Advanced Search
umbrella site table of contents purchase content feedback help button home button home button

Gudbjartsson T, Aranki S, Cohn LH. Mechanical/Bioprosthetic Mitral Valve Replacement.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:951986.

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Similar articles in this book
Right arrow Author home page(s):
Tomas Gudbjartsson
Sary Aranki
Lawrence H. Cohn
Google Scholar
Right arrow Articles by Gudbjartsson, T.
Right arrow Articles by Cohn, L. H.
Right arrow Articles citing this Article
Right arrow Search for Related Content
Right arrow Articles by Gudbjartsson, T.
Right arrow Articles by Cohn, L. H.
Related Collections
Right arrow Valve disease

Chapter 38

Mechanical/Bioprosthetic Mitral Valve Replacement

Tomas Gudbjartsson/ Sary Aranki/ Lawrence H. Cohn

????Mitral Stenosis
????Mitral Regurgitation
????Indications for Mechanical Valve Replacement
????Indications for Bioprosthetic Valve Replacement
????Mechanical Protheses
????Preoperative Management and Anesthetic Preparation
????Management of Cardiopulmonary Bypass for Mitral Valve Replacement
????Exposure of the Mitral Valve
????Minimally Invasive Mitral Valve Replacement
????Intracardiac Technique
????Associated Operations/Procedures
????Weaning Off Cardiopulmonary Bypass
????Early Results
????Late Results

Mitral valve surgery in the twentieth century began with Elliot Cutler's first operation at the Peter Bent Brigham Hospital in 1923.1 This was a mitral valvulotomy he had worked on for two years in the laboratory together with Samuel Levine, a Boston cardiologist. Two years later Dr. Suttar, an English surgeon, performed a mitral valvulotomy using his fingers to open up the commissures.2,3 The patient made an uneventful recovery, but Dr. Suttar did not perform any more mitral valvulotomies. It took two more decades until Dwight Harken and Charles Bailey independently continued the development of digital valvulotomy for rheumatic mitral stenosis.4,5 The results were dramatic and the operation gained popularity. This launched the modern area of cardiac surgery. But recurrence of the stenosis was still a major problem, even after the development of the cardiopulmonary bypass in the early 1950s, which enabled more complete open valvulotomy.

The next major step in the development of mitral valve surgery was the development of reliable, quality-controlled prosthetic heart valve devices in the late 1950s and early 1960s. For the first time devices were available that could effectively replace a diseased, nonreparable mitral valve with relative ease of implantation and assurance that the hemodynamic abnormalities from either mitral stenosis or regurgitation were corrected and maintained indefinitely.

The first successful prosthetic mitral valve replacement was a device implanted by Nina Braunwald at the National Institute of Health in 1959.6 This was a homemade device with artificial chordae made of polyurethane. Two years later the first reliable device for replacement of the mitral valve was produced on a commercial basis. This was the Starr-Edwards ball-and-cage mitral valve that resulted from the collaboration of Albert Starr, a cardiac surgeon in Portland, and Lowell Edwards, a mechanical engineer in Southern California.7 This prosthesis was a great success and became the "gold standard" for many years, until the late 1960s, when second- and third-generation prosthetic valves began to appear. Although reliable hemodynamically, it was soon found that the Starr-Edwards valve had significant thromboembolic potential, particularly in the small ventricle, and aggressive anticoagulation was required to control thromboembolic events.8,9 The Silastic ball in the original prosthesis also had to be corrected because of inadequate durability.

During the next decade a vide variety of different ball-and-disk valves were developed, and their profile was considerably reduced by alterations in both the height of the valve and the type of occluder (Fig. 38-1). After a number of experimental valves were evaluated (without Food and Drug Administration supervision), one valve emerged as the leading prototype for the 1970s: the Bj?rk-Shiley tilting-disk valve, which was developed by Viking Bj?rk in Stockholm and Earl Shiley in California.10 This valve had better hemodynamics (larger cross-sectional area and less hemolysis) than the Starr-Edwards valve and consequently had a lower thromboembolic potential.1113 However, problems with thrombosis occurred when the anticoagulation was altered. When an engineering change was made to correct this problem in a later model (a concave-convex disk), a fracture in the strut ensued and the Bj?rk-Shiley prosthesis was taken off the market.14

View larger version (27K):
[in this window]
[in a new window]
FIGURE 38-1 (A) Profiles of mechanical mitral valve prostheses. (B) Profile of the ON-X mitral valve.

A third-generation prosthetic valve was developed in the late 1970s that became the valve of the 1980s: the bileaflet St. Jude Medical valve, which had improved hemodynamics compared to older valves with less stagnation of blood, more complete opening of the leaflets, and reduced incidence of thromboembolism.1525 Several other disk prostheses are currently available (see Fig. 38-1), all with flow characteristics similar to the St. Jude valve but still with a small but definite risk of hemorrhage related to anticoagulant therapy and thromboembolism.

As the first, second, and third generations of prosthetic valves were developed, biologic or tissue replacement devices were developed concomitantly. The biologic valves showed a much lower frequency of thromboembolism and long-term anticoagulation seemed to be unnecessary.

In the 1960s, investigators began to use formalin fixation to sterilize and fixate fresh heterograft tissue.26,27 But when it became apparent that this fixation was unrealiable because of collagen breakdown in valve cusps resulting in fibrosis and calcifications, glutaraldehyde fixation of porcine tissue began.28 This fixative stabilized collagen bonding in the valve cusps and led to increased durability. The glutaraldehyde-fixed porcine aortic valve, principally developed by Hancock in the United States (1970) and Carpentier in Paris (1976), was the first commercially available bioprosthetic valve.29,30 These valves revolutionized mitral valve surgery by providing a biologic alternative that allowed long-term use without the need for lifelong warfarin anticoagulation. Both the Hancock and the Carpentier-Edwards valves became enormously popular in the 1970s and studies showed excellent 5-year durability (95%). But in the early 1980s structural valve dysfunction (SVD) became more apparent, with 15% to 20% of the prostheses failing within 10 years. The rate of deterioration seemed to accelerate in younger patients, with the valve gradually wearing down as a result of different biologically mediated dysfunctional processes.3140

The first- and second-generation biologic valves were constructed from porcine aortic valves. Because of limited durability these valves have mostly been replaced by the third generation of biological valves, which still include porcine valves in addition to biomechanically engineered bovine pericardial valves. For this third generation of valves new technology has been incorporated aimed at improving valve longevity and hemodynamic function This has resulted in better mid-term results.4148 These techniques include low-pressure or no-pressure fixation, antimineralization processes of the tissues, and low-profile, semiflexible stents that better define the biomechanical properties of the leaflets.

This chapter discusses the surgical indications, operative techniques, and early and late follow-up after implantation of mechanical and bioprosthetic mitral valve devices. The valves that are discussed are those that are currently (2002) approved by the U.S. Food and Drug Administration (FDA). Figure 38-2 shows the current FDA-approved prosthetic mitral valve devices, including the Starr-Edwards ball-and-cage valve, the Omnicarbon tilting-disk valve, the Medtronic Hall tilting-disk valve, the St. Jude Medical bileaflet valve, the Carbomedics bileaflet valve, the ATS bileaflet valve, and the On-X bileaflet valve. The FDA-approved bioprosthetic valve devices are shown in Figure 38-3, and include the Hancock II porcine valve, the Carpentier-Edwards porcine valve, the Carpentier-Edwards pericardial valve, and the Mosaic porcine valve.

View larger version (216K):
[in this window]
[in a new window]
FIGURE 38-2 FDA-approved mechanical mitral valves. (A) Starr-Edwards ball-and-cage. (B) Medtronic-Hall tilting-disk. (C) Omnicarbon tilting-disk. (D) St. Jude Medical bifleaflet.

(Continued) FDA-approved mechanical mitral valves. (E) Carbomedics bileaflet. (F) ATS bileaflet. (G) ON-X bileaflet.


View larger version (129K):
[in this window]
[in a new window]
FIGURE 38-3 FDA-approved bioprosthetic mitral valves. (A) Hancock II porcine heterograft. (B) Carpentier-Edwards standard porcine heterograft. (C) Mosaic porcine heterograft. (D) Carpentier-Edwards pericardial bovine heterograft.


The indications for mitral valve replacement are variable and undergoing evolution. Because of increasing use of reparative techniques, particularly for mitral regurgitation, replacement or repair of a mitral valve often depends on the experience of the operating surgeon. Current indications for valve replacement pertain to those types of valve problems that are unlikely to be repaired by most surgeons or which have been shown to have poor long-term success after reconstruction. Indications are discussed according to (1) pathophysiologic states for needing operation, and (2) type of valve required (i.e., mechanical or bioprosthetic).

Mitral Stenosis

Mitral stenosis is almost exclusively caused by rheumatic fever, even though a definite clinical history only can be obtained in about 50% of patients. The incidence of mitral stenosis has decreased substantially in the United States in the last several decades because of effective prophylaxis of rheumatic fever. In some African and Asian countries, especially India, mitral stenosis is still very common. Two thirds of patients with rheumatic mitral stenosis are female.

The pathologic changes in rheumatic valvulitis are mainly fusion of the valve leaflets at the commissures; shortening and fusion of the cordae tendinae; and thickening of the leaflets due to fibrosis with subsequent stiffening, contraction, and calcification. Approximately 25% of patients have pure mitral stenosis, but an additional 40% have combined mitral stenosis and mitral regurgitation.49

Stenosis usually develops one or two decades after the acute illness of rheumatic fever with no or slow onset of symptoms until the stenosis becomes more severe. Limitation of exercise tolerance is usually the first symptom followed by dyspnea that can progress to pulmonary edema. New onset atrial fibrillation and risk for thromboembolism, hemoptysis, and pulmonary hypertension are other common symptoms in patients with mitral stenosis.

The diagnostic workup of the symptomatic patient with mitral stenosis should include a complete cardiac catheterization, including coronary angiography in any patient over the age of 40. Under age 40, echocardiographic findings of the mitral valve suffice in most symptomatic patients for the definition of mitral valve pathology unless there is a history of chest pain or coronary artery disease. Cardiac catheterization establishes the extent of mitral valve stenosis by determining valve gradients and valve area. Pulmonary artery pressure, which may be extremely high in long-standing cases of mitral stenosis, is also documented. In general, operation is prescribed when the mean valve area is 1.0 cm2 or less50,51 (normal mitral valve area: 46 cm2; however, with a "mixed" lesion of mitral stenosis and mitral regurgitation, the valve area in symptomatic patients occasionally may be as large as 1.5 cm2. Asymptomatic patients are generally not considered for surgery,50 but some authors recommend operation in asymptomatic patients with significant hemodynamic mitral stensosis (see Ch. 36).52 The degree of pulmonary artery pressure elevation secondary to mitral stenosis continues to be an area of concern for the mitral valve surgeon. Is there any level of pulmonary hypertension that is too high for mitral valve replacement in the current surgical era of improved intraoperative and postoperative care? There is still no definitive answer to this question, but most surgeons operate on patients with severe pulmonary hypertension (suprasystemic) with the knowledge that intensive postoperative respiratory and diuretic therapy are necessary to maintain relatively dry lungs and to reduce the risk of severe right ventricular failure. It has been known for over 25 years that after mitral valve replacement for mitral stenosis, pulmonary artery pressure decreases within hours in most patients and decreases more gradually over weeks and months in others.5358

The success with closed commissurectomies after World War II and the development of the Starr-Edwards valve in the early 1960s led to an enormous increase in operations for rheumatic mitral valve disease; that pattern became a decrease as rheumatic disease declined. In recent years, a small resurgence in rheumatic valve disease has been observed in emigr?s from Southeast Asia and Latin America. In the 1990s, balloon dilation of fibrotic, stenotic mitral valves became increasingly utilized.50,59,60 At the present time, percutaneous mitral balloon valve dilation is used in most cases of symptomatic noncalcified, fibrotic mitral stenosis. But even though this technique has been shown to be equivalent in the short run to closed mitral commissurectomy, especially in young patients, it is only indicated in a minority of patients, i.e., those with optimal valvular characteristiscs.50,61,62 Open mitral commissurotomy and valvuloplasty for such patients can be a successful operation,63 but other studies have shown better long-term results with mitral valve replacement using a mechanical valve.64 Many patients with chronic mitral stenosis now require valve replacement because the valve has developed significant dystrophic changes, including marked thickening and shortening of all chordae, obliteration of the subvalvular space, agglutination of the papillary muscles, and calcification in both annular and leaflet tissue. Aggressive decalcification and heroic reconstructive techniques for these extremely advanced pathologic valves generally have produced poor long-term results; nevertheless, some surgeons still advocate aggressive repairs in this subset of patients.65

Mitral Regurgitation

The etiology of mitral regurgitation is very diverse and the decision to recommend operation for patients with mitral regurgitation is more complex than for patients with mitral stenosis, except in cases of acute ischemic mitral regurgitation and endocarditis, where indications are more straightforward. The pathologic subsets that produce mitral regurgitation are related to a number of metabolic, functional, and anatomic abnormalities.66 These can be categorized into degenerative (mitral prolapse, ruptured/elongated chordae), rheumatic, infectious, and ischemic diseases of the mitral valve. Most of these entities are now amenable to mitral valve repair and reconstruction with and without the use of annuloplasty rings, as mentioned elsewhere in this book (see Ch. 37).

For any of the preceding major pathologic subsets, indica- tions for surgery in patients with mitral regurgitation vary from the asymptomatic patient with an enlarging but well-functioning left ventricle and atrium to severely depressed left ventricular function. Any symptomatic patient with significant mitral regurgitation (3+ to 4+) should be operated on, and operation should be considered in any relatively symptom-free individual if there is objective evidence of left ventricular deterioration and documented and significant increases in left ventricular end-systolic and end-diastolic volumes.6172

Regurgitation through the valve is usually measured with Doppler echocardiography, but MRI is another noninvasive technology for measuring the regurgitant flow and can provide measurements of ventricular end-diastolic/systolic volumes and ventricular mass.73 Left ventricular angiography can be helpful but is otherwise indicated for evaluating the coronary arteries preoperatively in patients older than 40 years.

It is important to stress that ejection fraction is a poor indicator of left ventricular function in patients with mitral regurgitation. Ejection fraction can be preserved in patients with irreversible left ventricular failure because of regurgitant flow through the valve.74,75 Depressed cardiac output (usually indicates severe left ventricular dysfunction, and results of surgery are not as favorable in these patients as they are in patients with normal ventricles.76 Compared to ejection fraction, measurements of end-systolic volume and diameter are more reliable noninvasive parameters to evaluate the status of the left ventricle and determine the optimal time for operation (see Ch. 36).77,78

Once the valve is exposed, indications for mitral valve replacement in patients with mitral regurgitation depend on the extent of the pathology in each patient and the reparative experience of the operating surgeon. Thus, in regurgitation from degenerative prolapsing myxomatous valves that have a high probability of reconstruction, mitral valve repair is indicated if the prolapse is generalized and local findings that decrease the probability of a successful repair are absent.63,7952 Similarly, if rheumatic mitral regurgitation, calcific deposits throughout the leaflet substance, and shortened chordae and papillary muscles are encountered, mitral valve replacement is the most prudent operation because the probability of successful repair is low.83 In ischemic mitral regurgitation, pathology that precludes satisfactory repair includes restrictive valve motion from shortened, scarred papillary muscles, an acutely infarcted papillary muscle, and rupture of chordae associated with extensive calcification of valve leaflets.8486 In endocarditis, mitral valve replacement may be required because of destruction of the valve leaflets and subvalvular mechanisms and annular abscess formation. Although repair of the valve and avoidance of prosthetic material are very desirable in septic situations, the extent of the destruction may preclude repair. Therefore, mitral valve replacement is required after careful debridement of the infectious tissue and reconstruction of the valve annulus.87,88

Indications for Mechanical Valve Replacement

Worldwide prosthetic (mechanical) mitral valve replacement is more common today than bioprosthetic mitral valve replacement, about 60% versus 40%, but in the United States the ratio is inverse. Currently available prosthetic valves in the United States, in descending order of popularity, are the bileaflet, the tilting-disk, and the ball-and-cage valve. For the young patient, the patient in chronic atrial fibrillation who requires long-term anticoagulation, or any patient who wants to minimize the chance of reoperation, a prosthetic valve should be chosen if valve replacement is required. The St. Jude Medical bileaflet valve is the most widely used prosthetic mitral valve at present because it has good hemodynamic characteristics and is easy to insert. Indications to choose one prosthetic or another vary primarily by surgeon preference and occasionally depending on the state of the annulus and whether or not there have been multiple previous operations. For example, infrequently the mitral annulus provides poor anchorage with subsequent perivalvular leak with the bileaflet or tilting-disk valve, which requires an everting suture technique. In this instance, the central-flow Starr-Edwards ball-and-cage valve with a bulky sewing ring may be chosen to reduce the probability of subsequent perivalvular leak. A low-profile mechanical valve is on the other hand preferable in a patient with a small left ventricular cavity to prevent obstruction of left ventricular outflow and impingement of the myocardium.

