Functional mitral regurgitation
- William H Gaasch, MD
William H Gaasch, MD
- Section Editor — Valvular Disease
- Professor of Medicine
- University of Massachusetts Medical School
- Tufts University School of Medicine
- Senior Consultant in Cardiology
- Lahey Clinic
In patients with functional or secondary mitral regurgitation (MR), the papillary muscles, chordae, and valve leaflets are normal. There are two major causes of this problem: ischemia and any cause of dilated left ventricle. In these settings, MR may result from one or both of the following :
- Annular enlargement secondary to left ventricular dilatation (figure 1)
- Papillary muscle displacement due to left ventricular remodeling, which results in tethering and excess tenting of the leaflet  (see "Cardiac remodeling: Basic aspects")
A rare cause of functional MR is standard right ventricular (RV) pacing. RV pacing simulates the effects of left bundle branch block, with dyssynchronous contraction of the left and right ventricles. This dyssynchrony may alter the timing and function of papillary muscles and mitral valve apparatus, resulting in MR that can be severe, even in the setting of otherwise normal cardiac structure and function . Dyssynchrony from either RV pacing or intrinsic conduction disease can be improved with biventricular (BiV) pacing. (See 'Cardiac resynchronization therapy' below and "Cardiac resynchronization therapy in heart failure: Indications".)
Functional MR in association with systolic heart failure will be reviewed here. There is clear overlap between functional and ischemic MR, since the reports of functional MR due to heart failure include patients with ischemic cardiomyopathy. The clinical features and management of ischemic MR, including MR in association with myocardial infarction, are discussed separately. (See "Ischemic mitral regurgitation".)
Echocardiographic studies of functional mitral regurgitation (MR) have shown that regurgitant flow varies during systole: there is an early systolic peak, a midsystolic decrease, and a late, smaller late systolic peak [4,5]. In one series, the respective values for regurgitant flow at these three time periods were 144, 13, and 62 mL/sec . These variations occur in association with parallel changes in regurgitant orifice area and are more closely associated with changes in transmitral pressure, which drives the leaflets toward closure, than mitral annular area .
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