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  • • Fibrous annulus of mitral valve (MV) is thin, incomplete ring of fibrous tissue

    • Most MVs have anterior and posterior leaflets, attached by thin fibrous chordae tendineae to papillary muscle

    • Closed during systole via action of papillary muscle contraction, open during diastole when LA pressure higher than LV pressure

    • Etiology includes:

    • -Rheumatic heart disease

      -Idiopathic MV calcification

      -Mitral valve prolapse (MVP)

      -Infective endocarditis

      -Ischemic MR

    Postinfarction papillary muscle rupture: 0.1% of coronary artery disease; congestive heart failure with new murmur days after myocardial infarction

    • MR results in LA hypertension, resulting in pulmonary congestion, dyspnea, pulmonary hypertension, RV failure

    • LV is subjected to chronic volume overload causing LV failure (unlike mitral stenosis)




  • • Causes of valve disease include:

    • -Rheumatic carditis (most common)

      -Valve collagen degeneration


    • Less common causes include:

    • -Collagen-vascular disease



      -Marfan syndrome

    • Valvular heart disease: 89,000 hospital discharges in 1998

    • 40% of MR caused by rheumatic disease

    • Risk factors of idiopathic MV calcification include:

    • -Hypertension

      -Aortic stenosis


      -Chronic renal failure

    • MVP is present in 3-4% of general population; 5% of patients with MVP have significant MR

    • Infective endocarditis accounts for 5% of MR cases

    • 3% of patients with severe coronary disease have ischemic MR; affects posterior leaflet primarily


Symptoms and Signs


  • • Exertional dyspnea, orthopnea, fatigue

    • Symptoms do not correlate with degree of MR

    • Hemoptysis

    • Atrial fibrillation (75% of severe cases)

    • Malaise, fever, chills in this setting: consider infective endocarditis

    • Angina is rare

    • Apical impulse displaced to left, palpable thrill at apex

    • High pitched holosystolic murmur radiating to axilla and back


Laboratory Findings


  • • ECG: LV hypertrophy; if sinus rhythm P mitrale may be present


Imaging Findings


  • Chest film

    • -LA and LV enlargement

      -RV enlargement

      -Pulmonary edema

      -Kerley B lines

    • Transesophageal echocardiography identifies site of regurgitation jet

    • Cardiac catheterization demonstrates LA v waves, elevated LV pressure

    • Cardiac index < 2.0 L/min/m2, wide AV oxygen difference indicate severe impairment


  • • Evaluate for endocarditis

    • Evaluate for secondary LV dysfunction


  • • 3 determinants of clinical severity:

    • 1. Degree of regurgitation

      2. LV function

      3. Etiology of valve disease


  • • Preload reduction (diuretics), afterload reduction (ACE inhibitors): Helps in increase forward output, decrease regurgitation

    • Operation: Repair vs replacement

    • Virtually all MVP can be repaired (posterior leaflet reconstruction and annuloplasty)

    • Ischemic regurgitation: Ring annuloplasty + coronary artery bypass grafting

    • Rheumatic disease, valve calcification, or endocarditis: Prosthetic valve replacement






  • • Symptomatic heart failure (NYHA class II or greater)

    • Asymptomatic, ejection fraction (EF) < 60%, end-systolic dimension > 45 mm, pulmonary hypertension exists, or new atrial fibrillation




  • • Significant LV dysfunction (EF < 45%) has higher operative mortality, worse long-term outcome




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