Indications for Bioprosthetic Valve Replacement

Patients in any age group in sinus rhythm who wish to avoid anticoagulation may prefer a bioprosthetic valve. This is especially true for patients in whom anticoagulation is contraindicated, for instance in patients with a history of gastrointestinal bleeding or those who have a high-risk occupation or lifestyle.89 A bioprosthetic valve is preferred in patients over age 70 and in sinus rhythm, since these valves deteriorate more slowly in older patients. In addition, as observed by Grunkemeier et al, some 60-year-olds may not outlive their prosthetic valves because of comorbid disease.90,91 Specifically, patients who require combined mitral valve replacement and coronary bypass grafting for ischemic mitral regurgitation and coronary artery disease have significantly reduced long-term survival as compared with patients who do not have concomitant coronary artery disease.92102; These individuals may avoid anticoagulation with little risk of reoperation.

As 20-year results have become available for various bioprostheses, it is clear that structural valve degeneration (SVD) is the most prominent drawback of these valves.31,33,103107 The durability of porcine valves is less with mitral bioprostheses than with aortic bioprostheses. The more rapid deterioration of mitral bioprostheses may be due to higher ventricular systolic pressures against the mitral cusps as compared with the diastolic pressures resisted by aortic bioprosthetic leaflets. Durability of bioprosthetic valves is directly proportional to age;108 deterioration occurs within months or a few years in children and young adults and only gradually over years in septuagenarians and octogenarians.33,40,42,43,92,93,103,109 Essentially all valves implanted into patients less than 60 years of age have to be replaced ultimately and valve failure is prohibitively rapid in children and in adults under 35 to 40 years of age; therefore, bioprosthesis are not advisable in these age groups.110,111 Nevertheless, there are still indications for mitral porcine bioprosthetic valves in young patients. In a woman who desires to become pregnant, a bioprosthesis may be used to avoid warfarin anticoagulation and fetal damage during pregnancy.112115 In patients with chronic renal failure and hypercalcemia related to hyperparathyroidism, bioprostheses have extremely limited durability and should therefore be avoided.

For the last decade there are several reports, mainly from European centers, utilizing unstented cryopreserved homografts116121 and stentless heterografts122124 for mitral valve replacements, particularly in patients with endocarditis. The prosthetic valve is transplanted, donor papillary muscles are reattached to recipient papillary muscles, and the annulus is sutured circumferentially. Only a few patients are included in these studies with a short follow-up, and long-term results are therefore not available. But recent reports suggest that these operations may be a feasible alternative to stented valve replacement in patients with endocarditis. Pulmonary autografts have also been used for replacing the mitral valve (Ross II procedure) but only in a few patients with very short follow-up.125,126

Mechanical Protheses

The designs of mechanical and bioprosthetic heart valves have evolved over the last four decades in an effort to develop the ideal replacement for the pathologic mitral valve. Biochemical and engineering advances have produced hemodynamic improvements and reduced morbidity from valve-related complications. The ideal valve, however, is not available, and the positive and negative characteristics of current valves must be considered when choosing the most appropriate valve for an individual patient. The optimal heart valve exerts minimal resistance to forward blood flow and allows only trivial regurgitant backflow as the occluder closes. The design must cause minimal turbulence and stasis in vivo during physiologic flow conditions. The valve must be durable enough to last a lifetime and must be constructed of biomaterials that are nonantigenic, nontoxic, nonimmunogenic, nondegradable, and noncarcinogenic. The valve also must have a low incidence of thromboembolism.

The opening resistance to blood flow is determined by the orifice diameter; the size, shape, and weight of the occluder; the opening angle; and the orientation of leaflet or disk occluders with respect to the plane of the mitral annular orifice for any given annular size. Least resistance to transvalvular blood flow during diastole for valves in the mitral position is provided by a large ratio of orifice to total annular area. A wide opening angle also improves the effective orifice area and results in decreased diastolic pressure gradients. With an increasing orifice diameter, however, more energy is lost across the valve as more backflow passes through the valve at end diastole and early systole. Table 38-1 shows hemodynamic assessments of each of the FDA-approved mitral valve prostheses for the most commonly used mitral valve sizes.16,24,25,46,127154 The results of in vivo assessments at rest by invasive (catheterization) or noninvasive (Doppler echocardiography) techniques are tabulated.

View this table:
[in this window]
[in a new window]
TABLE 38-1 Hemodynamics of mitral valve prostheses

Blood turbulence flowing across mitral valve devices results from impedance to forward or reverse flow. This impedance can be minimized by occluder design and orientation, central flow through the orifice, and limited struts or pivots extending into flow areas (Fig. 38-4). Hemolysis is the product of red blood cell destruction that is caused by cavitation and shearing stresses of turbulence, high-velocity flow, regurgitation, and mechanical damage during valve closure.155 Areas of perivalvular blood stagnation and turbulence increase platelet aggregation, activation of the coagulation proteins, and thrombus formation.

View larger version (19K):
[in this window]
[in a new window]
FIGURE 38-4 Flow characteristics of different mechanical valve designs. (a) Ball-and-cage. (B) Tilting-disk. (C) Bileaflet.

Dynamic regurgitation is a feature of all prosthetic valves and is the sum of the closing volume during occluder closure and the leakage volume that passes through the valve while it is closed. The closing volume is a function of the effective orifice area and the time needed for closure. Closure time is influenced by the difference between the opening and closing angles of the occluder and valve ring. Leakage volume is inherent to the design of the valve and depends on the amount of time the valve remains in the closed position.156 A small amount of regurgitant volume can be beneficial by minimizing stasis and reducing platelet aggregation; this decreases the incidence of valve thrombosis and valve-related thromboembolism.137

The Starr-Edwards Model 6120 is the only ball-and-cage mitral valve prosthesis currently approved for use in the United States by the FDA. It was introduced with its current design in 1965 after undergoing several engineering modifications and has been in use longer than any other type of mechanical valve (see Fig. 38-2A). The occluder is a barium-impregnated Silastic ball in a Stellite alloy cage that projects into the left ventricle. This valve has a large Teflon/polypropylene sewing ring that produces a relatively small effective orifice and larger diastolic pressure gradients as compared with other prosthetic valves of similar annular sizes. Leakage volumes are not inherent in the ball-and-cage design, and in contrast to other mechanical valves, the presence of regurgitation may indicate a pathologic process. The central ball occluder causes lateralization of forward flow and results in turbulence and cavitation that increase the risk of hemolysis and thromboembolic complications (see Fig. 38-4A). The incidence of thromboembolism has been shown to be higher with the Starr-Edwards valve compared to the bileaflet valves.9,157 Because the cage projects into the left ventricle, it is unwise to implant this valve in small left ventricles, where the cage may contact the ventricular wall or cause ventricular outflow obstruction.144

Tilting-disk mitral valve prostheses have better hemodynamic characteristics as compared with ball-and-cage valves (see Fig. 38-4B). The Medtronic Hall central pivoting-disk valve was introduced in 1977 and is based on engineering design modifications of the earlier Hall-Kaster valve (see Fig. 38-2B).158 The axis of the tilting disk was moved more centrally to allow greater blood flow through the minor orifice and to reduce stagnation in areas of low flow. The opening angle was originally increased to 78 degrees to decrease resistance to forward flow and later narrowed to 70 degrees when in vitro studies revealed an unacceptable regurgitant volume. The opening angle of 70 degrees produced regurgitation volumes of less than 5% of left ventricular stroke volume without significantly compromising forward flow. The disk occluder was allowed to slide out of the housing at the end of the closing cycle to provide a gap through which blood could flow to minimize stasis at the contact surfaces.158 The large opening angle and slim disk occluder along with a thinner sewing ring provide improved hemodynamics with comparably larger effective orifice areas and lower mean diastolic pressure gradients for each valve size. During implantation, the larger orifice should be oriented posteriorly when using the larger valve sizes to minimize the potential for disk impingement. Smaller valves (27 mm or less) should be oriented with the larger orifice anteriorly to optimize in vivo hemodynamics.136,159

The Omniscience tilting-disk valve is a second-generation device derived from improvements to the design of the Lillehei-Kaster pivoting-disk valve.160 This low-profile device has a pyrolytic disk eccentrically located in a one-piece titanium housing attached to a seamless Teflon sewing ring. Introduced in 1978, the Omniscience prosthesis includes several engineering modifications from prior devices in an effort to improve its hemodynamic function. The orifice-to-annular area ratio was increased to minimize resistance to forward flow. The opening angle of 80 degrees is relatively large to allow flow reserve in patients with high cardiac outputs and during exercise. Resulting increases in regurgitant volumes are minimized by the disk design. Turbulence is reduced by the curvature of the disk, and areas of stasis and shear stress are reduced by the eccentric location of the pivot axis, in an effort to decrease the risk of thrombosis, thromboembolism, and hemolysis. Retaining prongs are not utilized, and the lower profile reduces the risk of impingement.139 A potential hemodynamic disadvantage that has been the subject of debate is the possibility of incomplete disk opening in vivo. Clinical studies report postoperative mean opening angles of between 44.8 degrees136 and 75.9 degrees.161 Implicated factors causing this variation include valve sizing, orientation during implantation, and anticoagulation status.161,162 A subsequent generation of the Omniscience valve is the all-carbon Omnicarbon monoleaflet valve that was released in 2001 in the United States but has been in clinical use in Europe since 1984 (see Fig. 38-2C). The housing material is made of pyrolytic carbon instead of titanium. As a result of this change, the incidence of thromboembolism, valvular thrombosis, and reoperations was significantly decreased compared with that of the Omniscience valve protheses.163 For all of the tilting-disk valves meticulous surgical technique is important because retained leaflets or chordae can cause subvalvular interference and leakage.

The unique design of the bileaflet St. Jude Medical valve was introduced in 1977 and it is currently the prosthesis used most commonly worldwide (see Fig. 38-2D). Two separate pyrolytic carbon semi-disks in a pyrolytic carbon housing are attached to a Dacron sewing ring. The housing has two pivot guards that project into the left atrium. The bileaflet design produces three different flow areas through the valve orifice that provide overall a more uniform, central, and laminar flow than in the caged-ball and monleaflet tilting-disk design. The improved flow results in less turbulence and decreased transmitral diastolic pressure gradients156,164 (see Fig. 38-4C) at any annulus diameter size and cardiac output compared to caged-ball or single-leaflet tilting valves.165 The favorable hemodynamics in smaller sizes makes it especially useful in children.166 The central opening angle is 85 degrees, with a closing angle of 30 to 35 degrees, which, along with a thin sewing ring, provides a large effective orifice area for each valve size at the expense of greater regurgitant volumes, especially at low heart rates. Asynchronous closure of the valve leaflets in vivo also contributes to the regurgitant volume.167 The design of this prosthesis provides excellent hemodynamic function even in small sizes, in any rotational plane.168 The antianatomic plane, however, with the central slit between the leaflets oriented perpendicular to the opening axis of the native valve leaflets, decreases the potential risk of leaflet impingement by the posterior left ventricular wall.169

The Carbomedics bileaflet valve was approved by the FDA in 1986 (see Fig. 38-2E). This low-profile device is constructed of pyrolytic carbon and has no pivot guards, struts, or orifice projections to decrease blood flow impedance and turbulence through the valve.156 It has a rotatable sewing cuff design and is available with a more generous and flexible sewing cuff (the OptiForm variant) that confirms more easily to different patient anatomies. The leaflet opening angle is 78 degrees, which, with the bileaflet design, provides a relatively large effective orifice area and transvalvular diastolic pressure differences only slightly greater than the St. Jude Medical bileaflet valve. Rapid synchronous leaflet closure reduces closing regurgitant volumes to less than that of the Bj?rk-Shiley pivoting-disk prosthesis, which has an opening angle of 60 degrees. Leakage volume, however, is greater with Carbomedics valves because of backflow through gaps around pivots. Because of its narrow closing angle and large leakage volume, the Carbomedics valve does not reduce the relatively large regurgitant volume associated with the bileaflet design. Although this valve has good hemodynamic function overall, in the mitral position, the 25-mm Carbomedics valve has a relatively high diastolic pressure gradient and large regurgitant energy loss across the valve, especially at high flows. Hemodynamic studies suggest that the Carbomedics valve should be avoided in patients with a small mitral valve orifice.156

The ATS (Advancing The Standard) mechanical prosthesis has been in clinical use in the United States since 2000. Similar to the Carbomedics valve, the ATS valve is a low-profile bileaflet prosthesis with a pyrolytic housing and pyrolytic carbon leaflets containing graphite substrate (see Fig. 38-2F). The pivot areas are located entirely within the orifice ring and the valve leaflets hinge on convex pivot guides on the carbon orifice ring. This design minimizes the overall height of the valve and provides wider orifice area, and the absence of cavities in the valve ring theoretically reduces stasis or eddy currents that may develop. Valve noise, a bothersome problem for some patients, is also reduced by this design.170 The opening angle is up to 85 degrees and the sewing cuff is constructed of double velour polyester fabric that is mounted to a titanium stiffening ring, which enables the surgeon to rotate the valve orifice during and after implantation.

The prosthesis most recently approved by the FDA (2002) is the On-X valve. It has a bileaflet design similar to the St. Jude Medical, Carbomedics, and ATS prostheses with comparable hemodynamic performance, i.e., a relatively large orifice diameter and a wide opening angle (90 degrees) (see Fig. 38-2F). Instead of silicon-alloyed pyrolytic carbon, as used in the other mechanical prosthesis, the On-X valve is made of pure pyrolytic carbon. This material is stronger and tougher than silicon alloyed carbon171 and allows incorporation of hydrodynamically efficient features to the valve orifice, such as increased orifice length and a flared inlet that reduces transvalvular gradient.152 Early clinical results are promising172 and the valve produces very little hemolysis with postoperative levels of serum lactate dehydrogenase in the normal range.173



The porcine bioprosthetic mitral valves are designed to mimic the flow characteristics of the in situ aortic valve. The Hancock I mitral valve bioprosthesis was introduced in 1970. It has three glutaraldehyde-preserved porcine aortic valve leaflets on a polypropylene stent attached to a Dacron-covered silicone sewing ring. The design allows for central laminar flow through the valve, which tends to decrease diastolic pressure gradients and minimize turbulence.164 The stent, however, impedes forward flow and results in relatively large diastolic pressure gradients across the bioprosthesis. The stent and the large sewing ring contribute to effective orifice areas that are smaller than those of size-matched mechanical valves (see Table 38-1).

The Hancock II porcine bioprosthesis is the more modern version of the Hancock I prosthesis (see Fig. 38-3A). The stent is made of Delrin with a scalloped sewing ring and reduced stent profile. The leaflets are fixated in glutaraldehyde at low pressure and subsequently for a prolonged period at high pressure. To retard calcification, the leaflets are treated with sodium dodecyl sulfate.

The Carpentier-Edwards porcine valve utilizes a flexible stent to decrease the stress of leaflet flexion while maintaining its overall configuration (see Fig. 38-3B).144 The effective orifice-to-total-annulus area ratio for the Carpentier-Edwards valve is relatively small, but exercise studies show that the effective orifice area increases significantly with increased blood flow across the valve; diastolic gradients also increase, although to a lesser degree.131,138,174 Porcine bioprostheses in the mitral position should be avoided in patients with small left ventricles because of the possibility of ventricular rupture or left ventricular outflow obstruction caused by the large struts.174

The Mosaic porcine bioprosthesis is a third-generation bioprosthesis utilizing the Hancock II stent (see Fig. 38-3C). It was introduced in the United States in 2000 and has a Delrin stent, scalloped sewing ring, and reduced stent profile. The valve tissue is pressure-free fixed with glutaraldehyde and the prosthesis is treated with alpha oleic acid (AOA) to retard calcification.


