|
|
|
| Advanced Search | ||
|
||
Agnihotri AK, Madsen JC, Daggett WM Jr. Surgical Treatment of Complications of Acute Myocardial Infarction: Postinfarction Ventricular Septal Defect and Free Wall Rupture.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:681714.
|
||||||||||||||||||||||||||||||||||||||||||||||||||
Chapter 26 |
 |
?? INTRODUCTION |
|---|
 Top NextReferences |
|---|
An acute postinfarction ventricular septal defect is a perforation of the muscular ventricular septum occurring in an area of acutely infarcted myocardium. A ventricular septal rupture may be termed chronic when it has been present for more than 4 to 6 weeks. A postinfarction ventricular rupture is a perforation of the ventricular free wall occurring in an area of acutely infarcted myocardium.
|
?? POSTINFARCTION VENTRICULAR SEPTAL DEFECT |
|---|
| TopPreviousNextReferences |
|---|
In 1845 Latham2 described a postinfarction ventricular septal rupture at autopsy, but it was not until 1923 that Brunn3 first made the diagnosis antemortem. Sager4 in 1934 added the 18th case to the world literature and established specific clinical criteria for diagnosis, stressing the association of postinfarction septal rupture with coronary artery disease.
The treatment of this entity was medical and strictly palliative until 1956, when Cooley et al5 performed the first successful surgical repair in a patient 9 weeks after the diagnosis of septal rupture. These first patients who underwent similar repairs in the early 1960s usually presented with congestive heart failure, having survived for more than a month after acute septal perforation.6,7 The success of operation in these patients and the precipitous, acute course of other patients with this complication8 gave rise to the belief that operative repair should be limited to patients surviving for 1 month or longer.6,9 This, purportedly, allowed for scarring at the edges of the defect, which was thought to be crucial to the secure and long-lasting closure of the septal rupture.10,11
In the late 1960s, more rapid recognition of septal rupture following infarction led to the recommendation that operation be attempted earlier in patients who were hemodynamically deteriorating.1,3,12 The use of improved prosthetic materials accompanied the successful surgical repair of defects from 1 to 11 days old, as reported by Allen and Woodwark12 in 1966, Heimbecker et al13 in 1968, and Iben et al14 in 1969. Notable among these was a superb early study by Heimbecker et al of infarctectomy and its clinical application to patients with postinfarction ventricular septal defects. The surgical management of these patients was further refined by the inclusion of infarctectomy13,15,16 and aneurysmectomy17,18 and the development of techniques to repair perforations in different areas of the septum.19,20a,20b Over the last 15 years, it has become increasingly clear that in the majority of cases postinfarction ventricular septal rupture constitutes a surgical emergency. More recently, improved surgical techniques, newer prosthetic materials, enhanced myocardial protection, and improved perioperative mechanical and pharmacologic support have led to more favorable results in the surgical management of patients with postinfarction septal rupture.21,22
Postinfarction ventricular septal defects complicate approximately 1% to 2% of cases of acute myocardial infarctions and account for about 5% of early deaths after myocardial infarction.23,24 The average time from infarction to rupture has been reported to be between 2 and 4 days, but it may be as short as a few hours or as long as 2 weeks.2427 These observations correlate well with the pathological findings, which demonstrate that necrotic tissue is most abundant and ingrowth of blood vessels and connective tissue is only beginning 4 to 21 days following a myocardial infarction.28,29 Postinfarction ventricular septal defects occur in men more often than women (3 to 2), but more women experience rupture than what would be expected from the incidence of coronary artery disease in women.8 The age of patients with this complication ranges from 44 to 81 years, with a mean of 62.5 years. However, there is some evidence that the average age is increasing.22,24,30,31 The vast majority of patients who experience ventricular septal rupture do so after their initial infarction.24,31 The overall incidence of postinfarction ventricular septal rupture may have decreased slightly during the past decade as a result of aggressive pharmacologic treatment of ischemia and thrombolytic and interventional therapy in patients with evolving myocardial infarction, as well as the prompt control of hypertension in these patients.31
Angiographic evaluation of patients with postinfarction ventricular rupture indicates that septal rupture is usually associated with complete occlusion rather than severe stenosis of a coronary artery.32 On average, these patients have slightly less extensive coronary artery disease, as well as less developed septal collaterals than do other patients with coronary artery disease.33 The lack of collateral flow noted acutely may be secondary to anatomic configuration, edema, or associated arterial disease. Hill et al,34 in reviewing 19 cases of postinfarction ventricular septal rupture, found single-vessel disease in 64%, double-vessel disease in 7%, and triple-vessel disease in 29%. However, the frequency of single-, double-, and triple-vessel coronary artery disease is more evenly distributed in other series.27,35
Postinfarction ventricular septal defects are most commonly located in the anteroapical septum as the result of a full-thickness anterior infarction (in approximately 60% of cases). These anterior septal ruptures are caused by anteroseptal myocardial infarction following occlusion of the left anterior descending artery. In about 20% to 40% of patients, the rupture occurs in the posterior septum following an inferoseptal infarction, which is usually due to occlusion of a dominant right coronary artery or, less frequently, a dominant circumflex artery.36 Thus, ventricular septal perforations occur most frequently in 65-year-old men with single-vessel coronary disease and poor collateral flow who present 2 to 4 days following their first anterior myocardial infarction.
The infarct associated with septal rupture is transmural and generally quite extensive, involving, on average, 26% of the left ventricular wall in hearts with septal rupture, compared with only 15% in other acute infarctions.24 In an autopsy study, Cummings et al37 found that in patients with acute anterior or inferior infarctions, the amount of right ventricular infarction was much greater in the hearts with septal ruptures as compared to those without septal defects. Likewise, hearts with posterior septal rupture had more extensive left ventricular necrosis than did hearts with inferior infarctions and no septal defects.
Why certain hearts rupture and others do not is unclear at present. Slippage of myocytes during infarct expansion38 may allow blood to dissect through the necrotic myocardium and enter either the right ventricle or pericardial space.39 Hyaline degeneration of cardiomyocytes with subsequent fragmentation and enzymatic digestion may allow fissures to form, predisposing to rupture.40
There are two types of rupture: simple, consisting of a direct through-and-through defect usually located anteriorly; and complex, consisting of a serpiginous dissection tract remote from the primary septal defect, which is usually located inferiorly.41 Multiple defects, which may develop within several days of each other, occur in 5% to 11% of cases and are probably due to infarct extension. Since a successful surgical outcome is related to adequacy of closure of septal defects, multiple defects must be sought preoperatively if possible, and certainly at the time of operative repair.
