Sample-Chapter-36-from-Runge-Netter's-Cardiology-2nd Edition.pdf

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T1. 36. Mitral Valve Disease. Thomas R. Griggs. Mitral valve leaflets consist of thin, pliable, fibrous material. The two leaflets—anterior and posterior—open by.
Mitral Valve Disease

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Thomas R. Griggs

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itral valve leaflets consist of thin, pliable, fibrous material. The two leaflets—anterior and posterior—open by unfolding against the ventricular wall and close by apposition when the pressure in the left ventricle becomes greater than that in the left atrium. Mitral stenosis occurs when the mitral valve leaflets become stiffened, calcified, and unable to open completely during diastole. This process often involves the chordae tendineae in addition to the mitral valve leaflets. Mitral valve regurgitation occurs when the leaflets are unable to close completely in systole. In the United States, more than 20,000 patients annually require surgery for manifestations of mitral stenosis and mitral regurgitation, and thousands more require monitoring and treatment.

Etiology and Pathogenesis Mitral Stenosis

p0015 Rheumatic fever is responsible for a majority of cases of mitral

stenosis. The initial infection and its sequelae result in thickened valve leaflets and fusion of the commissure between the leaflets. Chordae tendineae are also affected and become thickened, fused, and shortened. Most valves that are affected by rheumatic fever show abnormalities of all these structures. Few patients with rheumatic mitral valve disease have pure mitral stenosis; most have a combination of stenosis and regurgitation, and many have aortic and tricuspid involvement. Approximately two thirds of mitral stenosis cases in the United States occur in women. p0020 The normal mitral valve cross-sectional area in diastole is 4 to 6 cm2. Blood flow is impaired when the valve orifice is narrowed to less than 2  cm2, creating a pressure gradient with exertion. A valve area smaller than 1 cm2 is considered critical mitral stenosis and results in a significant pressure gradient across the valve at rest with chronically increased left atrial (LA) pressures (Fig. 36-1). p0025 Chronically increased LA pressures associated with mitral stenosis, along with ongoing rheumatic inflammation, result in LA enlargement and a predisposition for atrial fibrillation. Valves affected by mitral stenosis are also vulnerable to recurrent thrombosis and implantation of bacteria that lead to infective endocarditis. p0030 The hemodynamic effects of chronic mitral stenosis include pulmonary venous and arterial hypertension; right ventricular (RV) hypertrophy, dilation, and failure; peripheral edema; tricuspid regurgitation; ascites; and hepatic injury with cirrhosis (Fig. 36-2). s0020

Dysfunction of any component of the mitral apparatus can cause mitral regurgitation. Mitral regurgitation also frequently occurs in the absence of primary mitral valve disease in patients with cardiomyopathy and ventricular dilation. When the cause of mitral regurgitation is primarily a valve defect, valve repair or replacement can correct the mitral regurgitation and improve long-term prognosis. When the valve leaks because the ventricle is dysfunctional and dilated, mitral repair or replacement may have little or no effect on symptoms or prognosis. With mitral regurgitation, blood is discharged during systole p0040 into the left atrium in addition to traveling its usual route through the aortic valve and into the aorta. If the regurgitant volume is large, LA remodeling occurs with dilation to accommodate increased volumes without intolerable LA hypertension (Fig. 36-3). Over time, as an increasing fraction of ventricular volume is regurgitant, the “forward” ventricular output is reduced, and symptoms and other findings of mitral regurgitation become obvious (Fig. 36-4). Patients are generally clinically well if the regurgitant fraction (regurgitant volume/total ejection volume) is less than 0.4. Patients with regurgitant fractions greater than 0.5 predictably develop left ventricular (LV) failure and have high morbidity and mortality. Any evidence of LV failure (LV ejection fraction 1.5 cm ) or MVA 60 mm Hg Pulmonary artery wedge pressure >25 mm Hg or New-onset atrial fibrillation and No LA thrombus or significant mitral regurgitation (3+ or 4+)

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Asymptomatic

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PR SA O M PE PL R E TY C O O F N E TE L N SE T V - N IE O R T FI N

LA, left atrial; MVA, mitral valve area; PMBV, percutaneous mitral balloon valvotomy. Recommendations are from Bonow RO, Carabello B, Chatterjee K, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 2008;52:1–142.

Rheumatic fever can affect all heart valves. Therefore, multiple valve disease must be considered in all patients. Special attention should be given to the possibility that echocardiography can underestimate the degree of aortic regurgitation in patients with severe mitral stenosis. Tricuspid stenosis may be

similarly underestimated or even undetected and may complicate the immediate postoperative recovery after mitral valve repair or replacement. Atrial fibrillation is a frequent cause of decompensation in p0565 patients with mitral stenosis and must be anticipated and

Table 36-2  Management Approach for Patients with Symptomatic Mitral Stenosis

Mildly symptomatic (NYHA class II)

Moderately to severely symptomatic (NYHA class III–IV)

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Consider Open Valvotomy or Mitral Valve Replacement

Periodic Follow-up

Consider PMBV

Mild stenosis (MVA >1.5 cm2) and Exercise test results: PASP 25 mm Hg MVG >15 mm Hg and Valve morphology favorable for PMBV and No LA thrombus or significant mitral regurgitation (3+ to 4+) Moderate or severe stenosis (MVA