Previous studies indicated poor durability of pericardial valves, namely, the Ionescu-Shiley valve, caused by leaflet tearing. This led to significant changes in design, including mounting of the pericardium completely within the stent, causing less leaflet abrasion and increased durability. The Carpentier-Edwards pericardial valve uses bovine pericardium as material to fabricate a trileaflet valve that is cut, fitted, and sewn onto a flexible Elgiloy wire frame for stress reduction (see Fig. 38-3D). The tissue is preserved with glutaralderhyde with no applied pressure and the leaflets are treated with the calcium mitigation agent XenoLogiX. Compared to the Carpentier-Edwards porcine bioprosthesis, the stent profile is reduced. Long-term durability for the Carpentier-Edwards pericardial valve is strong and compared to third-generation porcine valves, valve-related complications are similar (see discussion later in this chapter).

Hemodynamically, pericardial valves provide the best solution to flow problems. The design maximizes use of the flow area, which results in minimal flow resistance.175 Figure 38-5A shows how the cone shape of the open valve and circular valve orifice minimize flow disturbance compared to more irregular cone shape for the porcine valves that allow for central unimpeded flow (Fig. 38-5B).

View larger version (22K):
[in this window]
[in a new window]
FIGURE 38-5 Flow patterns for bioprosthetic valves. (A) Pericardial bioprosthesis. (B) Porcine bioprosthesis.

Structural valve deterioration is seen after long-term follow-up of patients with both porcine and pericardial bioprostheses and results in mitral stenosis or regurgitation or both. Hemodynamic studies early after operation and at 5 years reveal higher average diastolic pressure gradients and smaller effective orifice areas when compared in the same patients at the follow-up study. In some patients these changes are sufficiently severe to require reoperation as soon as 4 to 5 years postoperatively, and by 10 years the rate of primary tissue failure averages 30%. It then accelerates, and by 15 years postoperatively the actuarial freedom from bioprosthetic primary tissue failure has ranged from 35% to 71% (see Table 38-2). Most of these patients show hemodynamic evidence of valvular deterioration prior to any clinical signs or symptoms.131 Bioprosthetic valves have the advantage of low thrombogenicity, which must be weighed against poor long-term durability and subsequent hemodynamic deterioration and the risk of reoperation.

View this table:
[in this window]
[in a new window]
TABLE 38-2 Freedom from structural valve detorioration after mitral valve replacement with bioprotheses


Preoperative Management and Anesthetic Preparation

Congestive heart failure secondary to mitral stenosis can usually be treated with aggressive diuretic therapy and sodium restriction preoperatively. If the patient is in rapid atrial fibrillation, digoxin, beta blockers, and calcium channel antagonists can be used to slow down the ventricular rate. Patients with acute mitral regurgitation are often in cardiogenic shock, and they can be stabilized preoperatively with inotropes and arterial vasodilators to reduce systemic afterload. Intra-aortic balloon counterpulsation can also be used for this purpose. Symptoms of congestive heart failure in patients with chronic mitral regurgitation are treated with diuretics and oral vasodilators. The vasodilators lower the peripheral vascular resistance, and forward cardiac output is increased by reducing the regurgitant volume into the left atrium.

Preferred anesthesia for mitral valve replacement typically involves a combination of narcotic and inhalational agents.176 Ultimately, anesthetic management is dictated by the wide range of functional disabilities and hemodynamic abnormalities of patients who present for mitral valve replacement. For example, a cachectic patient with functional class IV mitral stenosis and severe pulmonary hypertension may require postoperative positive-pressure mechanical ventilation for 1 or 2 days to remove excess pulmonary fluid by diuresis, facilitate bronchial toileting, and provide optimal conditions for adequate gas exchange. Alternatively, young patients who require mitral valve surgery and present with less preoperative comorbidity may benefit from a short-acting, balanced anesthetic that can facilitate extubation within 6 hours following surgery.177

Monitoring should include arterial and venous lines, a urinary catheter, and a pulmonary artery catheter placed before bypass to measure pulmonary pressures and cardiac output. Following valve replacement, occasionally a left atrial catheter directly inserted through the left atrial incision can be helpful to allow measurement of pulmonary vascular resistance, but we do not use it routinely. Preoperative intravenous prophylactic antibiotics are administered to all patients and are continued for 2 postoperative days until lines are removed. Temporary ventricular pacing wires are placed, and in many instances temporary atrial pacing wires are placed for possible pacing or diagnosis of various atrial arrhythmias.

Management of Cardiopulmonary Bypass for Mitral Valve Replacement

Cardiopulmonary bypass is instituted by placing two right-angle cannulas into the superior and inferior venae cavae. We place a small (22F) plastic or metal cannula directly into the superior vena cava, above the sinoatrial node. The inferior caval cannula is placed at the entrance of the inferior vena cava, low in the right atrium. These insertion sites keep the caval catheters out of the operative field and yet maintain excellent bicaval drainage. An arterial cannula is placed in the distal ascending aorta. Bypass flows are approximately 1.5 L/min per m2, and moderate hypothermia (30?C) is used with vacuum-assisted suction. Myocardial protection includes antegrade and retrograde blood cardioplegia and profound myocardial hypothermia.178181 Retrograde cardioplegia is useful for all valve surgery to protect the ischemic left ventricle and to help remove ascending aorta bubbles. Antegrade cardioplegia, used as an initial loading dose, is augmented by intermittent retrograde cardioplegia every 20 minutes. This provides safer delivery of cardioplegia, because when the atrium is retracted during valve replacement, the aortic valve is distorted, and antegrade cardioplegia tends to fill the ventricle.

Exposure of the Mitral Valve

Evolution of meticulous and complicated methods of mitral valve repair and reconstruction has required optimal exposure of the mitral valve. In primary operations, median sternotomy, development of Sondergaard's plane, and incision of the left atrium close to the atrial septum provide excellent exposure.182,183 (Fig. 38-6). This incision is a ubiquitous one, and we have rarely seen indications for use of other incisions, such as the superior approach through the dome of the left atrium,186 the so-called biatrial incision popularized by Guiraudon et al,187 division of the superior vena cava,188,189 and the less common but occasionally useful trans-right atrial septal incision.186,190 The trans-right atrial incision has in some studies been related to higher incidence of junctional and nonsinus rhythm postoperatively,191 although this has not been confirmed by other studies.192

View larger version (33K):
[in this window]
[in a new window]
FIGURE 38-6 Exposure of the mitral valve. (A) Location of Sondergaard's plane. (B, C) Development of the interatrial plane. (D) Location of the left atrial incision. (E) Cross-sectional view.

Minimally Invasive Mitral Valve Replacement

Following advances in videoscopic and other minimally invasive techniques in many areas of surgery in the 1990s, similar techniques are now being increasingly used in cardiac surgery, especially in mitral valve surgery.

In 1996 we began minimally invasive valve surgery for patients who have isolated valvular pathology without concomitant coronary artery disease. Our experience at Brigham and Women's Hospital now totals over 400 patients, including mitral valve repairs and aortic and mitral valve replacements.

The minimally invasive approach for mitral valve surgery is usually accomplished with a 5- to 7-cm midline skin incision (Fig. 38-7A). The superior margin of the incision is 2 cm distal to the angle of Louis, and the incision then extends caudally to a point that is 2 cm proximal to the sterno-xyphoid junction. Partial lower sternotomy is performed with an oscillitating saw from the xyphoid process, up to the manubrium with angled incision made into the right 2nd intercostal space. The pericardium is incised vertically and pericardial stay sutures are placed at the right side of the pericardial edge (Fig. 38-7B). Suspension of the right side of the pericardial cradle to the sternal edges allows better exposure of the base of the heart. This approach allows excellent exposure of the left and right atrium and proximal ascending aorta. A slightly different approach is to access the right atrium through a right parasternal incision, excising the 3rd and 4th costal cartilage. This approach, which was used in some of the early cases of minimally invasive mitral surgery, was associated with significant incidence of lung herniation, and has been abandoned.

View larger version (54K):
[in this window]
[in a new window]
FIGURE 38-7 (A) Minimally invasive right thoracotomy and groin cannulation. (B) A right atrial incision is used to gain access to the mitral valve through the septum. (C) When the right atrium is incised, an incision is made in the atrial septum through the fossa ovalis. Retraction sutures, on both the right atrium and the atrial septum, of 2-0 silk, are then used to elevate the septum and to keep the left atrium open. The mitral valve will then be exposed (inset).

Cardiopulmonary bypass can be established in several different ways, depending upon the exposure of the ascending aorta and superior vena cava. The exposure depends on the habitus of the patient, as well as upon the relative sizes of the right atrium and ascending aorta. If easily accessible, the ascending aorta can be cannulated directly using a Seldinger technique with a flexible aortic cannula. Both femoral and internal jugular vein are cannulated percutaneously (see Fig. 38-7A). Percutaneous venous cannulation allows better visualization of the operative field, since none of the cannulas exit the sternotomy incision. We routinely use vacuum-assisted venous drainage, which allows the use of smaller diameter cannulas (21F femoral venous cannula, and 14F right internal jugular cannula). Tips of the cannulas are positioned in the distal parts of the superior and inferior vena cavae, respectively. The positioning of the cannulas is done under transesophageal echocardiographic guidance. After fibrillating the heart, the aortic cross-clamp is applied and antegrade blood cardioplegia is administered through the aortic root. Systemic temperature is lowered to 28?C. The valve is approached through the left atrium as described above, or more often the right atrium with a transseptal incision (see Fig. 38-7B). After the valve has been replaced with a standard technique, the atrium and septum (if opened) are closed with running 4-0 Prolene. Intracardiac air is always monitored by transesophageal echocardiography and alternate filling used to evacuate the air by manipulating the volume of the heart on bypass.

Safety and efficacy of minimally invasive mitral valve surgery have been confirmed in several reports.192195 Trauma seems to be less with the minimally invasive incisions, which is beneficial in regard to infections (including mediastinitis) and bleeding from the incision and the operative field, leading to lesser usage of homologous blood.193 There is also improved cosmesis with these incisions and postoperative pain seems to be considerably less than in patients with the median sternotomy. This can result in less requirement for pain medication, faster return to normal activity with less dependence on after-hospital stay, and after-hospital care without compromising results.

Femoral arterial and venous cannulation are tolerated well in the vast majority of patients, and are associated with minimal morbidity. One of the important technical aspects of cannulation is the use of a limited (23 cm) oblique suprainguinal incision just above femoral vessels. This incision, in contrast to the standard vertical incision, has been associated with minimal discomfort and low wound infection rate, since it does not transverse the inguinal skin crease, and is not exposed to stretching during hip flexion and ambulation. One of the rare potential risks of femoral arterial cannulation is the development of retrograde aortic dissection, or retrograde plaque embolization in patients with severe atherosclerotic disease of the descending aorta. We perform routine assessment of descending aorta with transesophageal echocardiography prior to cannulation. De-airing the heart is more complex because the apex of the heart is not accessible, the heart is only partially visible through the 5- to 7-cm incision, and the left atrial appendage cannot be invaginated. Flooding the operative field with continuous CO2 can be beneficial in reducing intracardial air, and by manipulating the volume of the heart on bypass and alternating the position of the patient, air can be effectively evacuated. This is done under the guidance of transesophageal echocardiography, which is used in most patients undergoing minimally invasive mitral surgery. If transesophageal echocardiography is contraindicated, for instance because of esophageal diverticulum, the assessment of the mitral apparatus as well as de-aring of the heart chambers can be performed with direct epicardial echocardiography. If concomitant coronary artery bypass graft is needed, a full sternotomy is necessary.

Intracardiac Technique

Operation entails secure fixation of a valve prosthesis to the annulus by reliable suture techniques without damage to adjacent structures or myocardium and without tissue interference with valve function. Implantation should prevent injury to anatomic structures surrounding the mitral valve annulus. Figure 38-8 shows the proximity of important cardiac structures near the mitral valve annulus. These include the circumflex coronary artery within the atrioventricular (AV) groove, the left atrial appendage, the aortic valve in continuity with the anterior mitral curtain, and the AV node.

View larger version (32K):
[in this window]
[in a new window]
FIGURE 38-8 Location of important structures surrounding the mitral annulus. (Courtesy of David Bichell, M.D.)

An accumulation of laboratory and clinical evidence indicates that preservation of papillary musclechordal attachments to the annulus is important for maintenance of left ventricular function. In patients with mitral stenosis with agglutinated, fibrotic chordae and papillary muscles, preservation of these structures probably has little effect on left ventricular dysfunction but does protect the AV groove from rupture by preserving the posterior leaflet. However, preservation of the posterior mitral leaflet may preclude an adequately sized prosthesis. If fibrotic, agglutinated chordae and the posterior leaflet are excised, placement of artificial Gore-Tex chordae to reattach the papillary muscles to the annulus may improve early and late preservation of cardiac output.196,197 In patients with mitral regurgitation, however, it is important to preserve as much of the papillary muscle and annular interaction as possible. This can be achieved by a variety of techniques, as shown in Figure 38-9. The anterior leaflet may be partially excised and brought to the posterior leaflet198 (Fig. 38-9) or can be partially excised and "furled" to the anterior annulus by a running Prolene suture (Fig. 38-9B).199201

View larger version (33K):
[in this window]
[in a new window]
FIGURE 38-9 Techniques to maintain annularpapillary muscle continuity. (A) An ellipse is removed from the posterior leaflet, and a flap is cut form the central portion of the anterior leaflet. The anterior flap is flipped to the posterior annulus and tacked to the caudad edge of the posterior leaflet and the posterior annulus. Sutures anchoring the prosthesis include the annulus and anterior and posterior leaflet remnants to which chordae are attached. (B) The anterior leaflet is partially excised, and remnants are "furled" to the annulus by sutures used to insert the prosthesis.

Experimental and clinical evidence suggest that preservation of the conical shape of the ventricle is important to maintain normal cardiac output,208 and that assumption of a globular shape from cutting papillary muscles is deleterious to left ventricular function. Furthermore, preservation of the posterior leaflet and chordae has dramatically reduced the incidence of perforation of the left ventricle and atrioventricular separation during mitral valve replacement.64,209212

Suturing techniques vary according to the type of valve that is implanted. The bioprosthetic valve is preferentially inserted with the sutures placed from ventricle to atrium (noneverting or subannular). This has been shown to be the strongest type of suturing technique to the mitral annulus and is used with this valve and the central-flow Starr-Edwards ball-and-cage valve (Fig. 38-10A).213

View larger version (30K):
[in this window]
[in a new window]
FIGURE 38-10 Suturing techniques for prosthetic mitral valve implantation. Noneverting (subannular) sutures placed from ventricle to atrium for bioprosthetic or Starr-Edwards valves. Everting (supra-annular) sutures placed from atrium to ventricle for bileaflet or tilting-disk valves.

To ensure adequate function of bileaflet or tilting-disk valves, everting sutures (atrium to ventricle to sewing ring) should be used (Fig. 38-10B). This technique pushes the prosthetic valve out into the center of the orifice and minimizes any tissue interference of the prosthetic valve leaflets. This is particularly important if annular-chordal attachments are preserved. Teflon pledgeted sutures, particularly with the thin sewing rings of the currently available bileaflet and tilting-disk valves, should be used. If a bioprosthetic valve is inserted, a dental mirror is used to ensure that no annular suture is wrapped around a stent strut. A running Prolene suture for implantation of mitral valves has been advocated by some surgeons.214216 This technique makes a very clean suture line with minimal knots but runs the risk of valve dehiscence if an infection occurs.217

Prior to closure, the left atrial appendage is ligated by suture or stapled to prevent clot formation in patients with chronic atrial fibrillation, enlarged left atrium, or left atrial thrombus.218,219 The atrium is closed by a running Prolene suture, making sure that endocardial surfaces are approximated. If needed, a left atrial catheter can be inserted through the suture line.

Associated Operations/Procedures

Coronary bypass is the most common procedure performed with mitral valve replacement and should be performed first. This reduces lifting of the heart after the rigid mitral valve prosthesis is in place, which can cause rupture of the myocardium or the atrioventricular groove. This also allows cardioplegia to be delivered through the bypass grafts.

Tricuspid valve repair or replacements are usually performed after replacing the mitral valve. In these cases the mitral valve is often approached through the right atrium and a transseptal incision. After the mitral valve prosthesis is in place, the septum is closed and the aortic cross-clamp removed before proceeding with the tricuspid valve procedure.220

When both the aortic and mitral valves are replaced at the same operation, most surgeons begin with excising the aortic valve before proceeding with the mitral valve procedure. When excising the anterior mitral valve leaflet care must be taken not to injure the aortic annulus and the intra-annular region. The aortic valve is then sewn in after the mitral valve is in place.