Of the small number of patients who survive the early period of ventricular septal rupture, 35% to 68% go on to develop ventricular aneurysms25,34 through the process of ventricular remodeling.42 This compares with a 12% incidence of aneurysm formation in patients suffering an infarction but no septal rupture,43 and probably relates to the size and transmural nature of the infarction associated with septal rupture. Postinfarction septal rupture, especially in the posterior septum, may be accompanied by mitral valve regurgitation due to papillary muscle infarction or dysfunction. In approximately one third of cases of septal rupture, there is a degree of mitral insufficiency, usually functional in nature, secondary to left ventricular dysfunction with mitral annular dilation, which usually resolves with repair of the defect.33
The most important determinant of early outcome following postinfarction ventricular septal rupture is the development of heart failure (left, right, or both). The associated cardiogenic shock leads to end-organ malperfusion, which may be irreversible. The degree to which heart failure develops depends on the size of the ventricular infarction and the magnitude of the left-to-right shunt. Left ventricular dysfunction due to extensive necrosis of the left ventricle is the primary determinant of congestive heart failure and cardiogenic shock in patients with anterior septal rupture, while right ventricular dysfunction secondary to extensive infarction of the right ventricle is the principal determinant of heart failure and cardiogenic shock in patients with posterior septal rupture.35,44,45 However, the development of congestive heart failure and cardiogenic shock in a patient with postinfarction ventricular septal defects is not explained solely by the degree of damage sustained by the ventricle.46
The magnitude of the left-to-right shunt is the other key variable in the development of hemodynamic compromise. With the opening of a ventricular septal defect, the heart is challenged by an increase in pulmonary blood flow, and a decrease in system blood flow as a portion of each stroke volume is diverted to the pulmonary circuit. As a consequence of the sudden increase in hemodynamic load imposed upon a heart already compromised by acute infarction, and possibly by a ventricular aneurysm, mitral valve dysfunction, or a combination of these problems, a severe low cardiac output state results. The normally compliant right ventricle is especially susceptible to failure in this circumstance.47,48 Patients with posterior ventricular septal rupture and right ventricular dysfunction may display shunt reversal during diastole because the end-diastolic pressure in the right ventricle can be higher than in the left.39,49 Ultimately, persistence of a low cardiac output state results in peripheral organ failure.
The typical presentation of a ventricular septal rupture is that of a patient who has suffered an acute myocardial infarction and who, after convalescing for a few days, develops a new systolic murmur, recurrent chest pain, and an abrupt deterioration in hemodynamics. The development of a loud systolic murmur, usually within the first week following an acute myocardial infarction, is the most consistent physical finding of postinfarction ventricular septal rupture (present in over 90% of cases). The murmur is usually harsh, pansystolic, and best heard at the left lower sternal border. The murmur is often associated with a palpable thrill. Depending on the location of the septal defect, the murmur may radiate to the left axilla, thereby mimicking mitral regurgitation.26 Up to half of these patients experience postinfarction chest pain in association with the appearance of the murmur.24 Coincident with the onset of the murmur, there is usually an abrupt decline in the patient's clinical course, with the onset of congestive failure and often cardiogenic shock. The findings of cardiac failure that occur acutely in these patients are primarily the result of right-sided heart failure, with pulmonary edema being less prominent than that occurring in patients with acute mitral regurgitation due to ruptured papillary muscle.50
The electrocardiographic findings in patients with acute septal rupture relate to the changes associated with antecedent anterior, inferior, posterior, or septal infarction. The localization of infarction by ECG correlates highly with the location of the associated septal perforation. In our review31 of 55 patients with postinfarction septal rupture, the location of the defect corresponded to the territory of transmural infarction as determined by ECG in all but three patients. Up to one third of patients develop some degree of atrioventricular conduction block (usually transient) that may precede rupture,51 but there is no pathognomonic prognostic indicator of impending perforation. The chest radiograph usually shows increased pulmonary vascularity consistent with pulmonary venous hypertension.
It is important to realize that the sudden appearance of a systolic murmur and hemodynamic deterioration following infarction may also result from acute mitral regurgitation due to ruptured papillary muscle. Distinguishing these two lesions clinically is difficult, but a number of points may help. First, the systolic murmur associated with a septal rupture is more prominent at the left sternal border, whereas the murmur resulting from a ruptured papillary muscle is best heard at the apex. Second, the murmur associated with septal perforation is loud and associated with a thrill (in over 50% of patients), whereas the murmur of acute mitral regurgitation is softer and has no associated thrill.8 Third, septal rupture is often associated with anterior infarctions and conduction abnormalities, whereas papillary muscle rupture is commonly associated with an inferior infarction and no conduction defects.52 Finally, it should be noted that septal rupture and papillary muscle rupture may coexist following infarction.20a,53,54
Until recently, the mainstay of differentiating septal rupture from mitral valve dysfunction has been right heart catheterization using the Swan-Ganz catheter.55 With septal rupture, there is an oxygen saturation step-up between the right atrium and pulmonary artery. Step-up in oxygen saturation greater than 9% between the right atrium and pulmonary artery confirms the presence of a shunt.56 The pulmonary-to-systemic flow ratios (Qp/Qs), obtained from oxygen saturation samples, range from 1.4:1 to greater than 8:1 and roughly correlate with the size of the defect.57 In contrast, with acute mitral regurgitation secondary to papillary muscle rupture, there are classic giant V-waves in the pulmonary artery wedge pressure trace. It should be noted, however, that up to one third of patients with septal rupture also have mild mitral regurgitation secondary to left ventricular dysfunction.58
Advances in transthoracic and transesophageal echocardiography, especially color flow Doppler mapping, have revolutionized the diagnosis of both the presence and site of septal rupture.5861 Echocardiography can detect the defect, localize its site and size, determine right and left ventricular function, assess pulmonary artery and right ventricular pressures, and exclude coexisting mitral regurgitation or free wall rupture. Smyllie et al60 reported a 100% specificity and 100% sensitivity when color flow Doppler mapping was used to differentiate ventricular septal rupture from acute severe mitral regurgitation following acute myocardial infarction. It also correctly demonstrated the site of septal rupture in 41 of 42 patients. Widespread use of this technology has, for the most part, replaced thermodilution catheter insertion, which in outlying hospitals, where patients are often seen first, may be time consuming and difficult to accomplish. Indeed, the trend toward early surgical referral and prompt operative repair is at least partially explained by the more widespread use of color Doppler echocardiography for diagnosis in peripheral centers.22
The necessity of preoperative left heart catheterization with coronary angiography has been a matter of debate. On one hand, left heart catheterization provides important information concerning associated coronary artery disease, left ventricular wall motion, and specifics of valvular dysfunction, which are all important in planning operative correction of postinfarction septal rupture. In most series62 over 60% of patients with septal rupture have significant involvement of at least one vessel other than the one supplying the infarcted area. Bypassing associated coronary artery disease may increase long-term survival when compared with patients with unbypassed coronary artery disease.62 However, left heart catheterization has disadvantagesit is time consuming and can contribute to both the mortality and morbidity of these already compromised patients.22 Thus, some centers do not carry out preoperative left heart catheterization.63,64 Others use it selectively, avoiding invasive studies in patients with septal rupture caused by anterior wall infarction, which is associated with a much lower incidence of multiple-vessel disease than septal defects resulting from posterior infarctions.22 The issue of concomitant coronary bypassing is discussed in greater detail below.
Reviews by Oyamada and Queen,65 Sanders et al,8 and Kirklin et al66 reveal that nearly 25% of patients with postinfarction septal rupture and no surgical intervention died within the first 24 hours, 50% died within 1 week, 65% within 2 weeks, 80% within 4 weeks; only 7% lived longer than one year. Lemery et al67 reported that of 25 patients with postinfarction ventricular septal defects treated medically, 19 died within one month. Thus, the risk of death following postinfarction ventricular septal defect (VSD) is highest immediately after infarction and septal rupture, and then gradually declines. Interestingly, there are reports of spontaneous closure of small defects, though this is so rare that it would be unreasonable to manage a patient with the expectation of closure.
Recently, the SHOCK Trial (Should We Emergently Revascularize Occluded Coronaries in Cardiogenic Shock) provided intriguing data on the outcome of medically managed patients with shock and postinfarction VSD.68 The multi-institutional study tracked 55 patients in cardiogenic shock from postinfarction VSD. Rupture occurred a median of 16 hours after infarction, and the median time to the onset of shock was 7.3 hours. Twenty-four patients were managed medically; the remaining 31 patients comprised a high-risk surgical group. There were only 7 survivors, of whom 6 had surgery to the repair the defect.
