1. Normal physiology (control) is compared to that of acute mitral regurgitation (chordal rupture), compensated mitral regurgitation, and decompensated chronic mitral regurgitation. The sudden opening of a new pathway for regurgitant flow into the left atrium increases left atrial pressure and preload (sarcomere length), in turn mildly increasing end-diastolic volume because resting sarcomere length is still 90% of maximum length. Afterload (end-systolic stress) is decreased, allowing more complete left ventricular ejection fraction, reducing end-systolic volume. These changes in loading increase ejection fraction and total stroke volume, but because 50% of the total stroke volume is lost to regurgitation (regurgitant fraction), forward stroke volume is decreased. Therefore, despite normal contractile fraction and increased ejection fraction, the patient presents with the hemodynamics of congestive heart failure. In the presence of decompensated chronic mitral regurgitation, muscle damaged caused by prolonged severe volume overload reduces the effectiveness of ventricular ejection and end-systolic volume increases. There is a further increase in diastolic volume, which is not compensatory, resulting in a decrease in total and forward stroke volumes. EDV, end diastolic volume; ESS, end-systolic stress; ESV, end-systolic volume; MR, mitral regurgitation; SL, sarcomere length. Modified with permission from O’Gara P, Sugeng L, Lang R, et al: The role of imaging in chronic degenerative mitral regurgitation. JACC Cardiovasc Imaging Mar;1(2):
Source: DEGENERATIVE MITRAL VALVE DISEASE, Hurst's The Heart, 14e
Citation: Fuster V, Harrington RA, Narula J, Eapen ZJ. Hurst's The Heart, 14e; 2017 Available at: Accessed: November 10, 2017
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