Weaning Off Cardiopulmonary Bypass

We use transesophageal echocardiography for every valve operation and particularly for mitral valves, where excellent images can be obtained. If transesophageal echocardiography is contraindicated (e.g., because of esophageal disease), direct epicardial echocardiography can be used. The echocardiograms provide information about valve and left ventricular function, possible retained material in the left atrium including thrombus, and removal of intracardiac air.221223

A careful de-airing at the end of the operation is essential. The heart is vented through the left atrium and the ascending aorta and sometimes the left ventricle. Before the aortic cross-clamp is removed, the patient's head is lowered and the lungs inflated carefully to dislodge any air bubbles in the pulmonary vein. The operation table is then tilted from side to side, the left atrial appendage inverted, and the cardiac chambers aspirated if necessary. Once de-airing maneuvers are completed, and after the patient is completely rewarmed, venous return is partially occluded, and the heart is gradually volume loaded. Pulmonary artery pressures are monitored carefully. Pharmacologic agents, such as amrinone or dobutamine, particularly for right ventricular overload, are often used.

Postoperative care is directed toward the resumption of normal cardiac output, respiratory function, temperature control, electrolyte management, adequate renal flow, and prophylaxis against bleeding. Patients with low cardiac output are managed with a variety of pharmacologic agents after providing adequate volume loading. Left atrial and especially pulmonary arterial catheters are particularly helpful in determining optimal balancing of volume loading and myocardial function in the first hours following operation.224

Reduction of pulmonary interstitial fluid is aggressively pursued by diuresis in the intensive care unit in patients with severe pulmonary hypertension. Most patients with severe pulmonary hypertension can be extubated within 48 hours following surgery. Nutritional, respiratory, and general metabolic support are provided. Many patients with severe, long-standing mitral disease are cachectic and, despite preoperative nutritional support, are severely catabolic at the time of operation. These patients generally require longer periods of ventilatory support due to lack of respiratory muscle strength. They need aggressive nutritional support with nasogastric hyperalimentation to increase respiratory muscle strength. In patients with severe pulmonary hypertension and cardiac cachexia who require prolonged intubation, tracheostomy may be necessary to reduce ventilatory dead space and facilitate faster weaning and better pulmonary toilet. Tracheostomy is usually performed by the end of the first postoperative week.

Postoperative atrial arrhythmias are so common that their absence is unusual. Arrhythmias vary from rapid supraventricular tachycardias, usually atrial fibrillation, to junctional rhythm and heart block. These arrhythmias are treated by pharmacologic agents, pacemakers, or both. If rapid atrial fibrillation cannot be controlled pharmacologically and is destabilizing hemodynamically, emergency cardioversion is done to improve cardiac output. Pharmacologic management of supraventricular tachycardia is usually required but may precipitate the need for a prophylactic transvenous pacemaker if severe slowing of the heart rate occurs.

Anticoagulation is prescribed for all patients undergoing mitral valve replacement with either a mechanical or a bioprosthetic valve. In the first 6 weeks following operation, the incidence of atrial and other arrhythmias is high; thus these fluctuating rhythms mandate anticoagulation even if the basic rhythm is sinus. In addition to rhythm concerns, the left atrial incisions and the possibility of stasis in the left atrial appendage justify full anticoagulation with warfarin for all patients. Some surgeons advocate immediate intravenous heparin until therapeutic warfarin doses can be reached.225,226 Low molecular weight heparin (LMWH) can also be used.227 In our patients who are at high risk for thromboembolism, e.g., those with a large left atrium or an intra-atrial thrombus, we use dextran (500 mL every 24 hours) until the patient is anticoagulated with warfarin. We believe that this is safer than heparin in the early postoperative period and avoids blood accumulation in the pericardium.

The therapeutic International Normalized Ratio (INR) after mitral valve replacement is 2.5 to 3.5 depending on the type of valve, cardiac rhythm, and presence or absence of the aforementioned intraoperative risk factors for thromboembolism.51,218,219,225,227 Anticoagulation levels are in the low range for patients in sinus rhythm who received tissue valves. Patients who have mechanical valves need lifelong anticoagulation. Patients who have bioprosthetic valves are evaluated at 6 to 12 weeks for cardiac rhythm abnormalities. If they are in predominantly sinus rhythm, warfarin is stopped, and one aspirin tablet is given daily indefinitely. If the patient has continuous atrial fibrillation or fluctuating rhythms, anticoagulation with warfarin is continued. This is also true for patients with history of previous embolism or in whom thrombus is found in the left atrium at operation.

Warfarin is usually started on the second postoperative day. Addition of aspirin, 80 to 150 mg daily, together with warfarin may reduce the risk of thromboembolism.228 and should be given to all patients with prosthetic valves.166

Early Results

The hospital mortality for mitral valve replacement with and without coronary bypass grafting has decreased significantly since inception of mitral valve surgery. The current risk (2002) of elective primary mitral valve replacement with and without coronary bypass grafting is 5% to 9% in most studies (range 3.3% to 13.1%).24,25,42,43,47,104106,146,204,229233 Operative (30-day) mortality is related to myocardial failure, multisystem organ failure, bleeding, respiratory failure in the chronically ill, debilitated individual, diabetes, infection, stroke, and, very rarely, technical problems.102,234 Mortality is correlated with preoperative functional class, age, and preexisting coronary artery disease.233,235

Published results on mitral valve surgery have improved in recent years,236 probably because of preservation of papillary muscles, preventing midventricular rupture,209212 and preservation of the normal geometry of the left ventricle, which aids in the maintenance of early postoperative cardiac output.199,202,204206,208 Mitral valve replacement and coronary artery bypass surgery 15 to 20 years ago had an associated mortality of about 10% to 20%.17,94,237 This mortality risk also has decreased as myocardial protection has improved with the use of blood cardioplegia and retrograde methods of administration.178180 Some studies have indicated that the risk of combined mitral valve replacementcoronary artery bypass grafting is now no greater than that of mitral valve repair with an annuloplasty ring or mitral valve replacement without coronary artery bypass grafting.204,238 Other studies have shown significantly increased morbidity and mortality with the addition of coronary artery bypass graft.101 Figures from the database of the Society of Thoracic Surgeons indicate that both reoperation and emergency operation increase operative mortality (Fig. 38-11).239

View larger version (12K):
[in this window]
[in a new window]
FIGURE 38-11 Operative mortality for elective, urgent, emergency, and salvage procedures for primary operations and reoperations for mitral vavlular replacements. (Data used with permission from Society of Thoracic Surgeons.)

Late Results


In over 90% of patients following mitral valve replacement, functional class improves to at least class II. A small group of patients remain in class III or IV depending on left ventricular function prior to surgery or other coexisting morbidity.


The causes of late death in patients following mitral valve replacement are primarily chronic myocardial dysfunction, thromboemboli and stroke, endocarditis, anticoagulant-related hemorrhage, and coronary artery disease. The extent of left ventricular dysfunction and patient age, particularly if myocardial and coronary diseases are combined, also correlates with late mortality. The probability of survival after mitral valve replacement at 10 years is usually around 50% to 60% (range 42% to 81%, Table 38-3). 9,24,25,33,4048,103106,132,146,147,152,154,172,230233,240267 Long-term patient survival seems to be similar for patients with biologic and mechanical mitral valves.268271 Unlike patients with severe aortic regurgitation or aortic stenosis, arrhythmias seldom cause sudden death in patients following mitral valve replacement; however, a few die from thromboembolic stroke due to chronic atrial fibrillation.253 The fact that more than 50% of patients following mitral valve replacement are in chronic atrial fibrillation increases the propensity for thromboembolic stroke despite anticoagulation and for mechanical valve thrombosis if the anticoagulation protocol is altered. In addition, patients with older types of prosthetic valves who receive higher-intensity anticoagulation may develop severe anticoagulant hemorrhage.9,272

View this table:
[in this window]
[in a new window]
TABLE 38-3 Actuarial survival following mitral valve replacement

In patients with bioprosthetic valves, one of the important determinants of mortality is reoperation secondary to structural valve degeneration (Table 38-4).33,40,269,273276 Reoperative mitral valve replacement mortality has decreased significantly in the last 10 years to under 10%, even in patients who have required multiple mitral valve reoperations.178,180,277,278 At the Brigham and Women's Hospital, operative mortality was less than 6% for reoperative mitral valve operations from 1990 to 1995.178 Improved myocardial protection, earlier selection of patients for reoperation, and better perfusion techniques including frequent femorofemoral bypass to protect the right ventricle during incision and dissection of the heart are factors contributing to decreased mortality.178,204,275,276,279,280

View this table:
[in this window]
[in a new window]
TABLE 38-4 Freedom from reoperation


The major morbidity in patients following mitral valve replacement is structural valve deterioration of a bioprosthetic valve and thromboembolism and anticoagulant hemorrhage with a mechanical prosthesis. Both valve types develop perivalvular leak and infection.


Thromboembolism is perhaps the most common complication of both biologic and mechanical mitral prostheses but is more frequent in patients with mechanical valves. Chronic atrial fibrillation and local atrial factors, already discussed, increase the risk of thromboembolism in patients with mitral prostheses.20,31,40,249,273 A number of recent studies have summarized the thromboembolic potential of various valves.9,20,25,4044,46,47,104,105,146,149,151,154,157,161,172,225,230234,241,246,248250,252,254,255,257267,274,281,291 (Table 38-5), and it appears that the better the valve hemodynamics, the lower is the probability of thromboemboli. The incidence of thromboemboli in currently available bileaflet valves and tilting-disk valves is similar to that of bioprosthetic valvesabout 1.5% to 2.0% per patient-year. Thromboembolism in patients with mitral valve replacement is lower in those with a small left atrium, sinus rhythm, and normal cardiac output. It is much higher in patients with large left atria, chronic atrial fibrillation, and the presence of intra-atrial clot.218,219,292 Thrombosis of a mechanical valve, once a feared complication of tilting-disk valves,293295 is now relatively rare unless anticoagulation is stopped for any period of time. Valve thrombosis can be treated with thrombolytic agents if the patient is not in cardiogenic shock but requires surgery if the circulation is inadequate.296300

View this table:
[in this window]
[in a new window]
TABLE 38-5 Incidence of thromboembolism and anticoagulant-related hemorrhage


Bleeding related to anticoagulation is most commonly seen in the gastrointestinal, urogenital, and central nervous system and is usually proportionate to the INR. The incidence of anticoagulant-related hemorrhage has decreased markedly with hemodynamic improvements in mitral valve prostheses. New valves do not require the intensity of an anticoagulation of older prostheses. For example, the distinctive Starr-Edwards ball-and-cage valve requires an INR of 3.5 to 4.5.272 Patients with streamlined bileaflet or tilting-disk valves require an INR of between 2.5 and 3.5; thus the incidence of anticoagulant hemorrhage is significantly reduced in the newer, hemodynamically improved prostheses.243,301 Table 38-5 lists the incidence of anticoagulant hemorrhage with various bioprostheses and mechanical valves.


Structural valve degeneration (SVD) is the most important complication of the bioprosthetic valve. The probability of structural failure with currently available porcine valves (Hancock or Carpentier-Edwards) begins to increase 8 years after operation and reaches over 60% at 15 years.45,98,106,107,302 This finite durability is a major impediment to long-term success of these biologic prostheses, even though the failure rate in the patient 70 years of age or older is significantly less than in younger age groups.4145,9598,105,107,146,260,303 Structural valve degeneration presents as either mitral regurgitation from leaflet tear or as calcific mitral stenosis due to calcification of valve leaflets or as both. The appearance of a new murmur with new congestive symptoms should prompt a noninvasive investigation of the prosthesis and elective re-replacement if dysfunction is documented. Structural valve degeneration leading to reoperation is the cause for at least two thirds of the reoperations in patients with bioprostheses.40,276,278 The probabilities of structural valve degeneration at 5, 10, and 15 years of the four most commonly used biologic prostheses are shown in Table 38-6. 38,40,48,103107,146,147,242,251,257,274,287,296300,304,305 With current quality controls, the incidence of structural valve degeneration is virtually zero for bileaflet, tilting-disk, and ball-and-cage valves.

View this table:
[in this window]
[in a new window]
TABLE 38-6 Freedom from SVD by age


Perivalvular leak is an uncommon complication that is usually dependent on technical factors. Patient-related factors such as endocarditis or calcifications involving the annulus are also important. Perivalvular leak usually causes refractory hemolytic anemia in contrast to the more mild chronic hemolysis that is seen after implantation of some of the mechanical valves, especially the tilting-disk valves.306

Because of improved surgical techniques and the use of Teflon pledgets, the incidence of perivalvular leak has fallen, and is about 0% to 1.5% per patient-year for both mechanical and biologic valves.20,216,246,267,284,285,307 Perivalvular leak is slightly more common with the bileaflet valve than with the porcine valve because of the need for the everting suture technique and less bulky sewing ring.308,309 Surgery should be offered to all symptomatic patients and even patients with mild symptoms that require blood transfusions.310


Endocarditis is a feared complication after valve replacement, and prosthetic mitral valve endocarditis often presents difficult management problems related to timing of operation, type of operation, ability to securely fix the prosthesis, and operative and late survival. Mitral valve endocarditis is considerably less common than aortic prosthetic valve endocarditis,311,312 but when it does appear, it may present as septicemia, malignant burrowing infections, abscess formation, and septic emboli. With better antibiotic prophylaxis at the time of mitral surgery and improved prophylaxis for all patients having dental or other surgical procedures, the incidence of endocarditis is relatively low.

The incidence of prosthetic endocarditis is usually higher during the initial 6 months after surgery and thereafter declines to a lower but persistent risk.49 The probability of freedom from this morbid event is shown in Table 38-7 for both mechanical and bioprosthetic valves.9,24,25,4047,104,105,135,146,147,154,172,230233,239,241,242,247251,253255,257260,262265,267,274,283,285,288,290,291,303,304,313315 Biologic and mechanical valves seem to have a similar incidence of endocarditis, except for the initial months after valve implantation when mechanical prostheses carry a greater risk of infection.49,316

View this table:
[in this window]
[in a new window]
TABLE 38-7 Prosthetic valve endocarditis

The diagnosis and treatment of mitral perivalvular endocarditis are related to the infecting organism. The diagnosis is made by symptoms or the appearance of a new murmur, a septic embolus, or a large vegetation on echocardiogram. Blood cultures usually are positive, although a small percentage of patients have culture-negative endocarditis. Echocardiograms may show a rocking motion of the prosthesis and the presence of vegetations. The most frequent organisms are still Streptococcus and Staphylococcus; the latter is usually hospital acquired.317 Antibiotic therapy depends on the sensitivity of the organisms, but immediate high-dose intravenous therapy must begin as soon as possible. Experience indicates that a number of patients with bioprosthetic valvular endocarditis can be "cured" of low-potency organisms such as Streptococcus. However, it is unlikely that antibiotics alone can sterilize more virulent mitral valve infections, particularly Staphylococcus. These infections usually require urgent and sometimes emergent surgery because of invasion of the cardiac exoskeleton.

The surgical indications for mitral valve prosthetic endocarditis are persistent sepsis, congestive failure, perivalvular leak, large vegetations, or systemic infected emboli.87,318,319

Operative technique is similar to other mitral procedures with respect to anesthesia, monitoring, cardioplegia, left atrial incision, and exposure of the valve. Usually biologic valves are used for patients older than 65 years of age or younger patients with short life expectancy.311 Mechanical valves can be used in younger patients. Excision of the valve and debridement of the annulus and abscesses must be meticulous and extensive. All necrotic and infected tissue must be removed. After local application of an antibacterial solution such as Betadine and local antibiotic irrigation, the annulus and areas of tissue loss are reconstructed using autologous pericardium. Pericardium must be used to reconstruct the mitral valve annulus, and all sutures must be placed through the pericardial-lined annulus to obtain secure anchorage of the new prosthesis. Autologous pericardial pledgets can be made and used instead of conventional cloth pledgets to avoid synthetic material as much as possible. Examples of operative techniques for closure and repair of local abscesses and infectious destruction of the mitral valve annulus are shown in Figures 38-12 and 38-13.320

View larger version (28K):
[in this window]
[in a new window]
FIGURE 38-12 Preferred technique for inserting a mitral bioprosthesis in a patient with bacterial endocarditis. Pledgets are made from pericardium to minimize foreign material.


View larger version (31K):
[in this window]
[in a new window]
FIGURE 38-13 Repair of a mitral annular abscess using strips of pericardium. (A) Reconstruction of the annulus after debridement of the annulus. (B) The reconstructed annulus before insertion of the prosthesis.

Postoperative care should include at least 6 weeks of appropriate intravenous antibiotics. Hospital mortality is related primarily to ongoing sepsis, multisystem organ failure, or failure to eradicate the local infection and subsequent recurrent perivalvular leak.321,322 Recurrence of infection depends on the type of organism and the surgeon's ability to completely remove all areas of infection.318 Recurrence of infection is the single most important long-term complication.

