Ischemic Mitral Regurgitation

	INTRODUCTION

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Ischemic mitral regurgitation is mitral insufficiency caused by myocardial infarction.^1–7 Myocardial infarction always precedes ischemic MR. The leaflets and subvalvular apparatus are by definition normal. The disease must be distinguished from MR associated with coronary artery disease in which no cause and effect relationship exists. The prevalence of coronary arterial disease⁸ makes the association of myocardial infarction and nonischemic mitral insufficiency very common. The term ischemic mitral regurgitation excludes degenerative, myxomatous, and connective tissue valvular disease, spontaneous ruptured chordae tendineae, and other causes of acute or chronic mitral regurgitation due to infection, inflammation, trauma, congenital abnormalities (including mitral valve prolapse), annular calcification, or tumors. Mitral regurgitation associated with dilated cardiomyopathy and profound left ventricular (LV) dysfunction is a related phenomenon but should be considered etiologically distinct from IMR.

Intermittent MR that is completely attributable to transient ischemia is an infrequent⁶ associated condition that is a manifestation of coronary insufficiency similar to angina and should be treated as such.

The wide and often confusing clinical spectrum of IMR is due to the fact that the disease is a manifestation of postinfarction ventricular remodeling. The size, location, and transmurality of the myocardial infarction (MI) sets in motion left ventricular remodeling that determines the severity, time course, and clinical manifestation of IMR. The presentation may be either acute (with and without papillary muscle rupture and immediately life-threatening) or develop insidiously over time in association with congestive heart failure (CHF).

Ischemic mitral regurgitation is a disease of the myocardium (both infarcted and normally perfused) that disturbs mitral valvular function; MR to due other etiologies is a valvular disease that affects the myocardium. The cellular, molecular, and genetic effects on the myocardium of these two different causes of MR are probably unrelated. Lessons learned from experience with MR of nonischemic origin are not likely applicable to IMR. Recent clinical and laboratory studies are beginning to improve our understanding and approach to this vexing clinical problem.

	PREVALENCE

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All except the most recently reported series^6,7 of IMR are "contaminated" with large numbers of patients with CAD and associated structural mitral valve disease. Inclusion of such patients produces a heterogeneous population that is difficult to analyze.^9–14 With this caveat, we present the available data. Suffice to say, the problem is large and likely to grow as survival after acute myocardial infarction continues to improve.

Between 17% and 55% of patients develop a mitral systolic murmur or echocardiographic evidence of IMR early after acute myocardial infarction (AMI).^2,15–18 Of patients who have cardiac catheterization within 6 hours of the onset of symptoms of AMI, 18% have IMR.⁵ In 3.4% of these patients, the degree of mitral insufficiency is severe.⁵ Many of the murmurs early after acute myocardial infarction are transient and disappear by the time of discharge.^2,16

In one study, 19% of 11,748 patients who had elective cardiac catheterization for symptomatic coronary artery disease had ventriculographic evidence of mitral regurgitation.¹⁹ In most of these patients the degree of mitral insufficiency was mild, but in 7.2% of all patients the degree of regurgitation was 2+ or greater, and in 3.4% MR was severe with evidence of heart failure.¹⁹ In another study of consecutive cardiac catheterizations, 10.9% of 1739 patients with CAD had MR.²⁰

Collectively, these data indicate that IMR is frequent early after AMI, but in many patients is mild or disappears completely. The relatively high incidence of IMR (10.9% to 19%) in catheterized patients with symptomatic coronary artery disease suggests that chronic IMR persists in many patients after acute infarction and may subsequently develop in others.¹⁶ Approximately 12.6 million Americans have angina or a history of myocardial infarction, and untold millions more have asymptomatic coronary atherosclerosis.⁸ Using these figures,^8,19,20 the incidence of IMR in the United States is estimated to be 1.2 to 2.1 million patients, with approximately 425,000 patients having moderate or severe IMR with heart failure.^8,19

	PATHOLOGY

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Ischemic mitral regurgitation may present suddenly in association with AMI or chronically with CHF as a late manifestation of postinfarction ventricular remodeling. In all cases (by definition) the valve leaflets and subvalvular apparatus are structurally normal. Whether, when, and to what degree IMR develops is dependent on the size, transmurality, and location of the MI. Attempts to correlate IMR with the severity and distribution of coronary stenoses have added little to understanding of the disease.^19,20 Studies evaluating the distribution of wall motion abnormalities associated with IMR have been much more enlightening. Clinical studies published in the 1970s and 1980s were the first to suggest an association of IMR with posteroinferior myocardial infarctions. By auscultatory criteria IMR was found to be more common and severe after posterior infarction.^4,10,20,21 These studies also demonstrated that posterior infarctions were more likely to involve the papillary muscle and be transmural. Recent laboratory and clinical reports have confirmed and strengthened the association between IMR and transmural posteroinferior myocardial infarction.^6,22,23

In sheep, which have unvarying, left dominant coronary arterial anatomy,²³ ligation of the two most distal circumflex marginal arteries infarcts 21% of the left ventricular (LV) mass, includes the posterior papillary muscle, and produces progressively more severe MR as the left ventricle dilates over the subsequent 8 weeks.²³ Ligation of these vessels and the posterior descending coronary artery infarcts 32% of the LV mass and produces immediate MR.²⁴ Comparably sized infarctions in any other ventricular location, including those involving the anterior papillary muscle, do not produce significant MR.²⁵ These well-controlled animal experiments confirm the importance of infarct location on the development of IMR. They also suggest that infarct size is relevant to the acuity of presentation.

A report by Gillinov et al involving nearly 500 patients treated over 13 years at the Cleveland Clinic confirmed the clinical importance of infarct location and size on the development of IMR.⁶ In this study, 73% of patients had posterior wall motion abnormalities and 63% had inferior wall motion abnormalities. Virtually all were found by echocardiography to have evidence of posterior and/or inferior myocardial infarctions. While infarctions in other locations occurred, they were less common and probably represent the diffuse nature of coronary atherosclerosis that is present in most patients with IMR.⁶

Ruptured papillary muscle causes acute, often life-threatening IMR after AMI. The posterior papillary muscle is involved three to six times more commonly than is the anterior muscle.^26–30 Either the entire trunk of the muscle or one of the heads to which chordae attach may rupture; in most series partial rupture is more common^27,28,30; in a few the reverse is true.^26,31 The extent of the infarct averages approximately 20%^21,25 but varies widely. Complete rupture occurs most commonly within the first week after acute infarc- tion.^25,30 Partial rupture may be delayed up to 3 months.^27,30

AMI may also produce sudden, severe mitral insufficiency without rupture of a papillary muscle. These patients are usually described euphemistically as having "papillary muscle dysfunction,"^16,26,27,30 and, indeed, the papillary muscle does not contract, but this expression tends to minimize a dangerous clinical situation. The associated (again, usually posterior) left ventricular wall at the base of the affected papillary muscle is invariably involved with a large infarction^28,30 that is often hemorrhagic and friable.²⁸

