The term “ischemic valvular disease” defines valve regurgitation due to ventricular ischemia or ventricular infarction is classified by the term “ischemic valvular disease.” This definition excludes preexisting valvular diseases in patients presenting with coronary artery disease. The leaflet tissue often appears normal. For this reason, the valve dysfunction is sometimes called “functional regurgitation,” a terminology that might suggest a potential reversibility of the regurgitation (which is rarely the case) and the absence of organic lesions (which is never the case). The regurgitation is actually the result of mitral valve lesions involving the annulus, the papillary muscle, and the configuration of the left ventricle, which are parts of the mitral valve complex. In addition, the leaflet tissue can be affected by secondary lesions in long-lasting progression of mitral regurgitation. Whatever semantic considerations it is important to describe the regurgitation using the functional classification, which serves as a guideline to valve reconstruction.
An ischemic valvular disease is a myocardial disease producing a valve dysfunction.
PATHOPHYSIOLOGY
Type I Mitral Regurgitation (Normal Leaflet Motion)
Type I mitral regurgitation refers to a lack of leaflet coaptation with normal leaflet motion. This relatively rare condition (less than 10% of ischemic mitral regurgitation cases) is seen in basal infarctions. The lack of leaflet coaptation is due to an annular dilatation predominant in the posteromedial segments of the annulus (i.e., P2, P3, and PC segments).
Type II Mitral Regurgitation (Leaflet Prolapse)
Type II ischemic mitral valve regurgitation is rarely observed today. The usual cause is papillary muscle rupture or elongation. In most instances, the lesion involves the posteromedial papillary muscle, which has a more tenuous vascularization than the anterolateral papillary muscle. Complete rupture of a papillary muscle is much less frequent nowadays than in the past because of improved management of acute myocardial infarctions and early revascularization by interventional cardiology. Today, type II ischemic mitral regurgitation is generally due to partial rupture of a papillary muscle or to papillary muscle elongation following infarction and fibrosis.
Type IIIb Mitral Regurgitation (Systolic Restricted Leaflet Motion)
Type IIIb mitral regurgitation is by far the most frequent valve dysfunction following ventricular ischemia or infarction. In the past, the main cause of regurgitation was thought to be “papillary muscle dysfunction.” Experimental studies in our laboratory in the 1980s using sheep demonstrated that papillary muscle dysfunction caused by formaldehyde injection of the posterior papillary was unable to produce mitral valve regurgitation ( Fig. 29-1 ). A significant regurgitation could only be obtained by extending the formaldehyde infiltration to the adjacent myocardium, resulting in wall motion abnormality. This observation has now been validated as the main mechanism of ischemic mitral valve regurgitation. It is well accepted that type IIIb ischemic mitral regurgitation results from lateral and apical displacement of the papillary muscles, mostly the posteromedial papillary muscle and its supporting ventricular wall. The resulting tethering typically involves the P2, P3, and PC leaflet segments of the mitral valve (see Fig. 14-1 ). A tethering can also be seen at the belly of the anterior leaflet attributable to excess traction on one or more main chordae. We use the term “effet de mouette” *
* See Glossary .
(seagull deformation) to describe the image of the anterior leaflet seen at echocardiography.
The severity and localization of leaflet tethering vary according to the type of myocardial infarction. In anterior myocardial infarction the dilatation is usually global with leaflet tethering involving both the anterior and the posterior leaflets. In posterolateral myocardial infarction, leaflet tethering is predominant in the P2, P3, and PC segments. There is not always a perfect correlation between the degree of papillary muscle displacement and the severity of mitral regurgitation because of variations in myocardial contractility and loading conditions.
Type IIIb ischemic mitral valve regurgitation results from complex changes in left ventricular configuration, papillary muscle position, and annular dimensions.
In long-lasting type II and type IIIb ischemic regurgitation, annular dilatation is often observed as an associated lesion. The dilatation is predominant in the P3 and PC areas with a pronounced asymmetry of the annulus. Here again, the degree of deformation does not necessarily correlate with the severity of mitral regurgitation.
CLINICAL PRESENTATION
A myocardial infarction can result in the appearance of ischemic mitral valve regurgitation immediately or at a later time.