Mitral valve replacement by mechanical or bioprosthetic valves revolutionized the care of patients with severe mitral valve disease. Reconstructive operations of the mitral valve have now assumed an equally important role for mitral regurgitation. A number of advanced lesions of the mitral valve still require mitral valve replacement with reliable devices. The bileaflet, tilting-disk, and ball-and-cage prosthetic valves are extremely reliable in terms of durability but require long-term anticoagulation and have a high risk of thromboembolism or thrombosis without anticoagulation. Bioprosthetic porcine valves, conversely, in patients in sinus rhythm do not need long-term anticoagulation and are used mainly in elderly patients who are not likely to outlive the valve and in women who plan to become pregnant and do not wish to accept the risks of warfarin or heparin. The long-term durability of these valves is limited, and the probability of valve failure at 15 years is at least 40%. Improvements in mechanical valve design and biologic valve preservation of collagen structure and resistance to calcification are ongoing and are the hopes for the future. In addition, there is renewed interest in homograft mitral valves, which may offer better long-term durability, as has been observed with cryopreserved homograft aortic valves. Improved valve design and development of better biomaterials will eventually improve clinical results; however, current FDA restrictions on the development and evaluation of new prosthetic valves have an important impact on this process.

  1. Cutler E, Levine S: Cardiotomy and valvulotomy for mitral stenosis: experimental observations and clinical notes concerning an operated case with recovery. Boston Med Surg 1923; 188:1023.
  2. Suttar H: Surgical treatment of mitral stenosis. BMJ 1925; 2:603.
  3. Harken DE, Ellis LE, Ware PF, Norman LR: The surgical treatment of mitral stenosis, I: valvuloplasty. N Engl J Med 1948; 239:801.
  4. Harken DE, Ellis LE, Ware PF, Norman LR: The surgical treatment of mitral stenosis, I: valvuloplasty. N Engl J Med 1948; 239:801.
  5. Bailey C: The surgical treatment of mitral stenosis (mitral comissurotomy). Dis Chest 1949; 15:377.
  6. Braunwald N, Cooper T, Morrow A: Complete replacement of the mitral valve. J Thorac Surg 1960; 40:1.
  7. Starr A, Edwards M: Mitral replacement: clinical experience with a ball valve prosthesis. Ann Thorac Surg 1961; 154:726.
  8. Cobanoglu A, Grunkemeier GL, Aru GM, et al: Mitral replacement: clinical experience with a ball-valve prosthesis: twenty-five years later. Ann Surg 1985; 202:376.[Medline]
  9. Miller DC, Oyer PE, Stinson EB, et al: Ten to fifteen year reassessment of the performance characteristics of the Starr-Edwards Model 6120 mitral valve prosthesis. J Thorac Cardiovasc Surg 1983; 85:1.[Medline]
  10. Bjork VO, Lindblom D The Monostrut Bjork-Shiley heart valve. J Am Coll Cardiol 1985; 6:1142.[Abstract]
  11. Nakano S, Kawashima Y, Matsuda H, et al: A five-year appraisal and hemodynamic evaluation of the Bjork-Shiley Monostrut valve. J Thorac Cardiovasc Surg 1991; 101:881.[Abstract]
  12. Jacobs M, Buckley M, WG Austen, et al: Mechanical valves: ten year follow-up of Starr-Edwards and Bjork-Shiley protheses. Circulation 1995; 72(suppl III): III-1.
  13. Thulin LI, Bain WH, Huysmans HH, et al: Heart valve replacement with the Bjork-Shiley Monostrut valve: early results of a multicenter clinical investigation. Ann Thorac Surg 1988; 45: 164.[Abstract]
  14. Ostermeyer J, Horstkotte D, Bennett J, et al: The Bjork-Shiley 70 degree convexo-concave prosthesis strut fracture problem (present state of information). Thorac Cardiovasc Surg 1987; 35:71.[Medline]
  15. Gabbay S, McQueen DM, Yellin EL, et al: In vitro hydrodynamic comparison of mitral valve prostheses at high flow rates. J Thorac Cardiovasc Surg 1978; 76:771.[Abstract]
  16. Chaux A, Gray RJ, Matloff JM, et al: An appreciation of the new St. Jude valvular prosthesis. J Thorac Cardiovasc Surg 1981; 81:202.[Abstract]
  17. Arom KV, Nicoloff DM, Kersten TE, et al: Six years of experience with the St. Jude Medical valvular prosthesis. Circulation 1985; 72:II153.
  18. Duncan JM, Cooley DA, Reul GJ, et al: Durability and low thrombogenicity of the St. Jude Medical valve at 5-year follow-up. Ann Thorac Surg 1986; 42:500.[Abstract]
  19. Edmunds LH Jr: Thrombotic and bleeding complications of prosthetic heart valves. Ann Thorac Surg 1987; 44:430.[Abstract]
  20. Czer LS, Chaux A, Matloff JM, et al: Ten-year experience with the St. Jude Medical valve for primary valve replacement. J Thorac Cardiovasc Surg 1990; 100:44.[Abstract]
  21. Fiore AC, Naunheim KS, D'Orazio S, et al: Mitral valve replacement: randomized trial of St. Jude and Medtronic-Hall prostheses. Ann Thorac Surg 1992; 54:68.[Abstract]
  22. Hayashi J, Oguma F, Tsuchida S, et al: Review of ten years' use of the St. Jude Medical prosthetic valve replacement and post-operative management at Nigata University Hospital. Acta Med Biol 1993; 41:81.
  23. O'Kane BC, Gladstone D, et al: The St. Jude prosthesis: a thirteen year experience. J Thorac Cardiovasc Surg 1994; 108:221.[Abstract/Free?Full?Text]
  24. Fiore AC, Barner HB, Swartz MT, et al: Mitral valve replacement: randomized trial of St. Jude and Medtronic Hall prostheses. Ann Thorac Surg 1998; 66:707.[Abstract/Free?Full?Text]
  25. Remadi JP, Baron O, Roussel C, et al: Isolated mitral valve replacement with St. Jude medical prosthesis: long-term results: a follow-up of 19 years. Circulation 2001; 103:1542.[Medline]
  26. Carpentier A: From valvular xenograft to valvular bioprosthesis: 19651970. Ann Thorac Surg 1989; 48:S73.
  27. Binet JP: Pioneering in heterografts. Ann Thorac Surg 1989; 48:S71.
  28. Carpentier A, Lemaigre G, Robert L, et al: Biological factors affecting long-term results of valvular heterografts. J Thorac Cardiovasc Surg 1969; 58:467.[Medline]
  29. Kaiser GA HW, Lukban SB, Litwak RS: Clinical use of a new design stented xenograft heart valve prosthesis. Surg Forum 1969; 20:137.[Medline]
  30. Carpentier A: Principles of Tissue Valve Transplantation. London, Butterworths, 1971.
  31. Cohn LH: Atrioventricular valve replacement with a Hancock porcine xenograft. Ann Thorac Surg 1991; 51:683.[Abstract]
  32. Pupello P, Bessone L, Blank R, et al: The porcine bioprosthesis: patient age as a factor in predicting failure in Bodnar E, Yacoub M (eds): Biological and Bioprosthetic Valves. New York, Yorke Medical Books, 1986; p 130.
  33. Bernal JM, Rabasa JM, Lopez R, et al: Durability of the Carpentier-Edwards porcine bioprosthesis: role of age and valve position. Ann Thorac Surg 1995; 60:S248.
  34. Geha AS, Laks H, Stansel HC Jr, et al: Late failure of porcine valve heterografts in children. J Thorac Cardiovasc Surg 1979; 78:351.[Abstract]
  35. Thandroyen FT, Whitton IN, Pirie D, et al: Severe calcification of glutaraldehyde-preserved porcine xenografts in children. Am J Cardiol 1980; 45:690.[Medline]
  36. Jamieson WR, Rosado LJ, Munro AI, et al: Carpentier-Edwards standard porcine bioprosthesis: primary tissue failure (structural valve deterioration) by age groups. Ann Thorac Surg 1988; 46: 155.[Abstract]
  37. Jamieson WR, Tyers GF, Janusz MT, et al: Age as a determinant for selection of porcine bioprostheses for cardiac valve replacement: experience with Carpentier-Edwards standard bioprosthesis. Can J Cardiol 1991; 7:181.[Medline]
  38. Jamieson WR, Burr LH, Miyagishima RT, et al: Structural deterioration in Carpentier-Edwards standard and supraannular porcine bioprostheses. Ann Thorac Surg 1995; 60:S241.
  39. Glower DD, White WD, Hatton AC, et al: Determinants of reoperation after 960 valve replacements with Carpentier-Edwards prostheses. J Thorac Cardiovasc Surg 1994; 107:381.[Abstract/Free?Full?Text]
  40. Akins CW, Carroll DL, Buckley MJ, et al: Late results with Carpentier-Edwards porcine bioprosthesis. Circulation 1990; 82:IV65.
  41. Pelletier LC, Carrier M, Leclerc Y, Dyrda I: The Carpentier-Edwards pericardial bioprosthesis: clinical experience with 600 patients. Ann Thorac Surg 1995; 60:S297.
  42. Poirer NC, Pelletier LC, Pellerin M, Carrier M: 15-year experience with the Carpentier-Edwards pericardial bioprosthesis. Ann Thorac Surg 1998; 66:S57.
  43. Marchand M, Aupart M, Norton R, et al: Twelve-year experience with Carpentier-Edwards PERIMOUNT pericardial valve in the mitral position: a multicenter study. J Heart Valve Dis 1998; 7: 292.[Medline]
  44. Neville PH, Aupart MR, Diemont FF, et al: Carpentier-Edwards pericardial bioprosthesis in aortic or mitral position: a 12-year experience. Ann Thorac Surg 1998; 66:S143.
  45. David TE, Ivanov J, Armstrong S, et al: Late results of heart valve replacement with the Hancock II bioprosthesis. J Thorac Cardiovasc Surg 2001; 121:268.
  46. Fradet GJ, Bleese N, Burgess J, Cartier PC: Mosaic valve international clinical trial: early performance results. Ann Thorac Surg 2001; 71:S273.[Abstract/Free?Full?Text]
  47. Thomson DJ, Jamieson WR, Dumesnil JG, et al: Medtronic Mosaic porcine bioprosthesis: midterm investigational trial results. Ann Thorac Surg 2001; 71:S269.[Abstract/Free?Full?Text]
  48. Takahara Y, Sudou Y, Murayama H, Nakamura T: [Long-term evaluation of the Carpentier-Edwards pericardial bioprosthesis]. Nippon Kyobu Geka Gakkai Zassh 1995; 43:1097.
  49. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  50. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  51. Bonow RO, Carabello B, de Leon AC Jr, et al: Guidelines for the management of patients with valvular heart disease: executive summary. A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). Circulation 1998; 98:1949.[Medline]
  52. Spencer FC: A plea for early, open mitral commissurotomy. Am Heart J 1978; 95:668.[Medline]
  53. Dalen JE, Matloff JM, Evans GL, et al: Early reduction of pulmonary vascular resistance after mitral-valve replacement. N Engl J Med 1967; 277:387.
  54. Kaul TK, Bain WH, Jones JV, et al: Mitral valve replacement in the presence of severe pulmonary hypertension. Thorax 1976; 31:332.[Abstract]
  55. Braunwald E, Braunwald N, Ross JJ, Morrow A: Effects of mitral valve replacement on the pulmonary vascular dynamics of patients with pulmonary hypertension. N Engl J Med 1965; 273: 509.
  56. Pasaoglu I, Demircin M, Dogan R, et al: Mitral valve surgery in the presence of pulmonary hypertension. Jpn Heart J 1992; 33:179.[Medline]
  57. Aris A, Camara ML: As originally published in 1988: Long-term results of mitral valve surgery in patients with severe pulmonary hypertension. Updated in 1996. Ann Thorac Surg 1996; 61:1583.[Free?Full?Text]
  58. Vincens JJ, Temizer D, Post JR, et al: Long-term outcome of cardiac surgery in patients with mitral stenosis and severe pulmonary hypertension. Circulation 1995; 92:II137.
  59. Reyes VP, Raju BS, Wynne J, et al: Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis. N Engl J Med 1994; 331:961.[Abstract/Free?Full?Text]
  60. Palacios IF, Tuzcu ME, Weyman AE, et al: Clinical follow-up of patients undergoing percutaneous mitral balloon valvotomy. Circulation 1995; 91:671.[Medline]
  61. National Heart, Lung, Blood Institute Ballon Valvuloplasty Registry: Complications and mortality of percutaneous balloon commissurotomy. Circulation 1992; 85:2014.[Medline]
  62. Tuzcu EM, Block PC, Palacios IF: Comparison of early versus late experience with percutaneous mitral balloon valvuloplasty. J Am Coll Cardiol 1991; 17:1121.[Abstract]
  63. Cohn LH, Allred EN, Cohn LA, et al: Long-term results of open mitral valve reconstruction for mitral stenosis. Am J Cardiol 1985; 55:731.[Medline]
  64. Glower DD, Landolfo KP, Davis RD, et al: Comparison of open mitral commissurotomy with mitral valve replacement with or without chordal preservation in patients with mitral stenosis. Circulation 1998; 98:II120.
  65. el Asmar B, Acker M, Couetil JP, et al: Mitral valve repair in the extensively calcified mitral valve annulus. Ann Thorac Surg 1991; 52:66.[Abstract]
  66. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  67. Carabello BA: Preservation of left ventricular function in patients with mitral regurgitation: a realistic goal for the nineties. J Am Coll Cardiol 1990; 15:564.[Medline]
  68. Mudge GH Jr,: Asymptomatic mitral regurgitation: when to operate? J Card Surg 1994; 9:248.[Medline]
  69. Stewart WJ: Choosing the "golden moment" for mitral valve repair. J Am Coll Cardiol 1994; 24:1544.[Medline]
  70. Ling LH, Enriquez-Sarano M, Seward JB, et al: Clinical outcome of mitral regurgitation due to flail leaflet. N Engl J Med 1996; 335:1417.[Abstract/Free?Full?Text]
  71. Tavel ME, Carabello BA: Chronic mitral regurgitation: when and how to operate. Chest 1998; 113:1399.[Free?Full?Text]
  72. Tribouilloy CM, Enriquez-Sarano M, Schaff HV, et al: Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications. Circulation 1999; 99:400.[Medline]
  73. Kizilbash AM, Hundley WG, Willett DL, et al: Comparison of quantitative Doppler with magnetic resonance imaging for assessment of the severity of mitral regurgitation. Am J Cardiol 1998; 81:792.[Medline]
  74. Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Echocardiographic prediction of survival after surgical correction of organic mitral regurgitation. Circulation 1994; 90:830.[Medline]
  75. Timmis SB, Kirsh MM, Montgomery DG, Starling MR: Evaluation of left ventricular ejection fraction as a measure of pump performance in patients with chronic mitral regurgitation. Cathet Cardiovasc Interv 2000; 49:290.[Medline]
  76. Kontos GJ Jr, Schaff HV, Gersh BJ, Bove AA: Left ventricular function in subacute and chronic mitral regurgitation: effect on function early postoperatively. J Thorac Cardiovasc Surg 1989; 98: 163.[Abstract]
  77. Borrow KM, Green LH, Mann T, et al: End-systolic volume as a predictor of postoperative left ventricular performance in volume overload from valvular regurgitation. Am J Med 1980; 68:655.[Medline]
  78. Wisenbaugh T, Skudicky D, Sareli P: Prediction of outcome after valve replacement for rheumatic mitral regurgitation in the era of chordal preservation. Circulation 1994; 89:191.[Medline]
  79. David TE, Armstrong S, Sun Z, Daniel L: Late results of mitral valve repair for mitral regurgitation due to degenerative disease. Ann Thorac Surg 1993; 56:7.[Abstract]
  80. Cohn LH, Couper GS, Aranki SF, et al: The long-term results of mitral valve reconstruction for the "floppy" valve. J Card Surg 1994; 9:278.[Medline]