In chronic IMR, sizes and ages of infarcts vary widely, but as Gillinov has documented the wall motion abnormalities are overwhelmingly located in the posteroinferior aspect of the LV, and usually involve the posterior papillary muscle.⁶ Wall motion scores in these patients vary widely,^22,32 but the more severe degrees of MR are associated with larger areas of myocardial asynergy.²² Kono et al noted that the LV is more spherical in patients with chronic IMR and heart failure than in patients with previous infarctions that do not produce MR.³³ Surgeons usually describe a dilated mitral annulus at reparative operations for chronic IMR,^34,35 but detailed measurements and information regarding prior infarctions, the electrocardiogram, and ventricular dimensions during the cardiac cycle are not reported. Izumi et al observed significant annular dilatation (> 3 cm) in 11 of 43 patients with chronic IMR and noted a high correlation with increased LV volume and centralization of the regurgitant jet.²² Severe LV enlargement may occur without any dilatation of the mitral annulus.^16,36 Unlike dilated cardiomyopathies³⁷ or degenerative or connective tissue MR,³⁸ the mitral annulus may or may not be dilated in chronic IMR.¹⁶ The annulus tends to dilate in proportion to LV volume²² and in these patients the left atrium is often enlarged.

	PATHOGENESIS

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Normal Valve Function

The mitral valve has six anatomic components: leaflets, chordae tendineae, annulus, papillary muscles, left ventricle (LV), and left atrium. The mitral annulus is saddle-shaped (actually a hyperbolic parabloid with two-directional curvature) with cephalad promontories near the mid portions of the anterior and posterior leaflets and caudad depressions at the commissures (Fig. 28-1).³⁹ This unique shape is present in all mammalian mitral valves and has been shown, using finite element analysis, to reduce leaflet, annular, and chordal stress.⁴⁰ Function of the normal mitral valve is wonderfully complex and involves precisely timed interactions among the six components. These interactions are most easily described by relating the changes in each of the six components during a cardiac cycle. For this description the cardiac cycle is divided into four periods: systole, diastole, isovolemic relaxation (IVR), and isovolemic contraction (IVC), as defined below.

View larger version (55K): [in this window] [in a new window]   FIGURE 28-1 Image of a human mitral annulus obtained using three-dimensional transesophageal echocardiography (TEE). The image is reconstructed from two-dimensional images sampled every 10 degrees using a rotational omni-probe gated for heart rate and respiration. The annulus is viewed from posterior annulus (near) to aorta (far). The pronounced saddle shape of the human mitral annulus is well demonstrated.

During isovolemic contraction (IVC), left atrial filling begins immediately after the mitral valve closes and before the aortic valve opens.⁴² Flow through the mitral valve briefly reverses as the leaflets coapt and bulge toward the atrium.⁴³ During systole the left atrium rapidly fills⁴² and reaches maximum near ES. The position of the annulus ascends (away from the apex) slightly during atrial contraction,^44–46 which occurs during late diastole, does not change during IVC, and descends progressively 1 to 1.5 cm toward the apex throughout systole.^42,46,47 The annulus asymmetrically⁴⁴ contracts⁴⁷ during atrial and ventricular systole and in humans reaches a minimal area (mean reduction of 27%) in mid systole.⁴⁸ Immediately after atrial contraction, the mitral leaflets approach each other and close within 20 to 60 milliseconds after pressure crossover when LV pressure exceeds LA pressure.⁴² Since the total area of leaflet tissue is approximately twice the total area of the annulus,^36,49 the apposition point of the two leaflets at the time of pressure crossover is very near the plane of the annulus.^50,51 At closure approximately 30% of the anterior cusp and 50% of the longer posterior cusp are in apposition.⁵⁰ Chordae tendineae attached to the free edges and body of the leaflets⁵⁰ restrict the upward movement of the slightly compliant leaflets and produce a tight seal along the line of apposition.⁵⁰ Chordal tension peaks in early systole and begins to fall slowly in late systole and rapidly during IVR.⁵² Papillary muscles begin to shorten during late IVC and throughout systole in synchrony with shortening of the adjacent ventricular wall.⁵³ The actual distance papillary muscles shorten is small and ranges between 2 and 4 mm.^37,54 During systole, the directions and timing of left ventricular contraction are not necessarily uniform throughout systole because of the complex anatomic arrangement of muscle bundles^55,56 and the timing produced by the impulse conduction pattern.⁵⁷ LV shortening is greater in both equatorial axes than in the long axis.⁵⁷ LV wall thickness increases during IVC and decreases rapidly during IVR.⁵⁸ Peak wall thickness occurs near ES, but timing of the exact peak varies slightly between ventricular wall segments. During systole the ventricle progressively twists counterclockwise (as viewed from the apex) along its longitudinal axis to reach a maximum at ES.⁵⁹

During IVR the left atrium begins to empty when left atrial pressure crosses over and exceeds LV pressure.^42,43 The atrium empties rapidly in early diastole and further diminishes with atrial contraction in late diastole just before IVC.⁶⁰ The LV may actually generate negative pressure in early diastole if left atrial pressures are low.⁶¹ During IVR, the mitral annulus to LV apex distance lengthens as the mitral annulus ascends in early diastole, descends slightly, and ascends again with atrial contraction.^42,45 The area of the mitral orifice increases slightly during IVR and continues to increase during diastole until it reaches a maximum just before the left atrium contracts.^44,48 In humans, the annular area index reaches a maximum of 3.9 ± 0.7 cm²/m².⁴⁸ As the annular area increases, its shape changes asymmetrically; most of the area increase is due to lengthening in the posterior and lateral parts of the annulus (away from the fibrous trigone).⁴⁴ During IVR the mitral leaflets separate approximately 30 milliseconds before left atrial pressure exceeds LV pressure.⁴² Peak blood flow through the valve occurs early in diastole, but the mitral leaflets reach their maximal open position before peak flow occurs and begin closing while flow is still accelerating.⁶²

The papillary muscles may shorten very slightly during early IVR,^41,53,54,63 but do not begin to lengthen until the beginning of diastole. Papillary muscles reach maximum length shortly after ED during IVC. Chordal tension decreases rapidly during IVR and remains near zero until late diastole, when a small increase occurs.^52,62 The left ventricle relaxes and dilates after ES and reverses the complex deformations of LV shape produced by systole. During early diastole, and the period of rapid filling, the ventricle dilates primarily along both equatorial axes and much less along the longitudinal, base-to-apex axis.⁵⁷ Only a little shape change occurs in mid diastole and after atrial contraction. Ventricular wall thickness decreases⁵⁸ primarily during IVR. Lastly, the ventricle rapidly untwists (rotating clockwise) during early diastole and more gradually during mid and late diastole.⁵⁹

Mechanism of Ischemic Mitral Regurgitation

The pathogenesis of both acute IMR in the absence of papillary muscle rupture and chronic IMR is complex. Experimental analysis of clinically relevant ovine models using tantalum marker imaging, sonomicrometry array localization, and three-dimensional echocardiography^64–69 as well as detailed clinical echocardiographic studies has more clearly elucidated the mechanism of the complex geometric and temporal perturbations that cause a structurally normal mitral valve to leak, often massively, early or late after a myocardial infarction.