Acute ischemic mitral regurgitation results from papillary muscle rupture or ventricular motion abnormality in the setting of acute myocardial infarction. The clinical presentation varies widely depending upon the functional type and severity of mitral regurgitation and the extent of myocardial damage. For example, a limited myocardial infarction resulting in papillary muscle necrosis and rupture (type II dysfunction) causes a severe mitral regurgitation, leading to pulmonary edema and cardiogenic shock. This usually occurs within the first week after a myocardial infarction. Of note, the same time frame applies to ventricular septal rupture, making the differentiation between these two entities clinically difficult. In septal rupture, the systolic murmur is loud and predominant at the left sternal border, whereas in ischemic mitral regurgitation the murmur is softer and predominant at the apex, without thrill. Because of the rapid equilibration of left ventricular and atrial pressures, a murmur of ischemic mitral regurgitation may not be audible. In this case echocardiography is particularly useful to make the right diagnosis. In type IIIb ischemic mitral acute regurgitation, the clinical presentation is often less dramatic. Most patients present with mild to moderate regurgitation as assessed by echocardiography.
Chronic ischemic mitral regurgitation results from progressive ventricular dilatation following myocardial infarction. Patients may have a clinical history of myocardial infarction in the absence of mitral regurgitation (or in the presence of mild regurgitation) that worsens over time. Severe ischemic mitral regurgitation can be asymptomatic or be associated with minimal symptoms for many years because the patient adapts his or her physical activity to the functional capacity of the heart. The diagnosis is often made when the patient exhibits dyspnea on exertion, fatigue attributable to low cardiac output, or the onset of atrial fibrillation. Another common scenario is a patient presenting with acute ischemia and diagnosed with mitral regurgitation from previous silent infarction.
ECHOCARDIOGRAPHY AND CORONARY ANGIOGRAPHY
Echocardiography allows assessment of the mechanism and severity of mitral valve regurgitation and ventricular size and function. The direction of the regurgitant jet on Doppler echocardiography gives some valuable information about the functional type of mitral regurgitation. Type I mitral regurgitation displays a central jet. In type II, the jet is opposite to the prolapsing leaflet and papillary muscle rupture can be identified ( Fig. 29-2 ). In type IIIb, as a result of posterolateral myocardial infarction, the jet is typically directed posteriorly over the restricted P3 segment ( Fig. 29-3 ). It can be a central jet, however, if there is massive annular dilatation. In type IIIb mitral regurgitation caused by anterior myocardial infarction, both leaflets are often tethered with a central jet ( Fig. 29-4 ). Echocardiography also permits identification of some of the lesions, such as papillary muscle rupture in type II, and assessment of the severity of leaflet tethering, the tenting area, and the depth of the displaced coaptation in type IIIb. Finally, quantitative measurement allows calculation of the regurgitant orifice area and volume. The assessment of the severity of regurgitation, however, may be rendered difficult by the variations in the loading conditions. This explains why the degree of regurgitation is often downgraded by intraoperative transesophageal echocardiography caused by afterload reduction induced by general anesthesia.
A coronary angiography is performed in all patients. In patients with type II mitral regurgitation, an occlusion of the right coronary artery or the posterior descending branch is generally observed. Patients with type IIIb mitral regurgitation usually present with triple-vessel coronary artery disease.
SURGICAL INDICATIONS
Severe acute ischemic mitral regurgitation requires emergency surgery in patients with cardiogenic shock and pulmonary edema who are refractory to medical therapy. In other patients, intensive medical therapy is instituted to optimize the hemodynamic status. In patients with preserved systemic pressure, the medical regimen includes sodium nitroprusside and diuretics to reduce the regurgitant volume while concomitantly increasing the forward stroke volume. In cardiogenic shock, systemic hypotension limits the use of vasodilators. Intraaortic balloon counterpulsation is used to restore the mean arterial blood pressure and reduce the afterload while at the same time increasing the cardiac output. Another advantage of intraaortic balloon counterpulsation is that it helps avoid administration of excessive doses of inotropic agents.
Mild to moderate acute mitral regurgitation does not require urgent surgery since it may be partially or completely reversible with medical treatment and/or occasional percutaneous coronary revascularization.
In chronic ischemic mitral regurgitation , two clinical scenarios can be encountered. Some patients are referred to the surgeon for congestive heart failure resulting from moderate to severe mitral regurgitation. These patients should benefit from a valve reconstruction and a complete coronary revascularization. Other patients who need complete coronary revascularization for symptomatic multivessel coronary disease may be diagnosed with an associated mild to moderate mitral regurgitation, raising the question of the necessity of valve repair. This condition carries an increased risk of long-term mortality and morbidity. Coronary revascularization alone does not reverse chronic mitral regurgitation. Thus patients with mild to severe mitral regurgitation should have concomitant mitral valve reconstruction and complete coronary revascularization. Whenever preoperative risk factors suggest that the operative mortality could be prohibitive, the surgical procedure can be preceded by transcutaneous revascularization. In patients who present with a severe ventricular dysfunction, a myocardium viability evaluation by magnetic resonance imaging or thallium study is warranted, particularly in the absence of angina.
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