  81. Cosgrove DM, Chavez AM, Lytle BW, et al: Results of mitral valve reconstruction. Circulation 1986; 74:I82.
  82. Braunberger E, Deloche A, Berrebi A, et al: Very long-term results (more than 20 years) of valve repair with Carpentier's techniques in nonrheumatic mitral valve insufficiency. Circulation 2001; 104:I8.
  83. Asmar BE, Perrier P, Couetil J, Carpentier A: Failures in reconstructive mitral valve surgery. J Med Liban 1991; 39:7.[Medline]
  84. Cohn LH, Rizzo RJ, Adams DH, et al: The effect of pathophysiology on the surgical treatment of ischemic mitral regurgitation: operative and late risks of repair versus replacement. Eur J Cardiothorac Surg 1995; 9:568.[Abstract]
  85. David T: Techniques and results of mitral valve repair for ischemic mitral regurgitation. J Card Surg 1994; 9(suppl II):II.
  86. Byrne JG, Aranki SF, Cohn LH: Repair versus replacement of mitral valve for treating severe ischemic mitral regurgitation. Coron Artery Dis 2000; 11:31.[Medline]
  87. Aranki SF, Adams DH, Rizzo RJ, et al: Determinants of early mortality and late survival in mitral valve endocarditis. Circulation 1995; 92:II143.
  88. Alexiou C, Langley SM, Stafford H, et al: Surgical treatment of infective mitral valve endocarditis: predictors of early and late outcome. J Heart Valve Dis 2000; 9:327.[Medline]
  89. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  90. Grunkemeier GL, Jamieson WR, Miller DC, Starr A: Actuarial versus actual risk of porcine structural valve deterioration. J Thorac Cardiovasc Surg 1994; 108:709.[Abstract/Free?Full?Text]
  91. Peterseim DS, Cen YY, Cheruvu S, et al: Long-term outcome after biologic versus mechanical aortic valve replacement in 841 patients. J Thorac Cardiovasc Surg 1999; 117:890.[Abstract/Free?Full?Text]
  92. Schoen FJ, Collins JJ Jr, Cohn LH: Long-term failure rate and morphologic correlations in porcine bioprosthetic heart valves. Am J Cardiol 1983; 51:957.[Medline]
  93. Jones EL, Weintraub WS, Craver JM, et al: Ten-year experience with the porcine bioprosthetic valve: interrelationship of valve survival and patient survival in 1,050 valve replacements. Ann Thorac Surg 1990; 49:370.[Abstract]
  94. DiSesa VJ, Cohn LH, Collins JJ Jr, et al: Determinants of operative survival following combined mitral valve replacement and coronary revascularization. Ann Thorac Surg 1982; 34:482.[Abstract]
  95. Jamieson WR, Burr LH, Munro AI, et al: Cardiac valve replacement in the elderly: clinical performance of biological prostheses. Ann Thorac Surg 1989; 48:173.[Abstract]
  96. Holper K, Wottke M, Lewe T, et al: Bioprosthetic and mechanical valves in the elderly: benefits and risks. Ann Thorac Surg 1995; 60:S443.
  97. Helft G, Tabone X, Georges JL, et al: Bioprosthetic valve replacement in the elderly. Eur Heart J 1995; 16:529.[Abstract/Free?Full?Text]
  98. David TE, Armstrong S, Sun Z: The Hancock II bioprosthesis at ten years. Ann Thorac Surg 1995; 60:S229.
  99. Angell WW, Pupello DF, Bessone LN, et al: Influence of coronary artery disease on structural deterioration of porcine bioprostheses. Ann Thorac Surg 1995; 60:S276.
  100. Jones EL, Weintraub WS, Craver JM, et al: Interaction of age and coronary disease after valve replacement: implications for valve selection. Ann Thorac Surg 1994; 58:378.[Abstract]
  101. Thourani VH, Weintraub WS, Craver JM, et al: Influence of concomitant CABG and urgent/emergent status on mitral valve replacement surgery. Ann Thorac Surg 2000; 70:778.[Abstract/Free?Full?Text]
  102. Edwards FH, Peterson ED, Coombs LP, et al: Prediction of operative mortality after valve replacement surgery. J Am Coll Cardiol 2001; 37:885.[Abstract/Free?Full?Text]
  103. Burdon TA, Miller DC, Oyer PE, et al: Durability of porcine valves at fifteen years in a representative North American patient population. J Thorac Cardiovasc Surg 1992; 103:238.[Abstract]
  104. van Doorn CA, Stoodley KD, Saunders NR, et al: Mitral valve replacement with the Carpentier-Edwards standard bioprosthesis: performance into the second decade. Eur J Cardiothorac Surg 1995; 9:253.[Abstract]
  105. Jamieson WR, Burr LH, Munro AI, Miyagishima RT: Carpentier-Edwards standard porcine bioprosthesis: a 21-year experience. Ann Thorac Surg 1998; 66:S40.
  106. Khan SS, Chaux A, Blanche C, et al: A 20-year experience with the Hancock porcine xenograft in the elderly. Ann Thorac Surg 1998; 66:S35.
  107. Corbineau H, Du Haut Cilly FB, Langanay T, et al: Structural durability in Carpentier Edwards Standard bioprosthesis in the mitral position: a 20-year experience. J Heart Valve Dis 2001; 10:443.[Medline]
  108. Cohn LH, Collins JJ Jr, Rizzo RJ, et al: Twenty-year follow-up of the Hancock modified orifice porcine aortic valve. Ann Thorac Surg 1998; 66:S30.
  109. Pupello DF, Bessone LN, Hiro SP, et al: Bioprosthetic valve longevity in the elderly: an 18-year longitudinal study. Ann Thorac Surg 1995; 60:S270.
  110. Jamieson WR, Tyers GF, Janusz MT, et al: Age as a determinant for selection of porcine bioprostheses for cardiac valve replacement: experience with Carpentier-Edwards standard bioprosthesis. Can J Cardiol 1991; 7:181.
  111. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  112. Jamieson WR, Miller DC, Akins CW, et al: Pregnancy and bioprostheses: influence on structural valve deterioration. Ann Thorac Surg 1995; 60:S282.
  113. Salazar E, Zajarias A, Gutierrez N, Iturbe I: The problem of cardiac valve prostheses, anticoagulants, and pregnancy. Circulation 1984; 70:I169.
  114. Sareli P, England MJ, Berk MR, et al: Maternal and fetal sequelae of anticoagulation during pregnancy in patients with mechanical heart valve prostheses. Am J Cardiol 1989; 63:1462.[Medline]
  115. Badduke BR, Jamieson WR, Miyagishima RT, et al: Pregnancy and childbearing in a population with biologic valvular prostheses. J Thorac Cardiovasc Surg 1991; 102:179.[Abstract]
  116. Acar C, Farge A, Ramsheyi A, et al: Mitral valve replacement using a cryopreserved mitral homograft. Ann Thorac Surg 1994; 57:746.[Abstract]
  117. Deac RF, Simionescu D, Deac D: New evolution in mitral physiology and surgery: mitral stentless pericardial valve. Ann Thorac Surg 1995; 60:S433.
  118. Gulbins H, Kreuzer E, Uhlig A, Reichart B: Mitral valve surgery utilizing homografts: early results. J Heart Valve Dis 2000; 9: 222.[Medline]
  119. Plunkett MD, Bond LM, Geiss DM: Allograft mitral valve replacement. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 1999; 2:95.[Medline]
  120. Kumar AS, Choudhary SK, Mathur A, et al: Homograft mitral valve replacement: five years' results. J Thorac Cardiovasc Surg 2000; 120:450.[Abstract/Free?Full?Text]
  121. Doty DB, Doty JR, Flores JH, Millar RC: Cardiac valve replacement with mitral homograft. Semin Thorac Cardiovasc Surg 2001; 13:35.[Medline]
  122. Vrandecic MO, Fantini FA, Gontijo BF, et al: Surgical technique of implanting the stentless porcine mitral valve. Ann Thorac Surg 1995; 60:S439.
  123. Walther T, Walther C, Falk V, et al: Early clinical results after stentless mitral valve implantation and comparison with conventional valve repair or replacement. Circulation 1999; 100:II78.
  124. Hofmann B, Cichon R, Knaut M, et al: Early experience with a quadrileaflet stentless mitral valve. Ann Thorac Surg 2001; 71:S323.[Abstract/Free?Full?Text]
  125. Kumar AS, Aggarwal S, Choudhary SK: Mitral valve replacement with the pulmonary autograft: the Ross II procedure. J Thorac Cardiovasc Surg 2001; 122:378.[Free?Full?Text]
  126. Mestres CA, Pomar JL: Mitral valve replacement with a pulmonary autograft: initial experience. J Heart Valve Dis 2000; 9:169.[Medline]
  127. Johnson AD, Daily PO, Peterson KL, et al: Functional evaluation of the porcine heterograft in the mitral position. Circulation 1975; 52:I40.
  128. Pyle RB, Mayer JE Jr, Lindsay WG, et al: Hemodynamic evaluation of Lillehei-Kaiser and Starr-Edwards prosthesis. Ann Thorac Surg 1978; 26:336.[Abstract]
  129. Chaitman BR, Bonan R, Lepage G, et al: Hemodynamic evaluation of the Carpentier-Edwards porcine xenograft. Circulation 1979; 60:1170.[Medline]
  130. Levine FH, Carter JE, Buckley MJ, et al: Hemodynamic evaluation of Hancock and Carpentier-Edwards bioprostheses. Circulation 1981; 64:II192.
  131. Pelletier C, Chaitman B, Bonan R, Dyrda I: Hemodynamic evaluation of the Carpentier-Edwards standard and improved annulus bioprostheses, in Cohn LH, Gallucci V (eds): Cardiac Bioprostheses; Proceedings of the Second International Symposium. New York, Yorke Medical Books, 1982; p 96.
  132. Sala A, Schoevaerdts JC, Jaumin P, et al: Review of 387 isolated mitral valve replacements by the Model 6120 Starr-Edwards prosthesis. J Thorac Cardiovasc Surg 1982; 84:744.[Abstract]
  133. Ubago J, Figueroa A, Colman T, et al: Hemodynamic evaluation of the Hancock bioprosthesis in the mitral position, in Cohn LH, Gallucci V (eds): Cardiac Bioprostheses; Proceedings of the Second International Symposium. New York, Yorke Medical Books, 1982; p 87.
  134. Medtronic Hall Prosthetic Heart Valve: 8 Year Experience. New York, Medtronic, 1985.
  135. Hall KV, Nitter-Hauge S, Abdelnoor M: Seven and one-half years' experience with the Medtronic-Hall valve. J Am Coll Cardiol 1985; 6:1417.[Abstract]
  136. Cordoba M, Almeida P, Martinez P, et al: Invasive assessment of mitral valve prostheses, in Rabago G, Cooley DA (eds): Heart Valve Replacement and Future Trends in Cardiac Surgery. New York, Futura, 1987.
  137. Horskotte D, Curtis J, Bircks W, Loogen F: Noninvasive evaluation of prosthetic heart valves, in Rabago G, Cooley DA (eds): Heart Valve Replacement and Future Trends in Cardiac Surgery. New York, Futura, 1987.
  138. Khuri SF, Folland ED, Sethi GK, et al: Six month postoperative hemodynamics of the Hancock heterograft and the Bjork-Shiley prosthesis: results of a Veterans Administration cooperative prospective randomized trial. J Am Coll Cardiol 1988; 12:8.[Abstract]
  139. Mikhail AA, Ellis R, Johnson S: Eighteen-year evolution from the Lillehei-Kaster valve to the Omni design. Ann Thorac Surg 1989; 48:S61.
  140. Tatineni S, Barner HB, Pearson AC, et al: Rest and exercise evaluation of St. Jude Medical and Medtronic Hall prostheses: influence of primary lesion, valvular type, valvular size, and left ventricular function. Circulation 1989; 80:I16.
  141. Johnston RT, Weerasena NA, Butterfield M, et al: Carbomedics and St. Jude Medical bileaflet valves: an in vitro and in vivo comparison. Eur J Cardiothorac Surg 1992; 6:267.[Abstract]
  142. Carbomedics Inc: Carbomedics prosthetic heart valve FDA-PMA summary of safety and effectiveness, thromboembolism and valve thrombosis complications. Application approved by FDA, September 29, 1993.
  143. Chambers J, Cross J, Deverall P, Sowton E: Echocardiographic description of the CarboMedics bileaflet prosthetic heart valve. J Am Coll Cardiol 1993; 21:398.[Abstract]
  144. Kirklin J, Barratt-Boyes B: Mitral valve disease with or without tricuspid valve disease, in Kirklin JW, Barratt-Boyes BG (eds): Cardiac Surgery, 2d ed. New York, Churchill Livingstone, 1993; p 463.
  145. Messner-Pellenc P, Wittenberg O, Leclercq F, et al: Doppler echocardiographic evaluation of the Omnicarbon cardiac valve prostheses. J Cardiovasc Surg (Torino). 1993; 34:195.[Medline]
  146. Aupart MR, Neville PH, Hammami S, et al: Carpentier-Edwards pericardial valves in the mitral position: ten-year follow-up. J Thorac Cardiovasc Surg 1997; 113:492.[Abstract/Free?Full?Text]
  147. Jasinski MJ, Kadziola Z, Keal R, Sosnowski AW: "Mosaic" Medtronic bioprosthetic valve replacement clinical results and hemodynamical performance. J Cardiovasc Surg (Torino) 2000; 41:181.[Medline]
  148. Fehske W, Kessel D, Kirchhoff PG, et al: Echocardiographic profile of the normally functioning Omnicarbon valve. J Heart Valve Dis 1994; 3:263.[Medline]
  149. Shiono M, Sezai Y, Sezai A, et al: Multi-institutional experience of the ATS open pivot bileaflet valve in Japan. Ann Thorac Cardiovasc Surg 1996; 1:21.
  150. Van Nooten G, Caes F, Francois K, et al: Clinical experience with the first 100 ATS heart valve implants. Cardiovasc Surg 1996; 4:288.[Medline]
  151. Westaby S, Van Nooten G, Sharif H, et al: Valve replacement with the ATS open pivot bileaflet prosthesis. Eur J Cardiothorac Surg 1996; 10:660.[Abstract]
  152. Chambers J, Ely JL: Early postoperative echocardiographic hemodynamic performance of the On-X prosthetic heart valve: a multicenter study. J Heart Valve Dis 1998; 7:569.[Medline]
  153. Hasegawa M: Clinical evaluation of ATS prosthetic valve by Doppler echocardiography: comparison with St. Jude Medical (SJM) valve. Ann Thorac Cardiovasc Surg 2000; 6:247.[Medline]
  154. Emery RW, Petersen RJ, Kersten TE, et al: The initial United States experience with the ATS mechanical cardiac valve prosthesis. Heart Surg Forum 2001; 4:346.[Medline]
  155. Horskotte D, Loogen F, Birckson B: Is the late outcome of heart valve replacement influenced by the hemodynamics of the heart valve substitute? in Horskotte D, Loogen F (eds): Update in Heart Valve Replacement: Proceedings of the 2nd European Symposium on the St. Jude Heart Valve. New York, Springer-Verlag, 1986; p 55.
  156. Butterfield M, Fisher J, Davies GA, Spyt TJ: Comparative study of the hydrodynamic function of the CarboMedics valve. Ann Thorac Surg 1991; 52:815.[Abstract]
  157. Agathos EA, Starr A: Mitral valve replacement. Curr Probl Surg 1993; 30:481.[Medline]
  158. Hall KV: The Medtronic-Hall valve: a design in 1977 to improve the results of valve replacement. Eur J Cardiothorac Surg 1992; (6 suppl 1):S64.
  159. Butchart E: Early clinical and hemodynamic results with Hall-Kaster valve, in Medtronic International Valve Symposium. Lisbon, Portugal, Congress Books, 1981.
  160. Grunkemeier GL, Starr A, Rahimtoola SH: Prosthetic heart valve performance: long-term follow-up. Curr Probl Cardiol 1992; 17:329.[Medline]
  161. Akalin H, Corapcioglu ET, Ozyurda U, et al: Clinical evaluation of the Omniscience cardiac valve prosthesis: follow-up of up to 6 years. J Thorac Cardiovasc Surg 1992; 103:259.[Abstract]
  162. DeWall R, Pelletier LC, Panebianco A, et al: Five-year clinical experience with the Omniscience cardiac valve. Ann Thorac Surg 1984; 38:275.[Abstract]
  163. Watanabe N, Abe T, Yamada O, et al: Comparative analysis of Omniscience and Omnicarbon protsthesis after aortic valve replacement. Jpn J Artif Organs 1989; 18:773.
  164. Emery RW, Nicoloff DM: St. Jude Medical cardiac valve prosthesis: in vitro studies. J Thorac Cardiovasc Surg 1979; 78:269.[Abstract]