ACUTE ISCHEMIC MITRAL REGURGITATION

Numerous studies have conclusively demonstrated that loss of papillary muscle shortening alone as result of acute ischemia does not cause MR.^49,70–74 The term "papillary muscle dysfunction" is, therefore, erroneous and should be avoided. With ischemia or infarction, the posterior papillary muscle elongates 2 to 4 mm in the sheep and dog^53,54; the tip moves 1.5 to 3 mm closer to the annulus.^54,75 These are very small changes, and echocardiographic studies in dog, sheep, and man uniformly fail to show mitral valve prolapse with acute IMR in the absence of papillary muscle rupture.^3,33,51,76 In the sheep model of acute IMR, the uninfarcted anterior papillary muscle contracts earlier and more vigorously than before infarction. This moves the tip 4 to 5 mm further away from the annular plane at mid systole than before infarction.⁶⁴ This discoordination of normal synchronous papillary muscle contraction has a complex effect on leaflet coaptation that has been meticulously characterized by Miller et al^67,68 using tantalum marker technology. It is sufficient to say that the interaction of these rather small changes in papillary muscle contraction dynamics and location cause subtle distortions of valvular leaflet coaptation that are not simply leaflet prolapse and tethering. Annular dilatation is at best mild (10% to 15%) and located primarily along the posterior annulus in the ovine model of acute IMR.^64–66,77 This degree of dilatation is within the physiologic range achieved by varying loading conditions in sheep.⁷⁸ Leaflet area in sheep exceeds the maximum annular area by 50% to 100%.⁷⁷ These data suggest that acute IMR results from a complex interaction of very small geometric and temporal changes that for the most part are not demonstrable by standard imaging techniques and are not discernible in a flaccid heart at the time of surgery.

CHRONIC ISCHEMIC MITRAL REGURGITATION

In chronic IMR mitral valve prolapse has been described⁷⁹ in occasional patients, but the vast majority have incomplete mitral valve closure due to papillary muscle and chordal restriction of leaflet motion.^{33,71,76,79–82} Pathologic studies consistently show fibrosis and atrophy of infarcted papillary muscles,^3,16,36,70 and none demonstrate papillary muscle or chordal elongation. Nevertheless, surgeons describe elongated chordae in some patients with myocardial infarction and MR.^6,34,35 Elongated chordae and mitral valve prolapse without MR probably antedate the infarction in these patients.^83,84 In a patient with preexisting mitral valve prolapse, ventricular infarction may cause the previously competent valve to leak. This hypothesis explains sporadic observations of mitral valve prolapse in patients with chronic IMR, but needs preinfarction echocardiograms for confirmation.

Ovine experiments using sonomicrometry array localization to study postinfarction MR that evolves during the first 8 weeks after infarction have added insight relevant to the pathogenesis of chronic IMR. In this model, a combination of asymmetric annular dilatation and leaflet tethering by both papillary muscles occurs to produce chronic IMR. The annular area dilates by at least 60% at all time points during systolic ejection, but the dilatation involves all of the muscular annulus. The posterior or mural portion of the annulus directly adjacent to the infarct moves away from the relatively fixed anterior commissure (at the anterior fibrous trigone) and stretches the anterior portion of the mural annulus and the posterior portion of the aortic-based annulus, which are remote from the infarct. This finding illustrates how a moderately sized (21% of the LV mass) localized infarct remodels and distorts remote, uninfarcted myocardium including the mitral valve annulus (Fig. 28-2A).⁸⁵

View larger version (15K): [in this window] [in a new window]   FIGURE 28-2 (A) Two-dimensional axial view of the mitral valve annulus and papillary muscle transducers before (solid line) and 8 weeks after infarction. Note the stretching of both the posterior part of the aortic portion of the annulus (Ao to PC) and the anterior part of the mural portion of the annulus (Ao to P1 to P2). Also, note how the portion of the annulus between P2 and PC along with the posterior papillary muscle tip (PPT) pulls away from the relatively fixed anterior commissure. (B) Two-dimensional saggital view of the sheep mitral annulus and its relationship to the LV and papillary muscles before and 8 weeks after infarction. Note how the PPT and the posterior annulus are retracted away form the anterior commissure. The heart shown in this figure is the same one shown in Figure 28-1.

The concept of leaflet tethering as a contributing factor in the pathogenesis of chronic IMR is not new.^86–88 Two recent echocardiographic reports, one studying the same sheep model presented here and one human study, demonstrated findings very consistent with the experimental results cited above. Otsuji et al applied a very effective three-dimensional echocardiographic technique to quantify leaflet tethering in the same ovine model.⁸⁶ These authors also reported mid-systolic distortions between both papillary muscle tips and the anterior commissure, but did not observe changes between papillary muscle tips and the posterior commissure or annular dilatation. Yiu used quantitative two-dimensional echocardiography to corroborate these findings clinically by comparing normal controls with a cohort of patients with varying degrees of chronic IMR.⁸⁸ They found that ventricular distortions, which most closely correlated with the degree of MR, occurred between the posterior papillary muscle tip and anterior commissure (R = 0.55) and posterior displacement of the anterior papillary muscle tip (R = 0.65).

To summarize, the geometric changes that lead to acute IMR are multiple but extremely subtle (< 5 mm) and are not reliably imaged by currently available clinical modalities. Chronic IMR involves larger changes (1–2 cm) that cause moderate annular dilatation and complex leaflet tethering along the anterior and mid leaflet coaptation line.

	NATURAL HISTORY

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After acute myocardial infarction (AMI), approximately 15% of mitral murmurs disappear by hospital discharge and another 15% are gone within several months.¹⁶ In patients with AMI who do not have an early mitral murmur, approximately 12% develop an MR murmur later.¹⁶ Thus roughly 15% of patients have some degree of MR months after AMI.¹⁹

The presence of MR after AMI as determined by color flow Doppler velocity mapping or cardiac catheterization increases the likelihood of pulmonary edema, cardiogenic shock, and death.^2,5,89 However, when adjusted for age, ejection fraction, heart failure, and other variables that affect mortality, the presence of MR is not an incremental risk factor for early death.⁵ Nevertheless, even mild or moderate MR after AMI doubles the 30-day and 3-year mortality to approximately 15% and 20%, respectively,⁵ as compared to patients without MR.⁹⁰

Without surgery, median survival following rupture of a papillary muscle trunk is three to four days.^26,27 Some patients with partial rupture or rupture of one head survive several weeks or a few months.^27,91 Overall, acute moderate or severe (3+ or 4+) IMR has a 30-day mortality of 24% and a 1-year mortality of 52%.⁵ The onset of cardiogenic shock reduces survival to a few days.

