Mitral Regurgitation from Ischemic Heart Disease

Acute Mitral Regurgitation Complicating Myocardial Infarction

Other Causes

Mitral regurgitation is a frequent complication of acute MI. When Doppler echocardiography is used for diagnosis, mitral regurgitation has been detected in up to 39% of patients early after an infarction. Substantial (moderate or severe) mitral regurgitation is present in 3% to 19% of patients and is an important predictor of mortality ( Fig. 10-1 ). Because papillary muscle rupture or necrosis occurs infrequently after acute infarction, other important causes of mitral regurgitation include (1) changes in configuration of the LV (remodeling), (2) global or segmental LV dysfunction, and (3) changes in function of the mitral valve resulting from leaflet prolapse, abnormal closure, or anular dilatation. Although papillary muscle dysfunction has been implicated as an important cause of ischemic mitral regurgitation, experimental and clinical studies employing two-dimensional (2D) echocardiography have demonstrated that it rarely is causative. LV systolic dysfunction, increased LV chamber sphericity, and regional asynergy of the inferoposterolateral wall overlying the posterior papillary muscle may be important determinants of developing mitral regurgitation. Van Dantzig and colleagues found that changes in the mitral valve anulus and leaflets were of limited importance in the pathogenesis of ischemic mitral regurgitation early after MI. Thus, although there is often no apparent structural abnormality of the mitral valve, changes in configuration and contractile function of the LV after an acute infarction prevent adequate coaptation of the leaflets and result in mitral regurgitation.

Chronic Mitral Regurgitation from Ischemic Heart Disease

Many patients with ischemic heart disease and chronic mitral regurgitation have coexisting mitral regurgitation caused by rheumatic fever, myxomatous degeneration, or other conditions. At operation, distinction between mitral regurgitation coexisting with ischemic heart disease and that caused by ischemic heart disease can be difficult because papillary muscle scarring or fibrosis is not always the result of earlier necrosis or adjacent MI. Chronic regurgitation through the mitral valve apparatus does follow acute MI in some patients. The regurgitation may be localized to the region of the posteromedial or anterolateral commissure or both. Causes include underlying papillary muscle ischemic dysfunction, papillary muscle scarring and shortening or even lengthening, previous rupture of a portion of the papillary muscle, asynergy of the adjacent LV wall, and LV remodeling, all of which can result from an earlier MI. Chronic regurgitation may also occur through the central part of the valve. This can result from restricted leaflet motion with increased leaflet tethering ( Figs. 10-2 and 10-3 ) and from anular dilatation secondary to ischemic LV dysfunction. Severity and degree of the dysfunction may vary over time according to the degree of remodeling (increased sphericity) that occurs in the individual patient after infarction.

Acute Mitral Regurgitation Complicating Myocardial Infarction

Papillary muscle rupture presents as an acute event within a few hours to 14 days after an MI in 1% to 3% of patients. The onset is usually characterized by pulmonary edema, hypotension, or both, typically 2 to 7 days after acute infarction. Rupture is signaled by worsening of the patient's clinical condition. Profound shock indicates gross mitral regurgitation from total rupture; less severe signs suggest less severe mitral regurgitation from partial rupture or LV dysfunction. A new apical systolic murmur can be heard provided cardiac output is adequate and the regurgitation is not severe. The murmur is frequently absent in total rupture and usually present in partial rupture. An apical third heart sound is common, and pulmonary edema is often seen on chest radiography. The heart is usually normal in size or only slightly enlarged, and the left atrium is small.

A pulmonary artery (Swan-Ganz) catheter can provide important information (e.g., excluding the presence of left-to-right shunting) and, when it is in the pulmonary artery wedge position, may demonstrate a prominent v wave on the pressure tracing. Echocardiography (2D or transesophageal) is a valuable diagnostic tool in mitral regurgitation associated with MI. It is used to differentiate between papillary muscle rupture and LV dysfunction. In the latter condition, extensive wall motion abnormalities are usually present. With papillary muscle rupture, the mitral leaflet becomes flail and prolapses into the left atrium during systole. The ruptured portion of the muscle may be directly visualized as a separate mass attached to the chordae. Left ventriculography may be performed to confirm the diagnosis of mitral regurgitation (or ventricular septal defect or occasionally both) and to define areas of impaired LV contraction or aneurysm formation. In critically ill patients, however, left ventriculography is unnecessary when precatheterization studies have established the diagnosis and only coronary angiography is performed. When the patient is seriously ill, an intraaortic balloon pump (IABP) should be used. If the patient's hemodynamic state remains unstable, cardiopulmonary bypass (CPB) can be established using a percutaneous technique (see “Cardiopulmonary Bypass Established by Peripheral Cannulation” under Special Situations and Controversies in Section III of Chapter 2 ). These devices can be left in place until cardiac catheterization is completed and the patient is taken to the operating room.