  165. Nair CK, Mohiuddin SM, Hilleman DE, et al: Ten-year results with the St. Jude Medical prosthesis. Am J Cardiol 1990; 65:217.[Medline]
  166. Braunwald E: Valvular heart disease, in Braunwald E (ed): Heart Disease, A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, WB Saunders, 2001.
  167. Champsaur G, Gressier M, Niret J, et al: When are hemodynamics important for the selection of a prosthetic heart valve? in Horskotte D, Loogen F (eds): Update in Heart Valve Replacement: Proceedings of the 2nd European Symposium on the St. Jude Heart Valve. New York, Springer-Verlag, 1986; p 71.
  168. D'Alessandro L, Narducci C, Pucci A, et al: The use of mechanical valves in the treatment of valvular heart disease in Horskotte D, Loogen F (eds): Update in Heart Valve Replacement: Proceedings of the 2nd European Symposium on the St. Jude Heart Valve. New York, Springer-Verlag, 1986.
  169. Laub GW, Muralidharan S, Pollock SB, et al: The experimental relationship between leaflet clearance and orientation of the St. Jude Medical valve in the mitral position. J Thorac Cardiovasc Surg 1992; 103:638.[Abstract]
  170. Sezai A, Shiono M, Orime Y, et al: Evaluation of valve sound and its effects on ATS prosthetic valves in patients' quality of life. Ann Thorac Surg 2000; 69:507.[Abstract/Free?Full?Text]
  171. Ely JL, Emken MR, Accuntius JA, et al: Pure pyrolytic carbon: preparation and properties of a new material, On-X carbon for mechanical heart valve prostheses. J Heart Valve Dis 1998; 7:626.[Medline]
  172. Laczkovics A, Heidt M, Oelert H, et al: Early clinical experience with the On-X prosthetic heart valve. J Heart Valve Dis 2001; 10:94.[Medline]
  173. Birnbaum D, Laczkovics A, Heidt M, et al: Examination of hemolytic potential with the On-X(R) prosthetic heart valve. J Heart Valve Dis 2000; 9:142.[Medline]
  174. Gallucci V, Valfre C, Mazzucco A, et al: Heart valve replacement with the Hancock bioprosthesis: a 5- to 11-year follow-up. Cohn LH, Gallucci V (eds): Cardiac Bioprostheses: Proceedings of the Second International Symposium. New York, Yorke Medical Books, 1982.
  175. Black MM, Cochrame TT, Lawford PV: Design and flow characteristics, in Bodner E, Frater R (eds): Replacement Cardiac Valves. New York, McGraw-Hill, 1992; p 1.
  176. Jacson JM, Thomas SJ: Valvular heart disease, in Kaplan J, Reich D, Konstadt S (ed): Cardiac Anaesthesia. Philadelphia, WB Saunders, 1999; p 727.
  177. D'Attellis N, Nicolas-Robin A, Delayance S, et al: Early extubation after mitral valve surgery: a target-controlled infusion of propofol and low-dose sufentanil. J Cardiothorac Vasc Anesth 1997; 11:467.[Medline]
  178. Cohn LH, Aranki SF, Rizzo RJ, et al: Decrease in operative risk of reoperative valve surgery. Ann Thorac Surg 1993; 56:15.[Abstract]
  179. Buckberg GD: Antegrade/retrograde blood cardioplegia to ensure cardioplegic distribution: operative techniques and objectives. J Card Surg 1989; 4:216.[Medline]
  180. Singh AK: Warm retrograde cardioplegia: protection of the right ventricle in mitral valve operations. J Thorac Cardiovasc Surg 1993; 106:370.
  181. Buckberg GD: Development of blood cardioplegia and retrograde techniques: the experimenter/observer complex. J Card Surg 1998; 13:163.[Medline]
  182. Sondergaard T, Gotzsche M, Ottosen P, Schultz J: Surgical closure of interatrial septal defects by circumclusion. Acta Chir Scand 1955; 109:188.
  183. Larbalestier RI, Chard RB, Cohn LH: Optimal approach to the mitral valve: dissection of the interatrial groove. Ann Thorac Surg 1992; 54:1186.[Abstract]
  184. Hirt SW, Frimpong-Boateng K, Borst HG: The superior approach to the mitral valveis it worthwhile? Eur J Cardiothorac Surg 1988; 2:372.[Abstract]
  185. Saksena DS, Tucker BI, Lindesmith GG, et al: The superior approach to the mitral valve: a review of clinical experience. Ann Thorac Surg 1971; 12:146.[Medline]
  186. Utley JR, Leyland SA, Nguyenduy T: Comparison of outcomes with three atrial incisions for mitral valve operations: right lateral, superior septal, and transseptal. J Thorac Cardiovasc Surg 1995; 109:582.[Abstract/Free?Full?Text]
  187. Guiraudon GM, Ofiesh JG, Kaushik R: Extended vertical transatrial septal approach to the mitral valve. Ann Thorac Surg 1991; 52:1058.[Abstract]
  188. Selle JG: Temporary division of the superior vena cava for exceptional mitral valve exposure. J Thorac Cardiovasc Surg 1984; 88:302.[Abstract]
  189. Barner HB: Combined superior and right lateral left atriotomy with division of the superior vena cava for exposure of the mitral valve. Ann Thorac Surg 1985; 40:365.[Abstract]
  190. Kon ND, Tucker WY, Mills SA, et al: Mitral valve operation via an extended transseptal approach. Ann Thorac Surg 1993; 55:1413.[Abstract]
  191. Kumar N, Saad E, Prabhakar G, et al: Extended transseptal versus conventional left atriotomy: early postoperative study. Ann Thorac Surg 1995; 60:426.[Abstract/Free?Full?Text]
  192. Cosgrove DM 3rd, Sabik JF, Navia JL: Minimally invasive valve operations. Ann Thorac Surg 1998; 65:1535.[Abstract/Free?Full?Text]
  193. Cohn LH, Adams DH, Couper GS, et al: Minimally invasive cardiac valve surgery improves patient satisfaction while reducing costs of cardiac valve replacement and repair. Ann Surg 1997; 226:421.[Medline]
  194. Tam RK, Ho C, Almeida AA: Minimally invasive mitral valve surgery. J Thorac Cardiovasc Surg 1998; 115:246.[Free?Full?Text]
  195. Greelish JG, Cohn LH, Leacche M, et al: Early and late results of minimally invasive mitral valve surgery suggests earlier operations for mitral valve disease. J Thorac Cardiovasc Surg (in press).
  196. Cohn LH, Couper GS, Aranki SF, et al: The long-term results of mitral valve reconstruction for the "floppy" valve. J Card Surg 1994; 9:278.
  197. David TE, Bos J, Rakowski H: Mitral valve repair by replacement of chordae tendineae with polytetrafluoroethylene sutures. J Thorac Cardiovasc Surg 1991; 101:495.[Abstract]
  198. Douglas JJ: Mitral Valve Replacement. Philadelphia, WB Saunders, 1995.
  199. David TE: Mitral valve replacement with preservation of chordae tendinae: rationale and technical considerations. Ann Thorac Surg 1986; 41:680.[Abstract]
  200. David TE, Armstrong S, Sun Z: Left ventricular function after mitral valve surgery. J Heart Valve Dis 1995; 4(suppl 2):S175.
  201. Reardon MJ, David TE: Mitral valve replacement with preservation of the subvalvular apparatus. Curr Opin Cardiol 1999; 14:104.[Medline]
  202. Lillehei C, Levy M, Bonnabeau R: Mitral valve replacement with preservation of papillary muscles and chordae tendinae. J Thorac Cardiovasc Surg 1964; 47:532.
  203. Cohn LH, Kowalker W, Bhatia S, et al: Comparative morbidity of mitral valve repair versus replacement for mitral regurgitation with and without coronary artery disease. Ann Thorac Surg 1988; 45:284.[Abstract]
  204. Cohn LH, Couper GS, Kinchla NM, Collins JJ Jr: Decreased operative risk of surgical treatment of mitral regurgitation with or without coronary artery disease. J Am Coll Cardiol 1990; 16:1575.[Abstract]
  205. Miki S, Ueda Y, Tahata T, Okita Y: Mitral valve replacement with preservation of chordae tendineae and papillary muscles. Updated in 1995. Ann Thorac Surg 1995; 60:225.[Free?Full?Text]
  206. Horskotte D, Schulte HD, Bircks W, Strauer BE: The effect of chordal preservation on late outcome after mitral valve replacement: a randomized study. J Heart Valve Dis 1993; 2:150.[Medline]
  207. Okita Y, Miki S, Ueda Y, et al: Left ventricular function after mitral valve replacement with or without chordal preservation. J Heart Valve Dis 1995; 4(suppl 2):S181.
  208. Okita Y, Miki S, Ueda Y, et al: Mid-term results of mitral valve replacement combined with chordae tendineae replacement in patients with mitral stenosis. J Heart Valve Dis 1997; 6:37.[Medline]
  209. Asano K, Yagyu K: [Mitral valve replacement with preservation of the posterior leaflet, chordae tendineae and papillary muscles (modified MVP)]. Nippon Geka Gakkai Zasshi 1985; 86:233.[Medline]
  210. Cobbs BW Jr, Hatcher CR Jr, Craver JM, et al: Transverse midventricular disruption after mitral valve replacement. Am Heart J 1980; 99:33.[Medline]
  211. Spencer FC, Galloway AC, Colvin SB: A clinical evaluation of the hypothesis that rupture of the left ventricle following mitral valve replacement can be prevented by preservation of the chordae of the mural leaflet. Ann Surg 1985; 202:673.[Medline]
  212. Karlson KJ, Ashraf MM, Berger RL: Rupture of left ventricle following mitral valve replacement. Ann Thorac Surg 1988; 46:590.[Abstract]
  213. Chambers EP Jr, Heath BJ: Comparison of supraannular and subannular pledgeted sutures in mitral valve replacement. Ann Thorac Surg 1991; 51:60.[Abstract]
  214. Cooley DA: Simplified techniques of valve replacement. J Card Surg 1992; 7:357.[Medline]
  215. Antunes MJ: Technique of implantation of the Medtronic-Hall valve and other modern tilting-disc prostheses. J Card Surg 1990; 5:86.[Medline]
  216. Ibrahim M, O'Kane H, Cleland J, et al: The St. Jude Medical prosthesis: a thirteen-year experience. J Thorac Cardiovasc Surg 1994; 108:221.
  217. Dhasmana JP, Blackstone EH, Kirklin JW, Kouchoukos NT: Factors associated with periprosthetic leakage following primary mitral valve replacement: with special consideration of the suture technique. Ann Thorac Surg 1983; 35:170.[Abstract]
  218. Spencer F: Acquired Disease of the Mitral Valve, 4th ed. Philadelphia, WB Saunders, 1983.
  219. DiSesa VJ, Tam S, Cohn LH: Ligation of the left atrial appendage using an automatic surgical stapler. Ann Thorac Surg 1988; 46:652.[Abstract]
  220. Cohn LH: Tricuspid regurgitation secondary to mitral valve disease: when and how to repair. J Card Surg 1994; 9:237.[Medline]
  221. Bach DS, Deeb GM, Bolling SF: Accuracy of intraoperative transesophageal echocardiography for estimating the severity of functional mitral regurgitation. Am J Cardiol 1995; 76:508.[Medline]
  222. Jaggers J, Chetham PM, Kinnard TL, Fullerton DA: Intraoperative prosthetic valve dysfunction: detection by transesophageal echocardiography. Ann Thorac Surg 1995; 59:755.[Abstract/Free?Full?Text]
  223. Orsinelli DA, Pasierski TJ, Pearson AC: Spontaneously appearing microbubbles associated with prosthetic cardiac valves detected by transesophageal echocardiography. Am Heart J 1994; 128:990.[Medline]
  224. Meister S, Wolf N: Postoperative management of patients with implanted valvular prostheses, in Morse D, Steiner RM., Fernandez J (eds): Guide to Prosthetic Cardiac Valves. New York, Springer-Verlag, 1985; p 179.
  225. Jegaden O, Eker A, Delahaye F, et al: Thromboembolic risk and late survival after mitral valve replacement with the St. Jude Medical valve. Ann Thorac Surg 1994; 58:1721.[Abstract]
  226. Heras M, Chesebro JH, Fuster V, et al: High risk of thromboemboli early after bioprosthetic cardiac valve replacement. J Am Coll Cardiol 1995; 25:1111.[Abstract]
  227. Ezekowitz MD: Anticoagulation management of valve replacement patients. J Heart Valve Dis 2002; 11(suppl 1):S56.
  228. Laffort P, Roudaut R, Roques X, et al: Early and long-term (one-year) effects of the association of aspirin and oral anticoagulant on thrombi and morbidity after replacement of the mitral valve with the St. Jude medical prosthesis: a clinical and transesophageal echocardiographic study. J Am Coll Cardiol 2000; 35:739.[Abstract/Free?Full?Text]
  229. Peterffy A, Nagy Z, Vaszily M, et al: Valve surgery combined with myocardial revascularisation: report of 62 cases. Scand J Thorac Cardiovasc Surg 1989; 23:25.[Medline]
  230. Santini F, Casali G, Viscardi F, et al: The Carbomedics prosthetic heart valve: experience with 1,084 implants. J Heart Valve Dis 2002; 11:121.[Medline]
  231. Aoyagi S, Oryoji A, Nishi Y, et al: Long-term results of valve replacement with the St. Jude Medical valve. J Thorac Cardiovasc Surg 1994; 108:1021.[Abstract/Free?Full?Text]
  232. Nistal JF, Hurle A, Revuelta JM, Gandarillas M: Clinical experience with the CarboMedics valve: early results with a new bileaflet mechanical prosthesis. J Thorac Cardiovasc Surg 1996; 112:59.[Abstract/Free?Full?Text]
  233. Butchart EG, Li HH, Payne N, et al: Twenty years' experience with the Medtronic Hall valve. J Thorac Cardiovasc Surg 2001; 121:1090.[Abstract/Free?Full?Text]
  234. Cohn LH, Allred EN, Cohn LA, et al: Early and late risk of mitral valve replacement: a 12 year concomitant comparison of the porcine bioprosthetic and prosthetic disc mitral valves. J Thorac Cardiovasc Surg 1985; 90:872.[Abstract]
  235. Remadi JP, Bizouarn P, Baron O, et al: Mitral valve replacement with the St. Jude Medical prosthesis: a 15-year follow-up. Ann Thorac Surg 1998; 66:762.[Abstract/Free?Full?Text]
  236. Birkmeyer NJ, Marrin CA, Morton JR, et al: Decreasing mortality for aortic and mitral valve surgery in Northern New England. Northern New England Cardiovascular Disease Study Group. Ann Thorac Surg 2000; 70:432.[Abstract/Free?Full?Text]
  237. Brais MP, Bedard JP, Goldstein W, et al: Mitral valve replacement with Hancock porcine bioprostheses: up to 7-year follow-up. Can J Surg 1985; 28:119.[Medline]
  238. Oury JH, Cleveland JC, Duran CG, Angell WW: Ischemic mitral valve disease: classification and systemic approach to management. J Card Surg 1994; 9:262.[Medline]
  239. Society of Thoracic Surgeons: Data Analysis of the Society of Thoracic Surgeons National Cardiac Surgery Database: The Fifth YearJanuary 1996. Minneapolis, Summit Medical Systems, 1996.
  240. Teply JF, Grunkemeier GL, Sutherland HD, et al: The ultimate prognosis after valve replacement: an assessment at twenty years. Ann Thorac Surg 1981; 32:111.[Abstract]
  241. Damle A, Coles J, Teijeira J, et al: A six-year study of the Omniscience valve in four Canadian centers. Ann Thorac Surg 1987; 43:513.[Abstract]
  242. Cohn LH, Collins JJ Jr, DiSesa VJ, et al: Fifteen-year experience with 1678 Hancock porcine bioprosthetic heart valve replacements. Ann Surg 1989; 210:435.[Medline]
  243. DiSesa VJ, Collins JJ Jr, Cohn LH: Hematological complications with the St. Jude valve and reduced-dose Coumadin. Ann Thorac Surg 1989; 48:280.[Abstract]
  244. Vallejo JL, Gonzalez-Santos JM, Albertos J, et al: Eight years' experience with the Medtronic-Hall valve prosthesis. Ann Thorac Surg 1990; 50:429.[Abstract]
  245. Bortolotti U, Milano A, Testolin L, et al: The CarboMedics bileaflet prosthesis: initial experience at the University of Padova. Clin Rep 1991; 4.