Chronic IMR of 2+ severity discovered at cardiac catheterization for symptomatic coronary artery disease has a 1-year mortality of approximately 17%; 1+ severity increases mortality to approximately 10% from about 6% if MR is not present.¹⁹ The one-year mortality for 3+ and 4+ IMR is approximately 40%,¹⁹ which is only slightly less than severe MR after acute infarction.⁵

	DIAGNOSIS AND MANAGEMENT

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As noted above, acute IMR and chronic IMR are clinically related entities that are pathophysiologically and etiologically distinct. Their presentation, diagnosis, treatment, and outcome are discussed separately below to emphasize this distinction.

Acute Postinfarction Mitral Regurgitation

In most patients, the presence of MR does not affect management of AMI. Postinfarction angina with mild or moderate MR without symptoms or signs of heart failure is managed similarly to postinfarction angina without MR. A minority of patients develop severe (3+ or 4+) MR with symptoms of heart failure, low cardiac output, or both.

Severe MR following AMI may be due to rupture of a papillary muscle trunk or tip or to displacement of a papillary muscle and distortion of subvalvular structures. Rupture of the trunk of a papillary muscle (Fig. 28-3) invariably causes immediate, severe MR with pulmonary edema and cardiogenic shock and requires prompt intervention for survival. Rupture of a papillary muscle tip usually produces severe MR, but can, rarely, be consistent with longer survival.^27,91 Acute, severe postinfarction MR without rupture is more common than papillary muscle rupture and may be associated with both large and small infarctions. Although the specific pathology varies, acute, severe postinfarction MR is a distinct, highly lethal clinical entity that invariably requires surgery for survival.

View larger version (202K): [in this window] [in a new window]   FIGURE 28-3 Surgical specimen from a patient who ruptured the trunk of the posterior papillary muscle three days after acute postero-inferior myocardial infarction.

PATHOPHYSIOLOGY

Acute, severe mitral regurgitation produces acute LV volume overload and immediately increases LV end-diastolic volume and preload and decreases end-systolic volume.⁹⁴ Volume of regurgitant flow depends upon the size of the incompetent valve opening during systole and the pressure difference between the LV and left atrium. This pressure difference is influenced by LV afterload, forward flow past the aortic valve, and myocardial contractile force. Acute MR enhances early diastolic filling of the ventricle and decreases end-systolic wall stress (afterload) and end-systolic elastance.⁹⁵ Myocardial oxygen consumption does not change because of reduced wall stress in late systole.⁹⁴ Stroke volume increases and initially cardiac output may be maintained by a tremendous increase in stroke volume. However, if the regurgitant fraction of the increased stroke volume is very large, the amount of forward flow past the aortic valve (i.e., cardiac output) decreases. With MR, ejection fraction increases in animals without LV infarction; in patients with infarction, ejection fraction varies widely.³¹ Left atrial, pulmonary capillary wedge, and LV end-diastolic pressures increase abruptly with acute MR; end-diastolic wall stress also increases markedly, and end-diastolic wall thickness and stiffness decrease slightly.⁹⁶ In patients with small atria, a prominent "v" wave appears.^28,97 Pulmonary vascular resistance increases rapidly and may cause right heart failure.⁹⁴

CLINICAL PRESENTATION

Acute, severe IMR usually presents abruptly with an acute onset of chest pain and/or shortness of breath. The age range of patients reflects the age range of myocardial infarction; the mean age is around 60. The syndrome is slightly more common in men than women. Recent series report that 17% to 20% of ischemic mitral regurgitation cases coming to surgery are for acute IMR.^6,7 Only a few patients have historical or electrocardiographic evidence of prior myocardial infarction and less than half have angina.^26,28,30 The disease presents as an acute myocardial infarction and occasionally may be silent.^28,30 Papillary muscle rupture may occur as early as the first day after infarction and nearly always within 7 days (mean approximately 4 days).^26,28,30

Typically, patients are short of breath and many rapidly develop pulmonary edema complicated by systemic hypotension. Most patients have a loud apical, holosystolic murmur that radiates to the left axilla⁹⁷; in some the murmur occurs in mid or late systole, and in others it may be absent⁹⁰ or difficult to hear because of pulmonary rales.²⁸ The most compelling findings are those of low cardiac output and congestive heart failure in the setting of AMI. Many patients develop cardiogenic shock characterized by systemic hypotension, oliguria, acidosis, and poor peripheral pulses and perfusion.⁹³ A few have cardiac arrest.³¹

DIAGNOSTIC STUDIES

Nearly all electrocardiograms are abnormal,^26,28,30 but only slightly more than half are diagnostic of AMI. Some of the nondiagnostic changes include right or left bundle branch block and nonspecific ST- and T-wave changes in the anteroseptal, lateral, or inferior leads.^26–28,30 Most patients are in sinus rhythm.^28,94 In autopsy series, the incidence of subendocardial infarctions is approximately equal to the incidence of transmural infarctions.^26,30 Frequently patients with ruptured papillary muscle have electrocardiographic evidence of an inferior infarction. When the ECG is diagnostic, inferior wall infarctions are much more common than anterior and lateral wall infarctions. Conduction abnormalities are relatively uncommon and are more often found in patients with postinfarction ventricular septal defects.⁹⁸

Chest x-rays nearly always show signs of pulmonary congestion, interstitial pulmonary edema, and pulmonary venous engorgement.²⁸ The heart may or may not be enlarged²⁶ and usually is not massively enlarged.

The differential diagnosis includes postinfarction ventricular septal defect, massive AMI without significant MR, and ruptured chordae tendineae without AMI. Right heart catheterization usually shows elevated pulmonary arterial pressures with prominent "v" waves reaching 40 mm Hg or higher.^28,31 Mean pulmonary artery wedge pressures are greater than 20 mm Hg unless cardiac output is very low. Mixed venous oxygen saturations are often well below 50% and reflect low cardiac output with indices that range from 1.0 to 2.9 L/m²/min.³¹ In the presence of a loud systolic murmur, absence of an oxygen step-up in the pulmonary artery is strong evidence against the diagnosis of postinfarction ventricular septal defect. Electrocardiographic evidence of AMI distinguishes acute IMR from acute chordal rupture, but in some instances the two diseases cannot be distinguished until after operation or death.²⁸

Transthoracic echocardiography (TTE) assesses the degree of MR, confirms wall motion abnormalities, and often demonstrates flail mitral leaflets. Transesophageal (TEE) echocardiography is the diagnostic imaging tool of choice. This modality definitively documents the degree of MR, associated wall motion abnormalities, and the status of the posterior papillary muscle.^99,100 Typically the left atrium is not enlarged, but the left ventricle shows signs of volume overload and segmental wall motion abnormalities. Color flow Doppler velocity mapping documents the presence of MR after myocardial infarction⁹⁰ and semiquantitates its severity.¹⁰¹ Ejection fractions vary widely, but do not reflect the extent of the LV infarction.