Despite the many advances in the nonoperative treatment of congestive heart failure and cardiogenic shock, including the intra-aortic balloon pump and a multitude of new inotropic agents and vasodilators, these do not supplant the need for operative intervention in these critically ill patients.
It has become clear that the early practice of waiting for several weeks after ventricular septal rupture before proceeding with surgery only selects out the small minority of patients in whom the hemodynamic insult is less severe and is better tolerated.19,35,69 Likewise, it has also become clear that to manage most patients supportively, in hopes of deferring operation, is to deprive the great majority of those with postinfarction ventricular septal rupture of the benefits of definitive surgery before irreversible damage due to peripheral organ ischemia has occurred.62,70
While we21 as well as others69 have advocated early surgery since the middle of the 1970s, some continue to prefer to defer operation in patients who are easily supported and exhibit no further hemodynamic deterioration.71,72 Persistence of congestive heart failure or marginal stabilization with rising blood urea nitrogen (BUN) and borderline urine output necessitate aggressive therapy and prompt operation. The routine use of the intra-aortic balloon pump, whenever technically feasible, frequently results in transient reversal of the hemodynamic deterioration. This period of stability often makes it possible to complete left heart catheterization before proceeding to operation but should not significantly delay definitive surgical treatment. Patients with septal rupture rarely die of cardiac failure per se, but rather of end-organ failure as a consequence of shock. Shortening the duration of shock by operating early is the only therapeutic solution for this group of patients and can yield dramatic results.31,73
Our experience and the experience of others suggest that patients in cardiogenic shock represent a true surgical emergency requiring immediate operative repair. Because deaths in these patients result from multisystem failure secondary to organ hypoperfusion, delay in operative repair for patients in cardiogenic shock represents a "failed therapeutic strategy." Those few patients who are completely stable, with no clinical deterioration, and who require no hemodynamic support, can undergo operative repair when convenient during that hospitalization. The large group of patients who are in an intermediate position between those with shock and those in stable condition should be operated on early (usually within 12 to 24 hours) after appropriate preoperative evaluation. Since the group of patients in stable condition constitutes 5% or less of the total population of patients with postinfarction ventricular septal rupture, the overwhelming majority of patients require prompt surgical treatment.
Rarely, because of a delayed referral, a patient will be seen for surgical therapy who is already in a state of multisystem failure or has developed septic complications. Such a patient is unlikely to survive an emergency operation and thus may benefit from prolonged support with an intra-aortic balloon pump before an attempted operative repair. We have found it necessary to treat a small number of patients (3 of 92) in this fashion. Baillot et al72 have reported individual successes with such an approach, which we consider the exception rather than the rule.
Because the natural course of the disease in unoperated patients is so dismal, the diagnosis of postinfarction ventricular septal rupture can be regarded as its own indication for operation.70 Preoperative management is directed towards stabilization of the hemodynamic condition so that peripheral organ perfusion can be best maintained while any further diagnostic studies are obtained and while deciding on the optimal time for surgical intervention. Although the early clinical course of patients with postinfarction ventricular septal rupture can be quite variable, 50% to 60% present with severe congestive heart failure and a low cardiac output state requiring intensive therapy.74
The goals of preoperative management are to: (1) reduce the systemic vascular resistance, and thus the left-to-right shunt; (2) maintain cardiac output and arterial pressure to ensure peripheral organ perfusion; and (3) maintain or improve coronary artery blood flow. This is best accomplished by the intra-aortic balloon pump (IABP). Counterpulsation reduces left ventricular afterload, thereby increasing cardiac output and decreasing the left-to-right shunt, as reported by Gold et al in 1973.75 In addition, IABP support is associated with decreased myocardial oxygen consumption, as well as improved myocardial and peripheral organ perfusion. Although counterpulsation produces an overall improvement in the patient's condition, a complete correction of the hemodynamic picture cannot be obtained.76 Peak improvement occurs within 24 hours and no further benefit has been observed with prolonged balloon pumping.77 Pharmacologic therapy with inotropic agents and diuretics should be instituted promptly. The addition of vasodilators (i.e., sodium nitroprusside or intravenous nitroglycerine) makes good theoretical sense, because it can decrease the left-to-right shunting associated with the mechanical defect, and thus increase cardiac output. However, these effects are often associated with a marked fall in mean arterial blood pressure and reduced coronary perfusion, both poorly tolerated in these critically ill patients. It must be stressed that pharmacologic therapy is intended primarily to support the patient in preparation for operation and should not in any way delay urgent operation in the critically ill patient. We now admit patients with postinfarction septal rupture directly to the surgical intensive care unit rather than to the coronary care or medical intensive care unit.
Other techniques that have been tried in an effort to improve the hemodynamics of patients with interventricular septal rupture include venoarterial extracorporeal membrane oxygenation (ECMO),78 and inflation of a balloon in the right ventricular outflow tract to decrease the left-to-right shunt.79 Neither has been proven reliable in clinical application. Use of a catheter-mounted axial flow pump (Hemopump) in stabilizing these patients is controversial because of the risk of acute pump failure due to catheter blockage from pieces of necrotic tissue.80
The first repair by Cooley et al5 of an acquired ventricular septal defect was accomplished using an approach through the right ventricle with incision of the right ventricular outflow tract. This approach, which was adapted from surgical techniques for closure of congenital ventricular septal defects, proved to be disadvantageous for many reasons. Exposure of the defect was frequently less than optimal, particularly for defects located in the apical septum. It involved unnecessary injury to normal right ventricular muscle and interruption of collaterals from the right coronary artery. Finally, it failed to eliminate the paradoxical bulging segment of infarcted left ventricular wall. Subsequently, Heimbecker et al13 introduced, and others adopted,16,25,81 a left-sided approach (left ventriculotomy) with incision through the area of infarction. Such an approach frequently incorporates infarctectomy and aneurysmectomy, together with repair of septal rupture.
Experience with a variety of techniques for closure of postinfarction ventricular septal rupture has led us to the evolution of eight basic principles (Table 26-1). Adherence to these principles in the closure of septal defects in different locations has led to the evolution of individualized approaches to apical, anterior, and inferoposterior septal defects.
|
Patients are anesthetized using a fentanyl-based regimen. Pancuronium is selected as the muscle relaxant so as to prevent bradycardia. Pulmonary bed vasodilators such as dobutamine are avoided to minimize the left-to-right shunt fraction. Preoperative antibiotics include both cefazolin and vancomycin given the fact that prosthetic material may be left in the patient.
Cardiopulmonary bypass is accomplished with bicaval venous drainage. Systemic cooling to 25?C is employed. Cardiac standstill is achieved with cold, oxygenated, dilute blood cardioplegia82,83 using antegrade induction followed by retrograde perfusion via the coronary sinus. Although a number of myocardial protection strategies are currently available, we82 and others45,84,85 continue to use cold oxygenated, dilute blood cardioplegia to protect the heart during surgical correction of a ventricular septal defect. A total of 1200 to 2000 mL of cardioplegia solution is delivered depending on the size of the heart and the degree of hypertrophy.86 Although we have not employed warm cardioplegic induction,87 we do administer warm reperfusion cardioplegia just before removing the aortic cross-clamp.88 Patients with multivessel coronary disease and critical coronary stenoses are revascularized before opening the heart in order to optimize myocardial protection. In most of these patients, saphenous vein rather than the left internal mammary artery is utilized.