  246. Rabelo R, Brasil J, Castro A, et al: CarboMedics bileaflet prosthesis: initial experience at the University of Padova. Clin Rep 1991; 4.
  247. Louagie Y, Noirhomme P, Aranguis E, et al: Use of the Carpentier-Edwards porcine bioprosthesis: assessment of a patient selection policy. J Thorac Cardiovasc Surg 1992; 104:1013.[Abstract]
  248. de Luca L, Vitale N, Giannolo B, et al: Mid-term follow-up after heart valve replacement with CarboMedics bileaflet prostheses. J Thorac Cardiovasc Surg 1993; 106:1158.[Abstract]
  249. Kratz JM, Crawford FA Jr, Sade RM, et al: St. Jude prosthesis for aortic and mitral valve replacement: a ten-year experience. Ann Thorac Surg 1993; 56:462.[Abstract]
  250. Peter M, Weiss P, Jenzer HR, et al: The Omnicarbon tilting-disc heart valve prosthesis: a clinical and Doppler echocardiographic follow-up. J Thorac Cardiovasc Surg 1993; 106:599.[Abstract]
  251. Sarris GE, Robbins RC, Miller DC, et al: Randomized, prospective assessment of bioprosthetic valve durability: Hancock versus Carpentier-Edwards valves. Circulation. 1993; 88:II55.
  252. Khan S, Chaux A, Matloff J, et al: The St. Jude Medical valve: experience with 1,000 cases. J Thorac Cardiovasc Surg 1994; 108: 1010.[Abstract/Free?Full?Text]
  253. Masters RG, Pipe AL, Walley VM, Keon WJ: Comparative results with the St. Jude Medical and Medtronic Hall mechanical valves. J Thorac Cardiovasc Surg 1995; 110:663.[Abstract/Free?Full?Text]
  254. Copeland JG 3rd: An international experience with the CarboMedics prosthetic heart valve. J Heart Valve Dis 1995; 4:56.[Medline]
  255. Copeland JG 3rd, Sethi GK: Four-year experience with the CarboMedics valve: the North American experience. North American team of clinical investigators for the CarboMedics prosthetic heart valve. Ann Thorac Surg 1994; 58:630.[Abstract]
  256. Hayashi J, Nakazawa S, Eguchi S, et al: Long-term outcome of patients who received Starr-Edwards valves between 1965 and 1977. Cardiovasc Surg 1996; 4:281.[Medline]
  257. Murakami T, Eishi K, Nakano S, et al: Aortic and mitral valve replacement with the Carpentier-Edwards pericardial bioprosthesis: 10-year results. J Heart Valve Dis 1996; 5:45.[Medline]
  258. Yamauchi M, Eishi K, Nakano K, et al: Valve replacement with the CarboMedics bileaflet mechanical prosthesis: clinical results at midterm. J Cardiovasc Surg (Torino). 1996; 37:285.[Medline]
  259. Godje OL, Fischlein T, Adelhard K, et al: Thirty-year results of Starr-Edwards prostheses in the aortic and mitral position. Ann Thorac Surg 1997; 63:613.[Abstract/Free?Full?Text]
  260. Glower DD, Landolfo KP, Cheruvu S, et al: Determinants of 15-year outcome with 1,119 standard Carpentier-Edwards porcine valves. Ann Thorac Surg 1998; 66:S44.
  261. Kuntze CE, Ebels T, Eijgelaar A, et al: Rates of thromboembolism with three different mechanical heart valve prostheses: randomised study. Lancet 1989; 1:514.[Medline]
  262. Camilleri LF, Bailly P, Legault BJ, et al: Mitral and mitro-aortic valve replacement with Sorin Bicarbon valves compared with St. Jude Medical valves. Cardiovasc Surg 2001; 9:272.[Medline]
  263. Misawa Y, Hasegawa T, Kato M: Clinical experience with the Omnicarbon prosthetic heart valve. J Thorac Cardiovasc Surg 1993; 105:168.[Abstract]
  264. Otaki M, Kitamura N: Six years' experience with the Omnicarbon valve prosthesis. Cardiovasc Surg 1993; 1:594.[Medline]
  265. Thevenet A, Albat B: Long term follow up of 292 patients after valve replacement with the Omnicarbon prosthetic valve. J Heart Valve Dis 1995; 4:634.[Medline]
  266. Iguro Y, Moriyama Y, Yamaoka A, et al: Clinical experience of 473 patients with the omnicarbon prosthetic heart valve. J Heart Valve Dis 1999; 8:674.[Medline]
  267. Torregrosa S, Gomez-Plana J, Valera FJ, et al: Long-term clinical experience with the Omnicarbon prosthetic valve. Ann Thorac Surg 1999; 68:881.[Abstract/Free?Full?Text]
  268. Hammermeister K, Sethi GK, Henderson WG, et al: Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trial. J Am Coll Cardiol 2000; 36:1152.[Abstract/Free?Full?Text]
  269. Cen YY, Glower DD, Landolfo K, et al: Comparison of survival after mitral valve replacement with biologic and mechanical valves in 1139 patients. J Thorac Cardiovasc Surg 2001; 122:569.[Abstract/Free?Full?Text]
  270. Grossi EA, Galloway AC, Miller JS, et al: Valve repair versus replacement for mitral insufficiency: when is a mechanical valve still indicated? J Thorac Cardiovasc Surg 1998; 115:389.[Abstract/Free?Full?Text]
  271. Sidhu P, O'Kane H, Ali N, et al: Mechanical or bioprosthetic valves in the elderly: a 20-year comparison. Ann Thorac Surg 2001; 71:S257.[Abstract/Free?Full?Text]
  272. Starr A: The Starr-Edwards valve. J Am Coll Cardiol 1985; 6:899.[Abstract]
  273. Myken PS, Caidahl K, Larsson P, et al: Mechanical versus biological valve prosthesis: a ten-year comparison regarding function and quality of life. Ann Thorac Surg 1995; 60:S447.
  274. Bortolotti U, Milano A, Mossuto E, et al: Porcine valve durability: a comparison between Hancock standard and Hancock II bioprostheses. Ann Thorac Surg 1995; 60:S216.
  275. Wideman FE, Blackstone EH, Kirklin JW, et al: Hospital mortality of re-replacement of the aortic valve: incremental risk factors. J Thorac Cardiovasc Surg 1981; 82:692.[Abstract]
  276. Perier P, Swanson J, Takriti A, et al: Decreasing operative risk in isolated valve re-replacement, in Bodnar E, Yacoub M (eds): Biological and Bioprosthetic Valves: Proceedings of the Third International Symposium. New York, Yorke Medical Books, 1986.
  277. Kazui T, Kimura N, Morikawa M, et al: [Reoperation of primary tissue failure of bioprosthesis in the mitral position]. Nippon Kyobu Geka Gakkai Zasshi 1991; 39:862.[Medline]
  278. Tyers GF, Jamieson WR, Munro AI, et al: Reoperation in biological and mechanical valve populations: fate of the reoperative patient. Ann Thorac Surg 1995; 60:S464.
  279. Cohn LH, Peigh PS, Sell J, DiSesa VJ: Right thoracotomy, femorofemoral bypass, and deep hypothermia for re-replacement of the mitral valve. Ann Thorac Surg 1989; 48:69.[Abstract]
  280. McGiffin DC, O'Brien MF, Galbraith AJ, et al: An analysis of risk factors for death and mode-specific death after aortic valve replacement with allograft, xenograft, and mechanical valves. J Thorac Cardiovasc Surg 1993; 106:895.[Abstract]
  281. Gallucci V, Bortolotti U, Milano A, et al: Isolated mitral valve replacement with the Hancock bioprosthesis: a 13-year appraisal. Ann Thorac Surg 1984; 38:571.[Abstract]
  282. Cortina JM, Martinell J, Artiz V, et al: Comparative clinical results with Omniscience (STM1), Medtronic-Hall, and Bjork-Shiley convexo-concave (70 degrees) prostheses in mitral valve replacement. J Thorac Cardiovasc Surg 1986; 91:174.[Abstract]
  283. Akins C, Buckley M, Daggett W, et al: Ten-year follow-up of the Starr-Edwards prosthesis, in Rabago G, Cooley DA (eds): Heart Valve Replacement and Future Trends in Cardiac Surgery. New York, Futura, 1987.
  284. Jamieson W, Burr L, Allen P, et al: Quality of life afforded by porcine bioprostheses illustrated by the new-generation Carpentier-Edwards porcine bioprosthesis, in Rabago G, Cooley DA (eds): Heart Valve Replacement and Future Trends in Cardiac Surgery. New York, Futura, 1987.
  285. Antunes MJ, Wessels A, Sadowski RG, et al: Medtronic Hall valve replacement in a third-world population group: a review of the performance of 1000 prostheses. J Thorac Cardiovasc Surg 1988; 95:980.[Abstract]
  286. Beaudet RL, Nakhle G, Beaulieu CR, et al: Medtronic-Hall prosthesis: valve related deaths and complications. Can J Cardiol 1988; 4:376.[Medline]
  287. Perier P, Deloche A, Chauvaud S, et al: A 10-year comparison of mitral valve replacement with Carpentier-Edwards and Hancock porcine bioprostheses. Ann Thorac Surg 1989; 48: 54.[Abstract]
  288. Akins CW: Mechanical cardiac valvular prostheses. Ann Thorac Surg 1991; 52:161.[Abstract]
  289. Jamieson WR, Fradet GJ, Miyagishima RT, et al: CarboMedics mechanical prosthesis: performance at eight years. J Heart Valve Dis 2000; 9:678.[Medline]
  290. Khan SS, Trento A, DeRobertis M, et al: Twenty-year comparison of tissue and mechanical valve replacement. J Thorac Cardiovasc Surg 2001; 122:257.[Abstract/Free?Full?Text]
  291. Ohta S, Ohuchi M, Katsumoto K, et al: [Comparison of long-term clinical results of the three models of the Bjork-Shiley valve prosthesis and the Omnicarbon valve prosthesis]. Nippon Kyobu Geka Gakkai Zasshi 1995; 43:1569.[Medline]
  292. Cohn LH, Sanders JH, Collins JJ Jr: Actuarial comparison of Hancock porcine and prosthetic disc valves for isolated mitral valve replacement. Circulation. 1976; 54:III60.
  293. Levantino M, Tartarini G, Barzaghi C, et al: Survival despite almost complete occlusion by chronic thrombosis of a Bjork-Shiley mitral prosthesis. J Heart Valve Dis 1995; 4:103.[Medline]
  294. Copans H, Lakier JB, Kinsley RH, et al: Thrombosed Bjork-Shiley mitral prostheses. Circulation 1980; 61:169.[Medline]
  295. Edmunds L: Thrombotic complications with the Omniscience valve. J Thorac Cardiovasc Surg 1989; 98:300.[Medline]
  296. Martinell J, Jimenez A, Rabago G, et al: Mechanical cardiac valve thrombosis: is thrombectomy justified? Circulation 1991; 84:III70.
  297. Roudaut R, Labbe T, Lorient-Roudaut MF, et al: Mechanical cardiac valve thrombosis: is fibrinolysis justified? Circulation 1992; 86:II8.
  298. McKay C: Prosthetic heart valve thrombosis: "what can be done with regard to treatment?" Circulation 1993; 87:294.[Medline]
  299. Silber H, Khan SS, Matloff JM, et al. The St. Jude valve: thrombolysis as the first line of therapy for cardiac valve thrombosis. Circulation 1993; 87:30.[Medline]
  300. Manteiga R, Carlos Souto J, Altes A, et al: Short-course thrombolysis as the first line of therapy for cardiac valve thrombosis. J Thorac Cardiovasc Surg 1998; 115:780.[Abstract/Free?Full?Text]
  301. Horstkotte D, Schulte HD, Bircks W, Strauer BE: Lower intensity anticoagulation therapy results in lower complication rates with the St. Jude Medical prosthesis. J Thorac Cardiovasc Surg 1994; 107:1136.[Abstract/Free?Full?Text]
  302. Jamieson WR, Miyagishima RT, Munro AI, et al: The Carpentier-Edwards supra-annular porcine bioprosthesis: clinical performance to 8 years of a new generation porcine bioprosthesis. J Card Surg 1991; 6:562.[Medline]
  303. Jamieson WR, Miyagishima RT, Burr LH, et al: Carpentier-Edwards porcine bioprostheses: clinical performance assessed by actual analysis. J Heart Valve Dis 2000; 9:530.[Medline]
  304. Bernal JM, Rabasa JM, Cagigas JC, et al: Valve-related complications with the Hancock I porcine bioprosthesis: a twelve- to fourteen-year follow-up study. J Thorac Cardiovasc Surg 1991; 101:871.[Abstract]
  305. Jamieson WR, Hayden RI, Miyagishima RT, et al: The Carpentier-Edwards standard porcine bioprosthesis: clinical performance to 15 years. J Card Surg 1991; 6:550.[Medline]
  306. Ahmad R, Manohitharajah SM, Deverall PB, Watson DA: Chronic hemolysis following mitral valve replacement: a comparative study of the Bjork-Shiley, composite-seat Starr-Edwards, and frame-mounted aortic homograft valves. J Thorac Cardiovasc Surg 1976; 71:212.[Abstract]
  307. Beaudet R, Nakhle G, Beaulieu R, et al: The Medtronic-Hall valve: evaluation of its complications and their effect on quality of life, in Rabago G, Cooley DA (eds): Heart Valve Replacement: Current Status and Future Trends. New York, Futura, 1987.
  308. Gallucci V, Mazzucco A, Bortolotti U, et al: The standard Hancock porcine bioprosthesis: overall experience at the University of Padova. J Card Surg 1988; 3:337.[Medline]
  309. Burckhardt D, Striebel D, Vogt S, et al: Heart valve replacement with St. Jude Medical valve prosthesis: long-term experience in 743 patients in Switzerland. Circulation 1988; 78:I18.
  310. Genoni M, Franzen D, Vogt P, et al: Paravalvular leakage after mitral valve replacement: improved long-term survival with aggressive surgery? Eur J Cardiothorac Surg 2000; 17:14.[Abstract/Free?Full?Text]
  311. Baumgartner WA, Miller DC, Reitz BA, et al: Surgical treatment of prosthetic valve endocarditis. Ann Thorac Surg 1983; 35:87.[Medline]
  312. Dismukes WE, Karchmer AW, Buckley MJ, et al: Prosthetic valve endocarditis: analysis of 38 cases. Circulation 1973; 48:365.[Medline]
  313. Carrier M, Martineau JP, Bonan R, Pelletier LC: Clinical and hemodynamic assessment of the Omniscience prosthetic heart valve. J Thorac Cardiovasc Surg 1987; 93:300.[Abstract]
  314. Pelletier LC, Carrier M, Leclerc Y, et al: Porcine versus pericardial bioprostheses: a comparison of late results in 1,593 patients. Ann Thorac Surg 1989; 47:352.[Abstract]
  315. Keenan RJ, Armitage JM, Trento A, et al: Clinical experience with the Medtronic-Hall valve prosthesis. Ann Thorac Surg 1990; 50:748.[Abstract]
  316. Calderwood SB, Swinski LA, Waternaux CM, et al: Risk factors for the development of prosthetic valve endocarditis. Circulation 1985; 72:31.[Medline]
  317. Bayliss R, Clarke C, Oakley CM, et al: The microbiology and pathogenesis of infective endocarditis. Br Heart J 1983; 50:513.[Abstract/Free?Full?Text]
  318. Miller DC: Determinants of outcome in surgically treated patients with native valve endocarditis (NVE). J Card Surg 1989; 4:331.[Medline]
  319. Verheul HA, van den Brink RB, van Vreeland T, et al: Effects of changes in management of active infective endocarditis on outcome in a 25-year period. Am J Cardiol 1993; 72:682.[Medline]
  320. Cachera JP, Loisance D, Mourtada A, et al: Surgical techniques for treatment of bacterial endocarditis of the mitral valve. J Card Surg 1987; 2:265.[Medline]
  321. Jault F, Gandjbakhch I, Rama A, et al: Active native valve endocarditis: determinants of operative death and late mortality. Ann Thorac Surg 1997; 63:1737.[Abstract/Free?Full?Text]
  322. Edwards MB, Ratnatunga CP, Dore CJ, Taylor KM: Thirty-day mortality and long-term survival following surgery for prosthetic endocarditis: a study from the UK heart valve registry. Eur J Cardiothorac Surg 1998; 14:156.

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Similar articles in this book
Right arrow Author home page(s):
Tomas Gudbjartsson
Sary Aranki
Lawrence H. Cohn
Google Scholar
Right arrow Articles by Gudbjartsson, T.
Right arrow Articles by Cohn, L. H.
Right arrow Articles citing this Article
Right arrow Search for Related Content
Right arrow Articles by Gudbjartsson, T.
Right arrow Articles by Cohn, L. H.
Related Collections
Right arrow Valve disease