Despite hemodynamic instability, most patients have a diagnostic cardiac catheterization primarily for definition of coronary arterial anatomy; however, the wisdom of prescribing cardiac catheterization for patients in cardiogenic shock is highly questionable in that revascularization of obstructed, remote coronary vessels is not likely to improve a patient's chances for immediate survival.⁹³ Approximately half of catheterized patients have single-vessel disease, most often of the right coronary artery.^28,31 Most of the remainder have three-vessel disease.^26–28,30 Ventriculography shows increased LV volume at both end diastole and end systole, severe MR, segmental wall motion abnormalities,¹⁰² and a wide range of ejection fractions, which are generally over 40% and frequently over 60%.^27,31 LV end-diastolic pressures are elevated with prominent left atrial "v" waves and moderate pulmonary hypertension. Occasional patients have mild or moderate tricuspid regurgitation. Cardiac output is usually low.

MEDICAL MANAGEMENT

The urgency and aggressiveness of initial management depends upon the presence or absence of cardiogenic shock and/or congestive heart failure. Because of the severity of MR, definitive therapy means surgery or rarely interventional cardiac catheterization. Beyond the need for diagnosis and brief attempts to stabilize the circulation, there is nothing to gain by deferring definitive therapy. In an intensive care unit, patients are monitored by continuous electrocardiogram, measurement of peripheral oxygen saturation, an arterial catheter with continuous display of arterial blood pressure, and a Swan-Ganz catheter to monitor central venous pressure, pulmonary arterial pressure, cardiac output (intermittently or ongoing), and mixed venous oxygen saturations. An additional intravenous access may be needed. If surgery is possible or probable, a blood sample should be sent for type and cross-match and routine blood work for hematology, electrolytes, glucose, renal function, and coagulation studies. Blood gases for arterial oxygen saturation, Paco₂, and pH are also obtained. Nasal prongs or mask provides supplemental oxygen. The decision to intubate and ventilate the patient is made on the basis of clinical assessment of respiratory distress, findings of pulmonary edema, low Pao₂, or elevated Paco₂.

The adequacy or inadequacy of the circulation must be assessed early before arrhythmias or cardiac arrest intervenes. The criteria for cardiogenic shock vary slightly between specialists, but systemic hypotension (peak pressure <80 mm Hg; mean pressure <55 mm Hg), mixed venous oxygen saturation less than 50%, thermodilution cardiac index less than 2.0 L/m²/min, metabolic acidosis, oliguria, and poor peripheral perfusion (pallor, cool extremities, faint peripheral pulses) are findings that collectively or in various combinations indicate that the circulation is not adequate. Even if the criteria for cardiogenic shock are not present, patients must be promptly worked up and carefully monitored to avoid either progressive or abrupt deterioration of the circulation. Necessary diagnostic studies are best performed as promptly as possible.

Circulatory performance must be optimized and carefully monitored. Drugs that least impair myocardial contractility or cause hypotension should be used to control arrhythmias. Electrical cardioversion is often the first choice for tachy-arrhthmias when cardiac output is low. Temporary pacing via skin electrodes or an intravenous catheter may be the best treatment of bradyarrhythmias and atrial flutter. Appropriate inotropic therapy should be used to optimize cardiac output. If organ perfusion is still unacceptable, an intra-aortic balloon pump may be needed to maintain coronary perfusion pressure, unload the LV, and to increase cardiac output. For patients who are not hypotensive, pharmacologic reduction of afterload using intravenous nitroglycerin¹⁰³ or nitroprusside improves cardiac output. Management of fluid volume is critical and best guided by ongoing measurements of central venous and pulmonary capillary wedge or diastolic pressures. Additional volume must be given cautiously in critically ill patients to avoid volume overload and acute decompensation of the ventricle. In less ill patients, additional crystalloid or colloid may improve cardiac output and restore urine flow.

DEFINITIVE THERAPY

Prompt surgery is the best chance for survival for most patients with acute, severe postinfarction MR. A few, highly selected patients without papillary muscle rupture early in their presentation have been treated by emergency percutaneous transluminal coronary angioplasty (PTCA) and/or thrombolytic therapy in an attempt to reduce the size of the infarct and thereby reduce MR.^5,79,104,105

PTCA or thrombolysis carried out within 4 hours of the onset of AMI may on occasion produce spectacular reversal of both the infarction and MR.^79,104,105 However, less rapid PTCA may not succeed in preempting the infarct and aborting MR.¹⁰⁵ PTCA and thrombolysis in catheterized patients are potentially worth trying if patients reach medical attention soon after the onset of symptoms, are sufficiently stable, and can be followed by echocardiography. However, in many patients PTCA and thrombolysis do not provide a favorable outcome.⁵ In one study, 17% of patients with acute IMR and successful thrombolysis died in hospital; in those with successful PTCA, 50% died shortly afterward, and 77% were dead in one year.⁵ Of the survivors, the majority continue to have 3+ or 4+ MR.⁵

For patients who have acute postinfarction angina with 1+ or 2+ MR, urgent myocardial revascularization is indicated to relieve angina and to prevent extension of the infarction. It is important to prevent progression of MR and the development of congestive heart failure or cardiogenic shock. This is usually accomplished by thrombolysis, PTCA, or an intracoronary arterial stent. If these measures are unsuccessful, operation is rarely completed in time to reverse the infarction, but early operation may reduce the size of the ultimate infarct.^106–108 The presence of mild to moderate IMR does not increase operative mortality,^109–111 but the presence of congestive heart failure is a risk factor.¹¹² In these patients, the mitral valve is generally not addressed unless intraoperative transesophageal echocardiography indicates 3+ or 4+ MR.

Indications for emergency surgery for acute, severe postinfarction MR vary among institutions^{5,28,29,31,93,113,114} and probably explain wide discrepancies in reports of hospital mortality.^32,113 In this group of patients, medical therapy does not produce survivors^27,28 and patients denied operation are not reported.²⁸ Aged patients are less likely to survive operation,^32,79 and there are only anecdotal reports of successful operation in octogenarians (Gorman JH III, personal communication). Other risk factors for hospital death are severe congestive heart failure, the number and severity of comorbid diseases such as renal or pulmonary problems, presence of an intra-aortic balloon pump, reduced ejection fraction, and greater number of diseased coronary arteries.³³ Contemporary concerns regarding costs and longevity beyond immediate hospital survival also influence indications for operation and reported mortality.

Operation for acute (within 30 days) severe, postinfarction MR consists of mitral valve repair or replacement with or without myocardial revascularization. Nearly all surgeons recommend revascularization of all significantly obstructed coronary vessels away from the site of the infarction,¹¹³ and improved methods of cardioplegia and the open-artery hypothesis support this recommendation even in patients with preoperative cardiogenic shock who have had cardiac catheterization. The wisdom of blind revascularization of remote coronary vessels in patients who have not had preoperative cardiac catheterization and revascularization of the infarct artery more than 4 to 6 hours after onset of pain is less clear.⁹³ On a statistical basis, only half of patients with acute IMR have multivessel coronary artery disease.^26,28,31 Revascularization of completed infarctions favorably influences subsequent ventricular remodeling.^107–109

OPERATION

Operation for acute, severe postinfarction MR is often urgent or an emergency; a high percentage of patients have an intra-aortic balloon pump inserted before induction of anesthesia.^31,93 Monitors include the electrocardiogram, arterial blood pressure, a Swan-Ganz catheter with mixed venous oxygen electrode, nasopharyngeal and rectal (or bladder) temperature, and a catheter for urine output. The heart is exposed through a midline sternotomy and needed saphenous vein is harvested simultaneously. Mammary arteries are less often used for revascularization because of the extra time needed and typically precarious condition of the patient. Both cavae are cannulated separately and the pericardial attachments around the superior and inferior cavae and the right pulmonary veins are dissected back. Most patients with acute IMR have small left atria. During cardiopulmonary bypass moderate systemic hypothermia is employed; the aorta is cross-clamped; and the heart is protected by cardioplegia (e.g., retrograde and antegrade cold blood with myocardial temperature monitoring). After opening the left atrium for decompression of the heart, planned coronary bypass grafts are constructed prior to exposing the mitral valve.