Chronic Mitral Regurgitation from Ischemic Heart Disease

Usually the patient presents with gradually increasing mitral regurgitation. When the murmur dates from an MI, an ischemic etiology is assumed. There may be cardiac enlargement, including left atrial enlargement, hypokinesia, and akinesia at the infarction site. An LV aneurysm may coexist (see Chapter 8 ). Positron emission tomography (PET) or dobutamine echocardiography may reveal chronically ischemic, hibernating myocardium that may respond to increased blood flow from coronary artery bypass grafting (CABG) alone. Gadolinium contrast-enhanced cardiovascular magnetic resonance reveals myocardial scarring, and if the posterior papillary muscle is extensively scarred (nonviable), mitral anuloplasty may be insufficient to eliminate ischemic mitral regurgitation. Other diagnostic criteria are the same as for other types of chronic mitral regurgitation (see Chapter 11 ).

Acute Mitral Regurgitation Complicating Myocardial Infarction

Rupture of a papillary muscle is an uncommon complication of acute MI ^W2 and currently is probably even less common, given the widespread use of thrombolytic and percutaneous interventional therapy for acute infarction. It is, however, a life-threatening complication, with only about 25% of patients treated nonsurgically surviving more than 24 hours after total rupture. Survival after partial papillary rupture is better; more than 70% of patients survive the first 24 hours, and about 50% survive more than 1 month. They are then considered to have chronic mitral regurgitation.

When the papillary muscle remains intact, the natural history of acute mitral regurgitation is less well defined. As previously noted, however, moderate or severe mitral regurgitation in the absence of papillary muscle rupture is present in 3% to 19% of patients early after an acute infarction and is an important predictor of mortality. Using multivariable analysis, Lehmann and colleagues found that mitral regurgitation of any degree (as detected by left ventriculography) was a predictor of cardiovascular mortality at 1 year (relative risk 7.5; CL 2%-29%; P = .0008). In the study of Lamas and colleagues, cardiovascular mortality during years of follow-up was also higher in patients who developed mitral regurgitation early after acute infarction than in those who did not (29% vs. 12%; P < .001). Grigioni and colleagues observed a direct and significant correlation between severity of mitral regurgitation as determined by echocardiography and long-term survival (see Fig. 10-1 ). They also observed that mitral regurgitation predicts mortality in excess of that anticipated on the basis of patient characteristics and degree of LV dysfunction.

Chronic Mitral Regurgitation from Ischemic Heart Disease

Mild or moderate mitral regurgitation without papillary muscle rupture is episodic in some patients, presumably a result of changing prevalence and distribution of ischemic myocardium, loading characteristics of the LV, and variations in LV function. Persistent and severe mitral regurgitation, often associated with moderate or severe LV dysfunction, worsens the prognosis for patients with poor LV function. Furthermore, increasing severity of mitral regurgitation has an increasingly adverse effect on survival, regardless of type of treatment ( Fig. 10-4 ).

Acute Mitral Regurgitation Complicating Myocardial Infarction

In critically ill patients with this complication of acute MI, IABP is begun as soon as the condition is recognized, or CPB is established by percutaneous technique if indicated (see “Cardiopulmonary Bypass Established by Peripheral Cannulation” under Special Situations and Controversies in Section III of Chapter 2 ). In the operating room, the patient is prepared and draped for CABG; the sternotomy, graft preparation, and preparation for CPB are expeditiously accomplished. CPB is established using two venous cannulae. If CPB was established percutaneously before bringing the patient to the operating room, the cannulations just described should be made and CPB established by a pump-oxygenator designed for use in the operating room. The peripheral lines are clamped but left in place. These cannulae are removed in the operating room at the end of the cardiac procedure.