The technique of apical amputation was described by Daggett et al in 1970.16 An incision is made through the infarcted apex of the left ventricle. Excision of the necrotic myocardium back to healthy muscle results in amputation of the apical portion of the left ventricle, right ventricle, and septum (Fig. 26-1A and B). The remaining apical portions of the left and right ventricle free walls are then approximated to the apical septum. This is accomplished by means of a row of interrupted mattress sutures of 0 Tevdek that are passed sequentially through a buttressing strip of Teflon felt, the left ventricular wall, a second strip of felt, the interventricular septum, a third strip of felt, the right ventricular wall, and a fourth strip of felt (Fig. 26-2A and B). After all sutures have been tied, the closure is reinforced with an additional over-and-over suture, as in ventricular aneurysm repair, to insure hemostasis of the ventriculotomy closure (not shown).
|
|
The approach to these defects is by a left ventricular transinfarct incision with infarctectomy (Fig. 26-3). Small defects beneath anterior infarcts can be closed by the technique of plication as suggested by Shumaker.89 This involves approximation of the free anterior edge of the septum to the right ventricular free wall using mattress sutures of 0 Tevdek over strips of felt (Fig. 26-4A). The transinfarct incision is then closed with a second row of mattress sutures buttressed with strips of felt (Fig. 26-4BD). An over-and-over running suture completes the ventriculotomy closure (not shown).
|
|
|
Closure of inferoposterior septal defects, which result from transmural infarction in the distribution of the posterior descending artery, has posed the greatest technical challenge.20a,20b Early attempts at primary closure of these defects by simple plication techniques similar to those used in the repair of anterior defects were frequently unsuccessful because of the sutures tearing out of soft, friable myocardium that had been closed under tension. This resulted in either reopening of the defect or catastrophic disruption of the infarctectomy closure. It was, in large part, the analysis of such early results that led to the evolution of the operative principles enumerated in Table 26-1.
Use of the following techniques has been associated with an improved operative survival. After the establishment of bypass with bicaval cannulation, the left side of the heart is vented via the right superior pulmonary vein. The heart is retracted out of the pericardial well as for bypass to the posterior descending coronary artery. The margins of the defect may involve the inferior aspects of both ventricles, or of the left ventricle only (Fig. 26-6A). A transinfarct incision is made in the left ventricle, and the left ventricular portion of the infarct is excised (Fig. 26-6B), exposing the septal defect. The left ventricular papillary muscles are inspected. Only if there is frank papillary muscle rupture is mitral valve replacement performed. When it is indicated, we prefer to perform mitral valve replacement through a separate conventional left atrial incision, to avoid trauma to the friable ventricular muscle. After all infarcted left ventricular muscle has been excised, a less aggressive debridement of the right ventricle is accomplished, with the goal of resecting only as much muscle as is necessary to afford complete visualization of the defect(s). Using this technique, delayed rupture of the right ventricle has not been a problem. If the posterior septum has cracked or split from the adjacent ventricular free wall without loss of a great deal of septal tissue, then the septal rim of the posterior defect may be approximated to the edge of the diaphragmatic right ventricular free wall using mattress sutures buttressed with strips of Teflon felt or bovine pericardium (Fig. 26-6C and D).
|
|
|
The concept that the preservation of left ventricular geometry plays a crucial role in the preservation of left ventricular function19,90 has laid the groundwork for a recent evolution in the surgical approach to postinfarction ventricular septal defectsthe technique of endocardial patch repair of postinfarction ventricular septal defects described by David,81,84 Cooley,91,92 and then by Ross93 in the early 1990s. This operative technique, which is an application to ventricular septal rupture repair of Dor's technique of ventricular endoaneurysmorrhaphy,90 involves intracavitary placement of an endocardial patch to exclude infarcted myocardium while maintaining ventricular geometry. Thus, instead of closing the septal defect, it is simply excluded from the high-pressure zone of the left ventricle. The recent impressive results obtained using infarct exclusion45 mandate that a detailed description of the technique be provided here. The following descriptions are taken from the work of David et al (with permission).39,45,84
In patients with anterior septal rupture, the interventricular septum is exposed via a left ventriculotomy, which is made through the infarcted anterolateral wall starting at the apex and extending proximally parallel to but 1 to 2 cm away from the anterior descending artery (Fig. 26-9A). Stay sutures are passed through the margins of the ventriculotomy to aid in the exposure of the infarcted septum. The septal defect is located and the margins of the infarcted muscle identified. A glutaraldehyde-fixed bovine pericardial patch is tailored to the shape of the left ventricular infarction as seen from the endocardium but 1 to 2 cm larger. The patch is usually oval and measures approximately 4 x 6 cm in most patients. The pericardial patch is then sutured to healthy endocardium all around the infarct (Fig. 26-9B). Suturing begins in the lowest and most proximal part of the noninfarcted endocardium of the septum with a continuous 3-0 polypropylene suture. Interrupted mattress sutures with felt pledgets may be used to reinforce the repair.92 The patch is also sutured to the noninfarcted endocardium of the anterolateral ventricular wall. The stitches should be inserted 5 to 7 mm deep in the muscle and 4 to 5 mm apart. The stitches in the patch should be at least 5 to 7 mm from its free margin so as to allow the patch to cover the area between the entrance and exit of the suture in the myocardium.39 This technique minimizes the risk of tearing muscle as the suture is pulled taut. If the infarct involves the base of the anterior papillary muscle, the suture is brought outside of the heart and buttressed on a strip of bovine pericardium or Teflon felt applied to the epicardial surface of the left ventricle. Once the patch is completely secured to the endocardium of the left ventricle, the left ventricular cavity becomes largely excluded from the infarcted myocardium. The ventriculotomy is closed in two layers over two strips of bovine pericardium or Teflon felt using 2-0 or 3-0 polypropylene sutures as illustrated in Figure 26-9C. No infarctectomy is performed unless the necrotic muscle along the ventriculotomy is sloughing at the time of its closure, and even then it is minimized, since infarcted muscle will not be exposed to left ventricular pressures when the heart begins to work (Fig. 26-9D). Alternatively, sutures can be passed through the ventricular free wall and through a tailored external patch of Teflon or pericardium (Fig. 26-10).71,88
|
|
|
Most other operative techniques that have resulted in successful management of postinfarction of ventricular septal rupture have adhered to the same general principles described above. For example, da Silva et al94 report a technique whereby a nontransfixing running suture has been used to secure a large prosthetic patch to the left side of the ventricular septum, with little or no resection of septum muscle. Tashiro et al95 described an extended endocardial repair in which a saccular patch of glutaraldehyde-fixed equine pericardium was used to exclude an anterior septal rupture. Usui et al96 reported the successful repair of a posterior septal rupture using two sheets of equine pericardium to sandwich the infarcted myocardium, including the septal defect and ventriculotomy. Others have modified the exclusion technique by use of tissue sealants to aid in the septal closure.97
Successful transcatheter closure of postinfarction ventricular septal rupture has been reported using several types of catheter-deployed devices. The largest experience is with the CardioSEAL device, a nitinol, double umbrella prosthesis.98 The device consists of two attached and opposing umbrellas formed by hinged steel arms covered in a Dacron meshwork that, theoretically, promotes endothelization. The arms are manually everted to allow the device to be passed through a narrow percutaneous deployment system. When extruded from the guiding catheter, the arms spring backward, resembling a "clamshell." The device approaches the septum via the systemic veins and through the atrial septum (or alternatively via the arterial system through the aortic valve). As reported by Landzberg and Lock,98 the experience at Boston Children's Hospital and Brigham and Women's Hospital indicates that, while the device can be routinely deployed in the setting of an acute infarction, the continued necrosis of septal tissue led to decompensation and death in 4 of 7 patients. In contrast, they reported success in 6 of 6 patients treated for residual or recurrent septal defects discovered after primary operative repair. Other catheter devices have also been attempted, which variable success, including the Amplatzer septal occluder and the Rashkind double umbrella.99
The best use of such devices in an overall treatment strategy is unclear. As a primary treatment, data suggest the devices have a high early failure rate, but their potential role in improving the risk of an unstable surgical patient is not yet well characterized. Currently, catheter approaches appear to be most effective in treatment of recurrent or residual defects, and we preferentially employ them for these conditions. Device development is an ongoing process, and the future undoubtedly will see use of new devices, especially in the high-risk patient with multisystem failure.