The left atrium is usually opened after dissecting the lateral interatrial septum. The incision extends behind the inferior vena cava. Valvular exposure can in some cases be difficult; better exposure may be obtained by opening the right atrium just anterior to the interatrial septum and then cutting the septum transversely toward (but not to) the anterior commissure of the tricuspid valve. Improved exposure may also be obtained by extending the atrial incision superiorly behind the superior caval–right atrial junction. The mobilized cava may be retracted strongly anteriorly or, if cannulated directly, it may be divided at the right atrial junction.

Replacement of the diseased valve is the most reliable option in these often critically ill patients regardless of the pathology of the acute IMR.⁷ It is important to preserve the chordal attachments to the annulus (Fig. 28-4). The prosthetic valve (usually mechanical) is sutured to the annulus with running or interrupted sutures. The choice of a mechanical or bioprosthetic valve is optional since durability and anticoagulation issues are relatively minor concerns in these patients. The atrial incisions are closed with running sutures and any proximal anastomses are completed before weaning the patient off cardiopulmonary bypass.

View larger version (41K): [in this window] [in a new window]   FIGURE 28-4 Okita's method for retaining chordal attachment to the mitral annulus during replacement of the mitral valve. (A) Diagram showing the mitral valve from the left atrium. The center of the anterior leaflet is excised (shaded area) and the leaflet is divided retaining the chordae from each papillary muscle attached to the residual anterior leaflet tissue. The posterior leaflet may be divided at its midpoint if necessary. (B) Remnants of the anterior leaflets are sutured to the annulus using a single stitch as shown. This tissue is later included in sutures used in sewing the valve to the annulus. (Modified slightly with permission from Okita Y, Miki S, Kusuhara K, et al. Analysis of left ventricular motion after mitral valve replacement with a technique of preservation of all chordae tendineae. J Thorac Cardiovasc Surg 1992; 104:786.)

RESULTS

Published results of mitral valve replacement, which is recommended by many surgeons for acute, severe IMR, are poor.^{28,29,31,32,93,113,115} Hospital mortality ranges from 31% to 69% and probably reflects the selection process more than quality of care. Variables that increase early mortality include patient age, cardiogenic shock, comorbid conditions, the amount of infarcted myocardium, and delay in operation.^27,28,31,32 More recent experience may be better^6,7,116 because of prompt diagnosis, early surgery, complete revascularization, and application of chordal preservation techniques that better preserve LV function.^117–121 Several techniques are available for preserving chordae (Fig. 28-4).^117,122,123 David reports a hospital mortality of 22% in 18 patients using chordal preservation techniques.¹¹⁶

Many surgeons do not recommend mitral valve repair for acute IMR,^{7,29,93,114,116} but others do.^6,33,122,124 Repair of the valve in acute IMR poses difficult problems. As demonstrated above, the anatomical derangements may be very subtle. A reasonable repair option is, therefore, undersized ring annuloplasty. In cases of papillary muscle rupture, successful reimplantation in conjunction with ring annuloplasty has been reported, but these patients are uncommon and usually much less ill.⁶ Intraoperative transesophageal echocardiography and color flow Doppler velocity mapping are essential adjuncts to operation to assess quality of the repair.^99,100 Long-term (5-year) survival in patients who survive the perioperative period is poor and even in modern reports hovers around 50%.^6,7

Chronic Ischemic Mitral Regurgitation

Between 10.9% and 19.0% of patients with symptomatic coronary arterial disease who have cardiac catheterization^19,20 and 3.5% to 7.0% of patients who have myocardial revascularization have IMR.^125–128 The majority of patients with IMR have chronic IMR, and most of these patients have 1+ or 2+ MR without heart failure.^{19,20,125–127}

In patients with chronic IMR, three major variables interrelate to produce the clinical spectrum of patients with varying combinations of symptomatic ischemia and heart failure. As with acute IMR, the three variables are: (1) the presence and severity of ischemia, (2) the severity of MR, and (3) the magnitude of LV dysfunction. Patients with obstructive coronary artery disease may have no symptoms or have stable, progressive, unstable, or postinfarction angina or its equivalent. Because of disabling symptoms, threat to LV mass or statistically shortened survival ischemia is a compelling problem that must be addressed therapeutically. The approach and methods do not materially differ from similar patients who do not have IMR. The severity of MR is the second variable. At present, 1+ or 2+ MR in patients without symptoms of heart failure does not compel invasive therapy for MR. More severe MR and/or symptoms of heart failure require evaluation for possible operation irrespective of the therapy needed for ischemia. The degree of LV dysfunction is the last variable and the most difficult to assess in the presence of MR. Symptoms of heart failure may be due to LV dysfunction, MR, or both.

PATHOPHYSIOLOGY

It is important to realize the clinical and laboratory data regarding mitral regurgitation without prior myocardial infarction are not confidently extrapolated to patients with chronic IMR. It is possible (and recently laboratory studies suggest likely)¹²⁹ that the myocardial insult of progressive MR is dwarfed by the dramatic changes inflicted on normally perfused myocardium as a result of postinfarction ventricular remodeling.¹³⁰

In patients with chronic IMR, LV volume and wall stress increase at end diastole^20,89,96,131 and LV mass increases progressively without an increase in end-diastolic wall thickness.¹³¹ Infarction contributes to LV dilatation by increasing diastolic wall stress and by stimulating myocyte hypertrophy and myocyte slippage in uninfarcted, remote areas.¹³² In patients with IMR who maintain a near normal ejection fraction, peak systolic wall stress increases¹³² and the velocity of shortening decreases,¹³³ but end-systolic volume and stress remain near normal.¹³¹ Cardiac output is reduced but maintained at asymptomatic or minimally symptomatic levels by an increase in preload (increased end-diastolic wall stress).¹³¹ However, in patients with reduced ejection fractions, both end-diastolic and end-systolic volumes and stresses increase and cardiac output and stroke volume fall; the increase in afterload cannot be overcome by increased myocardial contractility produced by the increased preload.¹³¹ Left atrial, LV end-diastolic, and pulmonary wedge pressures increase to two or three times normal values independent of ejection fraction¹³¹; often the atrial "v" wave disappears⁹⁷ as does atrial contraction. The left atrium enlarges.⁹⁷ In patients with chronic IMR, the LV enlarges asymmetrically,^16,20 particularly in the infarct and borderzone myocardium around the infarct.¹³⁴ Over time both the severity of MR²⁰ and loss of myocardial contractile strength worsen.^{16,20,130,133} The degree to which the MR exacerbates loss of contractile function induced by ventricular remodeling is an area of intense laboratory and clinical investigation.

