Ischemic mitral regurgitation (IMR), often termed functional mitral regurgitation, is mitral insufficiency as a result of myocardial ischemia or infarction. By definition, the mitral valve leaflets are structurally normal in IMR. The malcoaptation of the leaflets and resultant regurgitation of the mitral valve in IMR is a result of either acute papillary muscle dysfunction or rupture, or chronic changes with left ventricular remodeling and subsequent changes in geometry.
Ischemic mitral regurgitation (IMR) is associated with decreased quality of life and long-term survival. Although extensive mechanistic research has been conducted, the optimal management of IMR remains elusive. Clinical studies in the past often included MR of multiple etiologies, including degenerative or nonischemic origin and IMR grouped into the same category, leading to confusion and incorrect conclusions regarding the natural history and true long-term impact of IMR. It is important to distinguish IMR from mitral regurgitation resulting from nonischemic etiologies. Mitral regurgitation is often associated with coronary artery disease without a direct cause-and-effect relationship. Given the prevalence of coronary artery disease, the association of myocardial infarction and nonischemic mitral regurgitation is a common clinical association. IMR must be distinguished from mitral insufficiency caused by degenerative, rheumatic, congenital, and infectious etiologies, as well as that arising from idiopathic dilated cardiomyopathy. Our recognition of IMR as a distinct clinical entity has improved the understanding of the pathophysiology and natural history of this distinct disease process.
IMR can produce a variety of very variable clinical presentations depending on infarct characteristics and subsequent postinfarction ventricular remodeling. The size, location, and transmurality of the myocardial infarction (MI) sets in motion varying degrees of left ventricular remodeling that subsequently determine the severity, time course, and clinical manifestations of IMR. The presentation may be either acute and immediately life threatening, or develop insidiously over time in association with congestive heart failure (CHF).
The advancement in catheter-based intervention for coronary artery disease and medical therapy has resulted in dramatically improved survival from ischemic heart disease and acute myocardial infarctions (AMI). Although survival following an AMI has improved, there has been a subsequent increase in the incidence of congestive heart failure. The American Heart Association estimates that 5.7 million Americans were in various stages of congestive heart failure in 2006.1 An increasing number of ischemic cardiomyopathy patients will develop left ventricular dysfunction and IMR as a result of annular dilatation and/or papillary muscle displacement.
Early after an acute myocardial infarction (AMI), between 11 and 55% of patients develop clinical (mitral systolic murmur), echocardiographic, or angiographic evidence of IMR. A recent echocardiographic study investigating the incidence of mechanical complications after acute myocardial infarction found a significantly reduced incidence of mitral regurgitation in the percutaneous coronary intervention (PCI) era, but still noted a very large incidence of post-MI acute ischemic MR, 28 versus 53%.2 Many of the murmurs early after acute myocardial infarction are transient and disappear by the time of discharge without further intervention, implying ...