Of interest, two centers have reported using a standard Swan-Ganz balloon catheter from the groin to abolish the shunt in unstable patients with postinfarction septal rupture.100,101 Hemodynamic improvement was immediate in both patients, who underwent subsequent surgical repair of the defect.
Role of Ventricular Assist Devices
In patients who present for operation with evidence of potentially reversible multiorgan dysfunction, or in patients who have intractable failure following repair, there may be a role for temporary mechanical heart support. There have been anecdotal cases of unstable patients being successfully managed by mechanical support followed by definitive operation.102
The theoretical advantages that make mechanical support attractive as an initial therapy in very sick patients with postinfarction VSD include: (1) the potential to reverse end-organ dysfunction; (2) maturation of the infarct leading to firmer tissue, making the closure less prone to technical failure; and (3) recovery of the stunned and energy-depleted myocardium. In our limited experience, this strategy has shown promise, and we are evaluating its broader application based on careful preoperative risk assessment. However, there are potential hazards with mechanical support that are specific to the patient with postinfarction VSD. High right-to-left shunting across the ventricular septum has been reported to cause hypoxic brain injury in a postinfarction VSD patient placed on a HeartMate LVAD.103 This anecdotal observation suggests that either partial left heart support or preferably biventricular support should be considered when using mechanical assistance in these patients. In a report using the Hemopump axial flow device, 2 of 2 patients supported experienced lethal pump failure. Examination of the device at autopsy disclosed necrotic material clogging the catheter system.104
Simultaneous Myocardial Revascularization
There has been controversy in the literature concerning the advantages and disadvantages of concurrent coronary artery grafting in patients undergoing emergent repair of postinfarction ventricular septal rupture.25,30,64,73,105 Some have argued that revascularization provides no survival benefit and subjects patients to preoperative left heart catheterization, a time-consuming and potentially dangerous diagnostic procedure.63,64 Loisance et al105 base their policy of not revascularizing patients with postinfarction septal ruptures on the fact that none of their 20 long-term survivors (5 of whom were bypassed) had incapacitating angina or recurrent myocardial infarction. Piwnica et al106 reported a series of 28 survivors of early operative closure of postinfarction ventricular septal rupture, among whom only one had coronary artery grafting. Among the 24 patients for whom follow-up was complete, there were only 2 late deaths of cardiac origin. However, it is not clear from their report what the impact of associated coronary artery disease (revascularized or not) may have been on the course of the other 32 patients who did not survive operation.
Some groups use left heart catheterization and coronary bypassing selectively.22,30 Davies et al30 found that of 60 long-term survivors (median 70 months; range 1 to 174 months), only five patients developed exertional angina during follow-up and none required revascularization. Their current policy is to avoid left heart catheterization on patients in whom an acquired septal defect is suspected to be a consequence of their first anterior infarction, provided that the patient has no history of angina or electrocardiographic evidence of previous infarction in another territory.30 This approach is also based on the findings that multivessel disease is much less prevalent in those with an apical septal rupture as a result of anterior infarction.22
We and others35,45,74,93,107 have tended to employ coronary revascularization with increasing frequency. Our policy is to place aortocoronary grafts to principal epicardial coronary arteries that have severe proximal stenoses. In order to investigate the early and late effects of coronary artery revascularization, we previously reviewed our experience in patients undergoing repair of postinfarction septal rupture,73 and concluded that revascularization was of early and long-term benefit. In a more recent review, the effect of bypass was less dramatic, not achieving statistical significance (manuscript in preparation). Nevertheless, there is no information that would suggest any negative impact of bypass grafting, and we continue to perform bypasses routinely when the clinical presentation permits catheterization.
Weaning from Cardiopulmonary Bypass
Intraoperative transesophageal echocardiography is essential to assess ventricular function, ventricular dimensions, residual shunt, and mitral regurgitation when weaning from bypass. The two most common problems encountered in separating from bypass following repair of a postinfarction ventricular septal defect are low cardiac output and bleeding. Although the treatment of low cardiac output following cardiac surgery is beyond the scope of this chapter, a few agents and principles are worth mentioning. First, most of these patients will have had an intra-aortic balloon pump (IABP) inserted before surgery. If not, one should be inserted in the operating room, especially if the low output state is secondary to left ventricular dysfunction. Also, IABP may benefit patients with right ventricular failure by improving right coronary artery blood flow due to diastolic augmentation. We have found intravenous milrinone, a phosphodiesterase inhibitor, to be very effective in reversing low output states secondary to left ventricular dysfunction. Milrinone possesses a balance of inotropic and vasodilatory properties that together produce an increase in cardiac output and reduction in right and left filling pressures and systemic vascular resistance. It is less arrhythmogenic than dobutamine, causes less hypotension than amrinone, and is not associated with thrombocytopenia.108
Posterior defects are commonly associated with mitral regurgitation and right heart dysfunction secondary to extensive right ventricular infarction.37 Management of right heart failure is aimed at reducing right ventricular afterload while maintaining systemic pressure.100 Initial steps to manage right ventricular dysfunction include volume loading, inotropic support, and correction of acidosis, hypoxemia, and hypercarbia. If patients remain unresponsive to these measures, we have successfully treated right ventricular failure with a prostaglandin E1 infusion (0.52.0 ?g/min) into the right heart, counterbalanced with a norepinephrine infusion titrated into the left atrium.109 Inhaled nitric oxide (2080 ppm), which selectively dilates the pulmonary circuit, has also proven efficacious in the treatment of right heart failure.110
In our experience, inability to separate from bypass has been uncommon if the repair has been successful. However, if a patient cannot be weaned from bypass using conventional therapy and is less than 70 years old with no residual hemodynamically significant lesion, we consider using a ventricular assist device. Indications for a left ventricular assist device are a cardiac index less than 1.8 L/min per m2, a left atrial pressure above 18 to 25 mm Hg, a right atrial pressure below 15 mm Hg, and an aortic pressure below 90 mm Hg peak systolic. Indications for a right ventricular assist device are a cardiac index less than 1.8 L/min per m2, an aortic pressure below 90 mm Hg peak systolic, and a left atrial pressure less than 15 mm Hg despite volume loading to a right atrial pressure of 25 mm Hg with a competent tricuspid valve. Important points to remember when instituting ventricular assistance are:
To prevent postpump coagulopathy, we begin antifibrinolytic therapy with either aprotinin or 
-aminocaproic acid (Amicar) before commencing cardiopulmonary bypass. Half-dose aprotinin is administered by first giving an intravenous test dose of 10,000 KIU over 10 minutes (before administering blockers), and then loading patients with 1 million KIU over 20 minutes prior to bypass. Another 1 million KIU is given in the pump prime, and then 250,000 KIU/hr is administered for the duration of the surgery. Heparin is managed in the usual fashion with activated clotting times (ACT), but kaolin, not Celite, is used as the ACT activator. Since controversy surrounds the issue of increased renal dysfunction and perioperative thrombotic events in patients receiving aprotinin,112 we prefer to use Amicar in patients who (1) require aortocoronary bypasses, (2) are diabetic, or (3) have known renal dysfunction. Amicar is administered by loading patients with 10 g prior to commencing bypass and then adding another 10 g to the pump prime. During the procedure Amicar is continuously infused at 1 g/h for the duration of surgery. We avoid giving over 30 g of Amicar. Postpump suture line bleeding may be reduced by application of a fibrin sealant to the ventricular septum around the septal defect prior to formal repair.113 Biological glue may be effective in controlling bleeding suture lines following repair.114 As a last resort, Baldwin and Cooley115 have suggested insertion of a left ventricular assist device solely as an adjunct to the repair of friable or damaged myocardium to reduce left ventricular distension and thus control bleeding.