CLINICAL PRESENTATION

Most published series of chronic "ischemic mitral regurgitation" are of limited value because of "contamination" by inclusion of patients with nonischemic MR. Gillinov et al reported on 482 consecutive patients operated on for ischemic mitral regurgitation at the Cleveland Clinic over a 13-year period.⁶ The report is unique and highly informative because the authors excluded patients with nonischemic MR. All patients had normal leaflet and subvalvular structure and all had a previous myocardial infarction. A clear distinction was also made between patients having operation within 2 weeks of their infarction. In this study 78% of patients were over 60 years old and 54% were male. NYHA class II, II, or IV heart failure symptoms were present in 32%, 30%, and 36%, respectfully. Chronic IMR was present in 80% and 12% had an intra-aortic balloon pump placed prior to surgery. There was a history of an inferior MI in 73% and superior MI in 63%, and essentially all patients had posterior, inferior, or both types of infarction. The procedure was a reoperation in 23% and an emergency in 8%. Triple- or double-vessel coronary artery disease was present in 89%. Atrial fibrillation occurred in one third of the patients. Myocardial revascularization was performed at the time of valve surgery in 95%. These demographic data are remarkably similar to another excellent report published by Grossi et al from New York University.⁷

DIAGNOSTIC STUDIES

The primary purpose of diagnostic studies is to determine the severity of coronary arterial disease and its anatomy, the severity and mechanism of MR, and the degree of LV dysfunction. In chronic IMR, the ventricular geometry and function reflect remodeling due to both the MR and infarction; therefore, these patients may require diagnostic studies and perhaps operative procedures that are different from patients with CAD associated with MR. It is also important to define comorbidity of other organ systems by appropriate diagnostic studies dictated by the patient's history, physical examination, and screening laboratory findings.

In patients with IMR, the ECG usually shows evidence of a prior myocardial infarction.^{126,127,135,136} The incidence of arrhythmias varies but atrial fibrillation as noted earlier is quite common. In patients without failure and mild MR, heart size by chest x-ray is normal or slightly enlarged; the left atrium is seldom enlarged. In those with moderate or severe MR and/or severe LV dysfunction, the heart is enlarged and usually the left atrium is also enlarged.⁹⁷

Transthoracic echocardiography and TEE are useful in determining the etiology of MR. Two-dimensional echocardiography reliably detects ruptured chordae, annular calcification, and myxomatous degeneration, which are not features of chronic IMR, and differentiates rheumatic valve disease, endocarditis, and congenital deformities. Echocardiography also effectively assesses regional wall motion abnormalities and global LV function. The degree of MR is also well-quantified by color flow Doppler measurements.

Cardiac catheterization defines the coronary arterial pathology. Ventriculograms add little to the data provided by TTE or TEE and should be avoided especially in patients with impaired renal function. Measurements of chamber pressures and estimates of cardiac output contribute to the overall evaluation of LV function. Pulmonary hypertension, when present, is typically moderate and correlates with the degree of LV dysfunction and/or severity of MR.

INDICATIONS FOR SURGERY

Patients with symptomatic coronary artery disease that is not amenable to interventional cardiology are candidates for operation. The criteria for revascularization do not differ from patients without IMR; however, the presence of MR and/or severe LV dysfunction increases the risk of operation.^126,125,135 A decision not to expose the mitral valve is generally made preoperatively if the severity of MR is 1+ or 2+, and is confirmed in the operating room by transesophageal echocardiography and color flow Doppler velocity mapping before and after cardiopulmonary bypass and after manipulating afterload and preload.

The presence of severe IMR (3+ or 4+) and significant LV dysfunction has been a conventional indication for operative therapy on the mitral valve in addition to any bypass grafts needed to ameliorate symptoms of coronary ischemia. Valve repair or replacement in these patients simplifies weaning from cardiopulmonary bypass and early postoperative management. Whether or not restoring valve competency in these patients reduces heart failure symptoms or improves longevity has not been resolved by available clinical and laboratory data.

OPERATION

Operation is usually elective except in patients with uncontrolled symptoms of coronary ischemia who may require emergency or urgent operation to prevent infarction. Preoperative preparation and intraoperative monitors do not differ from other cardiac operations with the exception of transesophageal echocardiography and color flow Doppler velocity mapping. After induction of anesthesia, the degree of MR, anatomy of the valve, and dimensions and segmental wall motion of the LV are carefully assessed to determine whether or not the mitral valve needs to be addressed. Since anesthesia generally reduces systemic vascular resistance and afterload, assessment of the valve after administration of phenylephrine may unmask more severe MR. If the amount of MR is 2+, transfusion after aortic cannulation to increase preload to 1.5 to 2.0 times resting pulmonary capillary wedge pressure may unmask more severe MR and prompt a decision to expose and repair the valve.¹³⁷ If there is a significant discrepancy between the intraoperative degree of MR and that diagnosed by preoperative TEE, it is probably best to treat according to the preoperative value since this likely what the patient experiences under normal loading conditions. In patients with marginal LV function, a Swan-Ganz catheter with an oxygen electrode and a femoral arterial catheter for possible intra-aortic balloon insertion are recommended.

The heart is exposed via midline sternotomy; other incisions may be used to expose the mitral valve, but these compromise the ability to revascularize the heart. For patients who have only revascularization, cannulation, administration of cardioplegia, depth of systemic hypothermia, choice of conduit, and conduct of operation do not differ from revascularization operations without IMR. However, if there is any possibility that the mitral valve will be exposed, separate cannulation of both cavae through the right atrium may save time later.

For patients who require mitral valve repair or replacement, two venous cannulas are preferred and one of the specialized retractors for facilitating exposure of the mitral valve is used after the sternotomy and mammary arterial dissection. Pericardial attachments to both cavae and the right pulmonary veins are dissected away to mobilize the heart. After starting cardiopulmonary bypass, the left atrium is opened for decompression of the ventricle; the aorta is clamped and cardioplegia is given. Both antegrade and retrograde cold blood cardioplegia are recommended with myocardial temperature monitoring to minimize myocardial stunning and post–bypass LV dysfunction. Distal coronary arterial anastomoses are done first to reduce manipulation of the heart with possible rupture of the ventricle at the atrioventricular groove after mitral valve repair or replacement.

The left atrium is usually enlarged and accommodates a generous incision behind the interatrial septum. The atrial septum and right atrium are retracted to expose the valve. An initial inspection reveals the amount of annular dilatation and may indicate segments of the mural annulus that appear disproportionately elongated. Traction sutures in the annulus at each commissure elevate the valve and facilitate exposure of the leaflets, chordae, and papillary muscles. Careful inspection searching for ruptured, elongated, or sclerosed chordae; fibrotic, atrophied papillary muscle; and redundant or defective leaflet tissue is made. Most often the entire valve appears normal; sometimes the posterior papillary muscle seems slightly more yellowish brown than the rest of the ventricle and the posterior part of the mural annulus seems slightly elongated.

