Ischemic mitral valve regurgitation (IMR) [1] occurs as two related but distinct complications of myocardial infarction. Acute IMR (aIMR), as discussed in a previous chapter[2], may result from acute papillary muscle rupture following myocardial infarction. Patients with acute IMR usually present in extremis and often require urgent surgical intervention with increased perioperative risk.[3] Conversely, chronic IMR (cIMR), which will be the focus of this chapter, is a result of ventricular remodeling following myocardial infarction and has a more indolent progression. Chronic IMR occurs in approximately 25% of patients following myocardial infarction and in up to half of patients after myocardial infarction with left ventricular (LV) dysfunction and heart failure.[4][5][6][7][8][9] It is associated with poor outcomes that worsen in direct correlation to the severity of valvular insufficiency[1][2][9][10][11][12][13][14], with even mild cIMR resulting in significantly worse outcomes than similar ischemia without cIMR.[6][7][15][16] There were an estimated 1,181,000 hospitalizations for myocardial infarction in the United States in 2018, or approximately 1 every 27 seconds.[17] As the population ages and the incidence of coronary artery disease increases, the number of patients with cIMR will only continue to grow.
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