Epidemiology


Etiology


  • Acute: Papillary muscle rupture (post-MI), Infective Endocarditis (IE), Chordae tendineae rupture (MVP, trauma).
  • Chronic Primary: Mitral Valve Prolapse (MVP - most common in US) c, Rheumatic Heart Disease (developing countries), Myxomatous degeneration.
  • Chronic Secondary (Functional): LV dilatation (HFrEF), Ischemic cardiomyopathy (tethers leaflets).
    • This results in hypokinesis and outward displacement of the papillary muscle, creating increased tension on the attached chordae tendineae and preventing complete closure of the corresponding mitral valve cusp. t

Pathophysiology


Clinical features


  • Auscultation
    • S3 heart sound in advanced stages of disease
      • Indication of severity
      • vs S2-opening snap interval in Mitral stenosis, also a indication of severity
    • Holosystolic murmur (high-pitched, blowing)
      • Radiates to the left axilla and heard best over the apex (5th intercostal space at the left midclavicular line)
      • Intensity can be increased by increasing preload (e.g., leg raise) or afterload (e.g., handgrip) due to increased regurgitation.

Diagnostics


Treatment