Mechanisms of functional mitral regurgitation in cardiomyopathy secondary to anterior infarction

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It remains unclear why some patients with cardiomyopathy secondary to anterior infarction do, and others do not develop functional mitral regurgitation (MR).


Thirty-six patients after anterior infarction with ejection fraction (EF) below 35%, 18 with no/trivial and 18 with moderate/severe MR, underwent cardiac magnetic resonance imaging. Parameters describing the geometry of the mitral valve, subvalvular apparatus and left ventricle were measured.


The septolateral and commissure-to-commissure mitral annular diameters were bigger in patients with MR. The odds ratio (OR) of developing regurgitation was 25.0 (95% confidence interval [95% CI] 4.3-144.3; P < 0.001) for end-systolic septolateral mitral annulus diameter above 20 mm/m2. MR was less likely in patients with straighter posterior papillary muscle (OR 0.040, 95% CI 0.007-0.23; P < 0.001—for the angle between muscle axis and mitral annulus plane >81°), and more likely (OR 7.9, 95% CI 1.6-39.4; P = 0.008) with posterior papillary muscle tethering >23 mm/m2. Regurgitation was less likely (OR 0.032, 95% CI 0.003-0.33; P = 0.001) with anterolateral papillary muscle tip to ipsilateral mitral annulus distance in end-diastole longer than 13 mm/m2. Left ventricular EF, volumes and the overall end-systolic and end-diastolic wall thicknesses did not differ between the groups. Patients with MR had thinner myocardium proximal to the base of the anterior and distal to the base of the posterior papillary muscle.


Inferior extension of anterior infarction and more leaning posterior papillary muscle are the major components resulting in the development of ischaemic MR in patients with cardiomyopathy secondary to anterior infarction. Shorter chordae tendineae may constitute the anatomical background that makes the development of ischaemic MR more likely.

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