Myocardial management may include warm induction of cardioplegia and controlled aortic root reperfusion (see “Cold Cardioplegia, Controlled Aortic Root Perfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). Because an acute coronary occlusion is typically present, the coronary sinus route of administration should be employed for part of the cardioplegic infusion (see “Technique of Retrograde Infusion” under Cold Cardioplegia [Multidose] in Chapter 3 ). The distal anastomoses of the bypass grafts are performed before the mitral valve is repaired or replaced to avoid retracting the heart after a mitral prosthesis (valve or ring) has been inserted and thus prevent possible rupture of an area of infracted LV. The proximal anastomoses of the grafts can be performed either immediately after completing the distal anastomoses and before opening the left atrium, or after closing the left atrium. If the left atrium has been closed, these anastomoses can be performed with the aorta still occluded or after removing the aortic clamp and placing a partially occluding clamp on the aorta while rewarming is completed.

The approach to the mitral valve is generally through the left atrium, although an approach through the right atrium may be useful (see “Approach Across the Atrial Septum” under Special Situations and Controversies in Chapter 11 ). With acute total papillary muscle rupture, the mitral valve is replaced with a mechanical prosthesis or bioprosthesis. Because the mitral anular tissue is usually not thickened and may be more friable than normal, great care must be taken to (1) obtain adequate bites of tissue when placing the anular sutures and (2) avoid excessive traction on these sutures as the valve is lowered into position, to prevent them from pulling through the tissue. Pledgeted mattress or nonpledgeted simple interrupted sutures are preferred.

When the papillary muscle is not ruptured and the chordal mechanism is intact, or if only one head is ruptured and there is anular dilatation, reparative techniques and anuloplasty with or without use of an anuloplasty ring are preferable to valve replacement (see “Mitral Regurgitation Repair” under Technique of Operation in Chapter 11 ). If an anuloplasty ring or band is inserted, it is probably preferable to use one that is smaller than the sizer that fits the anulus. After CPB is discontinued and with cannulae still in place, competence of the valve is assessed, preferably by transesophageal echocardiography (TEE). Left atrial pressure should be at least 15 mmHg and systolic arterial pressure above 120 to 130 mmHg during the assessment. If the valve is not competent, CPB is reestablished, cardioplegia is reinfused, and the valve is either repaired again or replaced. The remainder of the operation is completed as usual. An IABP or temporary ventricular assistance may be needed (see “Treatment of Low Cardiac Output” under Cardiovascular Subsystem in Section I of Chapter 5 ).

Chronic Mitral Regurgitation from Ischemic Heart Disease

The techniques of repair and replacement of the chronically regurgitant mitral valve are described under “Technique of Operation” in Chapter 11 . Difficulties in intraoperative decision making result from (1) time-related variability in the magnitude of regurgitation caused by ischemic heart disease, (2) uncertainty about the precise morphologic basis of the regurgitation, and (3) frequency with which regurgitation is associated with poor LV function. These considerations require careful evaluation of regurgitation and need for mitral repair or replacement preoperatively, in the operating room before CPB is established, after repair while CPB is still in place, and after CPB is discontinued.

Evaluation includes careful assessment of the intraoperative TEE, visual examination of the morphology of the valve, and identification of the location and magnitude of the regurgitation. Identifying the location and assessing the magnitude of regurgitation are accomplished by TEE, recognizing that this technique may overestimate or underestimate the degree of regurgitation (see Fig. 10-2 ). When the circulation is intact, echocardiographic assessments should be made with left atrial pressure at least 12 to 15 mmHg and systolic pressure above 120 to 130 mmHg.

On direct visualization of the valve, diagnosis of an ischemic etiology for regurgitation is generally made by exclusion. The anulus appears normal or is only slightly dilated. The leaflets are usually normal in appearance, and the chordae tendineae are usually not shortened or elongated. The papillary muscles may be pale, scarred, or normal in appearance. In this setting, repair of the valve with some form of anuloplasty is usually possible (see Chapter 11 ). When regurgitation is severe both preoperatively and intraoperatively and dominates the clinical picture, mitral repair or replacement is indicated. When severity of regurgitation is variable preoperatively and variable and no more than moderate intraoperatively (particularly when severity lessens after the CABG portion of the operation is completed), and signs and symptoms of myocardial ischemia are dominant, the mitral valve may be left alone. However, this recommendation is controversial. Intermediate situations demand individual intraoperative decision making.

When a repair is performed, the functional status of the mitral valve is evaluated by TEE after discontinuing CPB, with the cannulae still in place and with the systolic arterial pressure above 120 to 130 mmHg. If the hemodynamic situation or the repair is unsatisfactory, CPB can be reestablished and the mitral valve repaired again or replaced. If mitral replacement is necessary, every effort should be made to preserve the chordae tendineae to the posterior leaflet or to both leaflets.