Highlights of Postoperative Care
Early postoperative diuresis and positive end-expiratory pressure ventilation are used to decrease the arterial-alveolar gradient induced by the increased extravascular pulmonary water associated with cardiopulmonary bypass. Once the patient has warmed, we commonly use an intravenous infusion of Lasix combined with mannitol (1 g of Lasix in 400 cc of 20% mannitol) at a rate of 1 to 20 cc per hour to keep the urine output greater than 100 cc per hour. If renal function has been compromised preoperatively, continuous venovenous hemofiltration (CVVH) is employed postoperatively.
Intractable postoperative ventricular arrhythmias secondary to reperfusion injury are sometimes difficult to control using standard therapy. We have been impressed with the efficacy of intravenous amiodarone in these situations (1020 mg/kg over 24 hours).116
Operative Mortality and Risk Factors for Death
Table 26-2 summarizes recently reported experience from several centers. Operative mortality, defined as death prior to discharge or within 30 days of operation, ranged from 30% to 50%. In the MGH experience of 114 patients, operative mortality was 37% (Fig. 26-12A). The risk for death was found to be very high initially, but dropped rapidly (Fig. 26-12B). We identified independent risk factors for early and late death using multivariate methods (Table 26-3). The most important predictor of operative mortality in our study, and in other reports, was preoperative hemodynamic instability. Patients in this group are usually in cardiogenic shock, are emergency cases, are on inotropic support, and usually have intra-aortic balloon pumps. Several variables are highly correlated with hemodynamic instability, and different multivariate models may use one or more of these indicators of severe hemodynamic failure in their final model. As previously discussed, the degree to which the patient's hemodynamics suffer depends both on the magnitude of the shunt and the size of the infarction.35,45,74,117119
|
|
|
|
|
Our review of the MGH experience underscored the large variability of risk to which patients could be segregated using a few clinical variables (Figs. 26-15 and 26-16), most notably indicators of hemodynamic instability (emergency surgery and use of inotropics). The result was that a small group of high-risk patients dramatically affected the overall mortality rate. We believe that this phenomenon makes it very difficult to compare mortality between institutions. A slight difference in practice patterns, such as a tendency of a surgeon or referring cardiologist to deny operation, could substantially affect results. Additionally, any difference in transport dynamics to certain centers could lead to loss of unstable patients, which could create another type of selection bias. In our opinion, these issues are by far the most important source of mortality differences in modern series.
|
|
There is limited information from other centers on results using the exclusion technique. Ross commented that he was enjoying improved results with the method, although instead of using a running suture he used interrupted buttressed mattress sutures, and added an epicardial patch.123 Cooley and others have also modified the method due to difficulty with the continuous suture line, and noted improved results with a decrease in mortality to 36.4% from a historical level of 46%.124 Our group has not been able to replicate the excellent Toronto results, with a disappointing 60% mortality in 10 patients who underwent the "exclusion" type repair (higher than the rate achieved historically with traditional techniques).
Regardless of the technique, the most common cause of death following repair of acute postinfarction ventricular septal defect was low cardiac output syndrome (52%). Technical failures, most commonly recurrent or residual VSD but including bleeding, were the second most common (23%). Other causes of death include sepsis (17%), recurrent infarction (9%), cerebrovascular complications (4%), and intractable ventricular arrhythmias.
Long-term results have been favorable as regards both mortality risk and functional rehabilitation. Actuarial survival at 5 years for most recent series generally ranges between 40% and 60% (see Table 26-2). Due to the overall high risk of the operation, it is rewarding to note that hospital survivors enjoy excellent longevity, with 1-, 5-, and 10-year survival of 91%, 70%, and 37%. They also are quite functionalamong 15 of our patients contacted during the most recent follow-up of long-term survivors, 75% were in NYHA functional class I, and 12.5% were class II.31
Gaudiani et al74 reported similar long-term results using an early operative approach. In their series, 88% of hospital survivors were alive at 5 years, with 74% of survivors in NYHA functional class I and 21% of survivors in class II. In the series of patients reported by Piwnica et al,105 there were 20 long-term survivors, of whom 8 were in class I and 12 were in class II. David et al45 have reported a 66% 6-year survival rate in patients operated on since 1980. Finally, Davies et al30 reported 5-, 10-, and 14-year survivals of 69%, 50%, and 37%. Eighty-two percent of patients were in NYHA functional class I or II.
Recurrent Ventricular Septal Defects
Recurrent or residual septal defects have been diagnosed by Doppler color flow mapping early or late postoperatively in 10% to 25% of patients.22 They may be due to reopening of a closed defect, to the presence of an overlooked defect, or to the development of a new septal rupture during the early postoperative period. These recurrent defects should be closed when they cause symptoms or signs of heart failure or when the calculated shunt fraction is large (Qp: Qs > 2.0). When they are small (Qp:Qs diuretic therapy, a conservative approach is reasonable and late spontaneous closure can occur.22 Intervention in the catheterization laboratory may be useful in closing symptomatic residual or recurrent defects postoperatively.
Chronic Ventricular Septal Defects
In 1987 Rousou et al reported successful closure of an acquired posterior ventricular septal defect by means of a right transatrial approach.125 Filgueira et al have used the transatrial approach for delayed repair of chronic acquired posterior septal defects.126 Approaching a postinfarction ventricular septal defect through the tricuspid valve should not be used in acute cases because of the friability of the necrotic septum, poor exposure, and because this technique does not involve infarctectomy, and thus cannot achieve the hemodynamic advantages of elimination of a paradoxically bulging segment of ventricular wall. However, the right heart approach can be used in chronic postinfarction ventricular septal defects when the septum is well scarred and the patch can be safely sutured to it from the right atrium. We emphasize that while the transatrial approach may be used selectively for the closure of chronic defects, it is unlikely to be an appropriate choice for the closure of acute defects, except perhaps in the rare circumstance when an infarct is localized to the septum with no evidence of necrosis of the free wall of the left ventricle.39
|
?? POSTINFARCTION VENTRICULAR FREE WALL RUPTURE |
|---|
| TopReferences |
|---|
William Harvey first described rupture of the free wall of the heart after acute myocardial infarction in 1647.127 In 1765, Morgagni reported 11 cases of myocardial rupture found at postmortem.128 Ironically, Morgagni later died of myocardial rupture.129 Hatcher and colleagues from Emory University reported the first successful operation for free wall rupture of the right ventricle in 1970.130 FitzGibbon et al131 in 1971 and Montegut132 in 1972 reported the first successful repairs of a left ventricular rupture associated with ischemic heart disease.
Autopsy studies reveal that ventricular free wall rupture occurs about 10 times more frequently than postinfarction ventricular septal rupture, occurring in about 11% of patients following acute myocardial infarction.23,133 The incidence has been found to be as high as 31% in autopsy studies of anterior myocardial infarction.134 Ventricular rupture and cardiogenic shock are now the leading causes of death following acute myocardial infarction, and together account for over two thirds of early deaths in patients suffering their first acute infarction.135 Postinfarction ventricular ruptures are more common in elderly women (mean age of 63 years) suffering their first infarction.136,137 In the prethrombolytic era, 90% of ruptures occurred within 2 weeks after infarction with the peak incidence at 5 days.138 In contrast, the time to cardiac rupture (not frequency of rupture) seems to be accelerated by thrombolysis and coronary reperfusion, sometimes occurring within hours from the onset of symptoms.139 Thus, free ventricular ruptures occur most frequently in hypertensive women over the age of 60 who develop symptoms within 5 days of their first transmural myocardial infarction.