The decision to repair or replace the valve is often difficult. Replacement is recommended in older patients with severe LV dysfunction, who do not easily tolerate prolonged cardiopulmonary bypass with cardioplegic arrest. A short operation ending with a competent valve offers the greatest chance of success. In other patients, repair is preferred if a competent valve is produced. Since repair of IMR does not address the primary pathology causing MR, a decision to repair carries the caveat of immediate replacement if unsuccessful

Gillinov's report demonstrated that mitral valve repair is effective (at least in the short term) in 97% of patients undergoing elective surgery for 3+ to 4+ chronic IMR. Ring annuloplasty was employed in 98% of these repairs and was the sole surgical maneuver on the valve in over 80%. There was a distinct inclination in this study to undersize the valvuloplasty ring; 79% of the rings were 30 mm or less. Iatrogenic mitral stenosis was not seen even in the patients who received 26-mm annuloplasty devices.⁶

Chordal sparing techniques^{117–119,122,123,138} are used if the valve is replaced. These methods have significantly reduced postoperative ventricular dysfunction observed after valve excision in the past and produce no more LV dysfunction than reparative operations.¹²³ Aged patients in sinus rhythm and patients with a life expectancy of less than 5 or 6 years who otherwise do not need anticoagulation are candidates for bioprosthetic valves; mechanical valves are recommended for others. The valve is inserted after excising^118,123 or transposing¹²² anterior leaflet tissue using running over and over sutures. Pledgeted interrupted mattress sutures are used only in patients with extremely friable atrial and annular tissue. The mural leaflet is plicated into the valve insertion suture line to prevent interference with the valve mechanism.

Prior to removing the aortic clamp, all air is evacuated from the ventricle and the mitral valve is kept incompetent using a transvalvular catheter with ventricular and atrial holes. Absence of air and assessment of ventricular wall motion is made by transesophageal echocardiography. Anticipated pharmacologic support is started and satisfactory LV contractility is established before loading the heart. After weaning, cardiopulmonary bypass is restarted if the LV begins to dilate and wall motion deteriorates; every effort is made to prevent any distention of the ventricle that might reduce myocardial contractile force.¹³⁸ Decisions for using intra-aortic balloon pumping or even temporary left ventricular assistance are better made early than after multiple attempts to wean from cardiopulmonary bypass have failed.

RESULTS

Myocardial revascularization alone in patients with chronic IMR has a higher hospital mortality than in patients without IMR.¹²⁸ Mild (1+) IMR increases operative mortality to 3.4% to 4.5%^{126–128,139} and moderate (2+) IMR raises operative mortality to 6% to 11%.^{126–128,140} Five-year survival is influenced by the severity of LV dysfunction at the time of operation, age, and comorbid disease.³³

Two-year survival for revascularization alone in patients with 1+ and 2+ MR is 88% and 78%, respectively.¹⁴¹ Five-year survival rates for patients with mild MR range between 70% and 80%.^{19,126,135,142} For moderate IMR, five-year survival ranges between 60% and 70%.^143,144 There are little data regarding the functional class and quality of life in revascularized patients with mild to moderate MR and no data regarding rates of progressive worsening of MR.

Historically, repair and revascularization of chronic IMR has an operative mortality that ranges from 3.0% to 29.4%^{37,38,114,142,145,146} and a rate of reoperation up to 14.7%.^122,145,147 These values are confirmed in the most recent reports.^6,7 The long-term durability of repairs for chronic (and acute) IMR is difficult to assess since death is a strong competing end point and repair failure is usually defined as a need for reoperation. The incidence and severity of recurrent MR that does not require reoperation are almost never reported. Mitral valve replacement and revascularization have a hospital mortality between 3% and 33%^{35,114,116,126–128,132,148–151} and average around 20%. Most of this reported experience with valve replacement occurred before chordal sparing became standard practice.^{126,127,148–151} In addition, many series combined patients who had myocardial revascularization and mitral valve replacement for any type of mitral disease.^{147–149,151–153} However, Grossi's recent report using modern techniques and a rigorous definition of IMR confirmed these statistics.⁷ In general, operation for IMR has a higher mortality than for other causes of mitral valve malfunction.^129,138,143 The choice of valve prosthesis does not appear to influence results. Risk factors for hospital death include age, congestive heart failure, severity of LV dysfunction, preoperative intra-aortic balloon pump, ejection fraction, number of diseased coronary arteries, and comorbid conditions.^32,101,137

Most reports indicate the 5-year survival after revascularization and mitral valve repair or replacement is between 30% and 40%.^{19,34,126,127,135} Gillinov's report again confirms these statistics. In his series 5-year survival in the propensity-matched best risk group was 58% for valve repair and 36% for replacement. This group had significantly fewer NYHA class IV patients and less severe MR preoperatively. In the propensity-matched poorer risk groups (more severe CHF, MR, and emergency surgery) and for the group as a whole (Fig. 28-5) there was no difference between repair and replacement and 5-year survival was uniformly less than 50%.⁶ These sobering 5-year survival data are depressingly similar to those for medically treated heart failure patients. As Miller has aptly stated, "successful revascularization and correction of IMR does relatively little in terms of ameliorating the ravages of previous LV infarction ...."¹⁵⁴

View larger version (14K): [in this window] [in a new window]   FIGURE 28-5 Survival after mitral valve surgery for all patients with ischemic mitral regurgitation. Each symbol represents a death according to Kaplan-Meier estimator. Vertical bars enclose asymmetric 68% confidence limits. Solid lines represent parametric survival estimates; these are enclosed between dashed 68% confidence limits. Numbers in parentheses are numbers of patients traced beyond that point. (Reproduced with permission from Gillinov AM, Wierup PN, Blackstone EH, et al: Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 2001; 122:1125.)

	A LOOK TO THE FUTURE

Top References

Recent work supports the concept that regional increases in wall stress of normally perfused myocardium adjacent to the infarction initiates production of oxygen free radicals, apoptosis, and alterations in collagen metabolism.^{130,160–163} Although much more work is needed to prove this hypothesis, the concept introduces the possibility of early surgical and/or medical interventions before LV remodeling occurs, rather than afterwards. Reperfusion of completed infarctions, although too late to save myocytes, attenuates LV dilatation,¹⁰⁹ improves survival, and alters collagen metabolism of the extracellular matrix.¹⁶³ Restraining infarct expansion preserves LV resting function and stabilizes LV geometry in a sheep model of anteroapical infarction,¹⁶⁴ alters collagen metabolism,¹⁶² and reduces the severity of chronic remodeling MR.¹⁶⁵ Preliminary work suggests that preventing infarct expansion using a partial LV wrap significantly reduces subsequent development of both MR and ventricular dilatation. These approaches, which address the hypothesis of stress-induced apoptosis, better address the pathogenesis of chronic ischemic MR and may eventually improve results in this large group of difficult patients.