Opinions differ as to the most common site of left ventricular rupture. The older literature suggests that the anterior wall is the most frequent site.140 However, more recent series have observed a preponderance of lateral and posterior wall ruptures.27,133,138 David141 has suggested that a lateral wall infarction is more likely to rupture than is an anterior or inferior one, but since anterior infarctions are much more frequent than lateral infarctions, overall the commonest site of rupture is the anterior wall. Like postinfarction ventricular septal rupture, free wall ruptures may be simple or complex.41 A simple rupture results from a straight through-and-through tear which is perpendicular to the endothelial and epicardial surfaces, whereas a complex rupture results from a more serpiginous tear, often oblique to the endocardial and epicardial surfaces.141 Batts et al138 reported 100 consecutive cases of left ventricular free wall rupture and found that half were simple ruptures and the rest were complex.
Pathogenesis and Pathophysiology
Left ventricle free wall rupture can be divided into three clinicopathological categories: acute, subacute, and chronic.142,143 An acute or "blow-out" rupture is characterized by sudden recurrent chest pain, electrical mechanical dissociation, profound shock, and death within a few minutes due to massive hemorrhage into the pericardial cavity. This type of rupture is probably not amenable to current management. A subacute rupture is characterized by a smaller tear, which may be temporarily sealed by clot or fibrinous pericardial adhesions. These usually present with the signs and symptoms of cardiac tamponade and, eventually, cardiogenic shock. Subacute rupture may mimic other complications of acute myocardial infarction such as infarct extension and right ventricular failure, and may be compatible with life for several hours or days or even longer.141 A chronic rupture with false aneurysm formation occurs when the leakage of blood is slow and when surrounding pressure on the epicardium temporarily controls the hemorrhage. Adhesions form between the epicardium and pericardium, which reinforce and contain the rupture.29 The most common clinical presentation of patients with false aneurysms of the left ventricle is congestive heart failure.144 A false aneurysm may also be an echocardiographic finding in an otherwise asymptomatic patient recovering from acute myocardial infarction. Angina, syncope, arrhythmias, and thromboembolic complications occur in a small percentage of patients.144 There are four major differences between a true and false aneurysm of the left ventricle:
Rupture of the free wall of the left ventricle may occur in isolation or with rupture of other ventricular structures such as the interventricular septum, papillary muscles, or right ventricle.144,147
The pathogenesis of cardiac rupture remains poorly understood. However, cardiac rupture occurs only with transmural myocardial infarctions and infarction expansion appears to play an important role in its pathogenesis.38,42,148 Infarct expansion is an acute regional thinning and dilatation of the infarct zone, seen as early as 24 hours following acute transmural myocardial infarction and not related to additional myocardial necrosis.149 This regional thinning and dilatation of the infarct zone is a consequence of slippage between muscle bundles, resulting in a reduction in the number of myocytes across the infarcted area.150 Infarct expansion increases the size of the ventricular cavity, with a consequent increase in wall tension (Laplace effect) that subjects the infarct zone to more tension and predisposes to endocardial tearing.141 Systemic hypertension aggravates the problem of thinning and dilatation of the infarct wall and increases the probability of rupture.151 Lack of collateral flow may also promote ventricular rupture.152
Since myocardial rupture occurs in regions of complete transmural myocardial necrosis, usually after extensive hemorrhagic transformation of the acute infarct,148,153,154 and because thrombolytic therapy is associated with the conversion of a bland infarct into a hemorrhagic infarct,155 there has been an ongoing concern that thrombolysis might increase the likelihood of ventricular rupture.156 Honan et al153 performed a meta-analysis of four large clinical trials (1638 patients) in which streptokinase was used to treat acute myocardial infarctions and concluded that the risk of cardiac rupture was directly related to the timing of thrombolytic therapy. Early treatment (within 7 hours from the onset of symptoms) decreased the risk of cardiac rupture, whereas late treatment (after 17 hours) increased the risk of this complication even though, surprisingly, the overall mortality rate was diminished when streptokinase was given late after acute infarction. In a prospective ancillary study of 5711 patients, Late Assessment of Thrombolytic Efficacy (LATE), Becker et al139 were unable to show an increased risk of cardiac rupture in patients treated with rt-PA 6 to 24 hours after the onset of symptoms. Thus, there is general agreement that early successful thrombolysis decreases the overall risk of cardiac rupture, probably by limiting the extent of necrosis resulting in a nontransmural instead of transmural infarct, but the impact of late thrombolytic therapy on cardiac rupture remains unclear.
The clinical picture of a subacute ventricular rupture is primarily that of pericardial tamponade with pulsus paradoxus, distended neck veins, and cardiogenic shock. The hemodynamics of tamponade include hypotension, right atrial and pulmonary capillary pressures greater than10 mm Hg, equalization of right atrial and pulmonary capillary pressures (with a difference of less than 5 mm Hg between both pressures), and right atrial pressure waveform exhibiting a deep x descent and blunted y descent.157 The identification of clinical or hemodynamic findings of cardiac tamponade should be followed by transthoracic or transesophageal echocardiography to confirm the presence of a pericardial effusion. Although 5% to 37% of patients with acute myocardial infarction but no rupture may develop a pericardial effusion,158 echocardiographic signs that increase the sensitivity and specificity for cardiac rupture include effusion thickness greater than 10 mm, echo-dense masses in the effusion, ventricular wall defects, and signs of tamponade (e.g., right atrial and right ventricular early diastolic collapse and increased respiratory variation in transvalvular blood flow velocities).136,159,160 Pericardiocentesis and aspiration of uncoagulated blood has been considered the most reliable criterion of subacute ventricular rupture161,162; however, false-positive and false-negative diagnoses have been reported.136,159 The demonstration of a clear pericardial fluid on pericardiocentesis definitively excludes cardiac rupture.159 Pericardiocentesis is of therapeutic value in some patients, often providing a short-term circulatory improvement.163 The certainty of diagnosis of cardiac rupture can be provided promptly using echocardiography.136
In an attempt to define symptomatic, electrocardiographic, and hemodynamic markers that may permit the prospective identification of patients prone to rupture of the heart after acute myocardial infarction, Oliva et al134 retrospectively studied 70 consecutive patients with rupture and 100 comparison patients with acute myocardial infarction but without rupture. They found a number of markers that were associated with a significant increase in the risk of rupture (Table 26-4). The presence of a lateral infarction, especially with associated inferior or posterior infarction, identified a subset of patients at increased risk for rupture. Persistent, progressive, or recurrent ST-segment elevation and, especially, persistent T-wave changes after 48 to 72 hours, or the gradual reversal of initially inverted T waves, are associated with an increased risk of rupture. Finally, the development of pericarditis, repetitive emesis, or restlessness and agitation, particularly two or three of these symptoms, conveyed predictive value.134 In a similar type of study, Pollak et al160 identified lateral wall involvement, history of hypertension, and age older than 65 years to be associated with a high risk of subacute left ventricular rupture following acute myocardial infarction.
|
Acute rupture of the free wall of the left ventricle is invariably fatal, with death usually occurring within minutes of the onset of recurrent chest pain.138,141,152 In most of these cases, the sequence of events leading to death is so rapid that there is not enough time for surgical intervention. In contrast, patients with a subacute rupture usually survive hours or days, rarely weeks, following the myocardial tear.143 Pollak et al160 found that in 24 cases of postinfarction subacute rupture, survival time (i.e., time from critical event to death) varied between 45 minutes and 6.5 weeks, with a median survival of 8 hours. N??ez et al166 found that in 29 cases of subacute rupture, 20 (69%) died within minutes of the onset of symptoms and 9 (31%) lived several hours, allowing time for treatment. Subacute ventricular ruptures are generally considered to be less common than acute free wall ruptures. In recent studies, with high autopsy rates, 21% to 42% of all postinfarction free wall ruptures followed a subacute course.160,167,168
Because of its rarity, the natural history of false aneurysm of the left ventricle has not been established.141 It is believed to have a poor prognosis because of its high probability of rupture145,169,170; however, there are patients in whom the diagnosis was made many years after myocardial infarction.144,171,172 The increasingly wide application of echocardiography after acute myocardial infarction gives promise of altering clinical outcome for many patients with the various forms of ventricular wall rupture.
Usually, the sequence of events leading to death is so rapid in patients with acute rupture of the free wall of the left ventricle that there is not time enough for surgical intervention.141 These patients usually die within minutes of the onset of recurrent chest pain.166 However, a high index of suspicion, combined with a novel technique of percutaneous intrapericardial infusion of fibrin glue immediately following pericardiocentesis,173,174 may afford at least a chance of survival in this surgically untreatable subgroup of patients.
In contrast, patients with subacute left ventricular rupture can be saved with surgery. Once the diagnosis of rupture of the free wall is established, the patient should be immediately transferred to the operating room. No time should be wasted attempting to perform coronary angiography.136,141,166,175 Inotropic agents and fluids should be started while preparing for surgery. Pericardiocentesis often improves hemodynamics temporarily,175 and insertion of an intra-aortic balloon pump may be beneficial, even though the principal problem is cardiac tamponade.162
The timing of surgery following the diagnosis of false aneurysm of the left ventricle is dependent upon the age of the myocardial infarction. When a false aneurysm is discovered within the first 2 to 3 months after coronary infarction, surgery is urgently recommended after coronary angiography and ventriculography because of the unpredictability of rupture.144,172 However, when the diagnosis is made several months or years after myocardial infarction, the urgency of the operation is not determined so much by the risk of rupture, but rather by symptoms and the severity of the coronary artery disease.141,171
SUBACUTE RUPTURE OF THE FREE WALL
As soon as the diagnosis of rupture of the free wall of the left ventricle is confirmed by echocardiography, the patient should be transferred to the operating room. In patients with tamponade, severe hypotension may result during the induction of anesthesia. Therefore, we usually complete the sterile preparation and draping of the patient before inducing anesthesia. Some even advocate femoral artery cannulation before the induction of anesthesia.176 A median sternotomy is performed and upon decompressing the pericardium, the blood pressure commonly rises quickly. This should be anticipated and controlled because hypertension can cause ventricular bleeding to start again, or may even increase the size of the ventricular rent.141 In most cases, however, the ventricular tear is sealed off by clot, and there is no active bleeding.
Traditionally, postinfarction rupture of the free wall of the left heart has been repaired on cardiopulmonary bypass136,143,157,161,162,166,176,177; however, some surgeons have suggested that cardiopulmonary bypass is not necessary except perhaps in patients with posterior wall rupture, severe mitral regurgitation, ventricular septal rupture, or graftable coronary artery disease.141,175 Although the ventricular tear can be repaired without aortic cross-clamping, cardiac standstill and left ventricular decompression make the procedure easier when the rupture is in the posterior wall of the left ventricle.141
Four surgical techniques have been used to control ventricular rupture. The first technique involves closing the rent with large horizontal mattress sutures buttressed with two strips of Teflon felt.130,178 This method is not recommended because the sutures are placed into necrotic, friable myocardium and can easily tear.136 The second method combines infarct excision and closure of the defect with interrupted, pledgeted sutures131,136,162,176 or a Dacron patch.179,180 This method usually requires aortic cross-clamping and is probably best reserved for those patients who have an associated ventricular septal defect.166 The third technique, described by N??ez et al,166 involves closing the defect with horizontal mattress sutures buttressed with two strips of Teflon felt, and then covering the closed ventricular tear and surrounding infarcted myocardium with a Teflon patch sutured to healthy epicardium with a continuous polypropylene suture (Fig. 26-17). Good control of active ventricular hemorrhage has been achieved with this method.136 The fourth method consists of simply gluing a patch of either Teflon175 or autologous gluteraldehyde-preserved bovine pericardium136,181,182 to the ventricular tear and infarcted area using a biocompatible glue of either fibrin (Tissucol, Immuno AG, Vienna, Austria), butyl-2-cyanoacrylate monomer (Histoacryl Blue, B. Braun, Melsungen AG, Germany), or gelatin-resorcin-formaldehyde (Pharmacie Centrale, C.H.V. Henry Mondor, Cr?teil, France). This technique does not necessarily require institution of cardiopulmonary bypass and may be the repair of choice when the ventricle is not actively bleeding.136,175
|
Acute false aneurysms are probably best repaired with an endocardial patch using the same methods as are used in repairing true ventricular aneurysms.141 Chronic anterior false aneurysms can usually be closed primarily if the neck is fibrotic. However, primary closure of the neck of a posterior false aneurysm may exacerbate mitral regurgitation, and therefore probably should be reconstructed with a patch of Dacron graft or glutaraldehyde-fixed bovine pericardium.144,147
SUBACUTE RUPTURE OF THE FREE WALL
The surgical experience with this entity is largely anecdotal. The single largest experience with surgical repair of postinfarction left ventricular free wall rupture was reported by Padr? et al.175 They treated 13 patients using a Teflon patch glued onto the ventricular tear and surrounding infarcted muscle, and utilized cardiopulmonary bypass in only 1 patient who presented with a posterior defect. All of their patients survived and were alive after a mean follow-up of 26 months. Eleven of them were asymptomatic and 2 had exertional angina.175 N??ez et al166 operated on 7 patients, 4 of whom survived. Recently the group at McGill University reported hospital discharge in 5 of 6 patients who received unsupported felt secured with cyanoacrylate glue.183 Coletti et al136 treated 5 patients and 4 survived. Pifarre et al162 treated 4 patients successfully, while Pappas et al180 treated 4 patients of whom 2 survived.
Although operative risk can not be determined from these small numbers, it is likely that without surgery all these patients would have died.141 It appears that patients who survive surgery tend to do well afterwards.141
FALSE ANEURYSM OF THE LEFT VENTRICLE
Komeda and David144 treated 12 patients with postinfarction left ventricular false aneurysms; 4 of them also had mitral valve replacements, 1 had repair of a fistula between the false aneurysm and the right ventricle, and 9 had coronary artery bypass surgery. There were 3 operative deaths, all in patients who needed mitral valve replacements. Of the 8 patients who underwent isolated repair of false aneurysms, all were alive after a mean follow-up of 62 months. Seven patients were asymptomatic and 1 had angina pectoris.144 Mackenzie and Lemole146 reported 14 cases of left ventricular false aneurysm, 12 of which were related to a previous myocardial infarction. There were 3 operative deaths. Long-term follow-up was not reported.
Overall, the literature suggests that patients who have isolated repair of false aneurysms of the left ventricle have low operative mortality.141
|
?? REFERENCES |
|---|
| Top |
|---|
: Prediction of rupture in acute myocardial infarction. Clin Cardiol 1988; 11:63.[Medline]
|
||||||||||||||||||||||||||||||||||||||||||||||||||
|
|
