Mechanisms and predictors of mitral regurgitation after high-risk myocardial infarction

Abstract

Background: Mitral regurgitation (MR) has been associated with adverse outcomes after myocardial infarction (MI). Without structural valve disease, functional MR has been related to left ventricular (LV) remodeling and geometric deformation of the mitral apparatus. The aims of this study were to elucidate the mechanistic components of MR after high-risk MI and to identify predictors of MR progression during follow-up.

Methods: The Valsartan in Acute Myocardial Infarction Echo substudy prospectively enrolled 610 patients with LV dysfunction, heart failure, or both after MI. MR at baseline, 1 month, and 20 months was quantified by mapping jet expansion in the left atrium in 341 patients with good-quality echocardiograms. Indices of LV remodeling, left atrial size, and diastolic function and parameters of mitral valve deformation, including tenting area, coaptation depth, anterior leaflet concavity, annular diameters, and contractility, were assessed and related to baseline MR. The progression of MR was further analyzed, and predictors of worsening among the baseline characteristics were identified.

Results: Tenting area, coaptation depth, annular dilatation, and left atrial size were all associated with the degree of baseline MR. Tenting area was the only significant and independent predictor of worsening MR; a tenting area of 4 cm(2) was a useful cutoff to identify worsening of MR after MI and moderate to severe MR after 20 months.

Conclusions: Increased mitral tenting and larger mitral annular area are determinants of MR degree at baseline, and tenting area is an independent predictor of progression of MR after MI. Although LV remodeling itself contributes to ischemic MR, this influence is directly dependent on alterations in mitral geometry.

Figure 1

Indices of geometric mitral valve deformation and LV remodeling. (A) Tenting area (red triangle), coaptation depth (blue line), MA diameter (basis of the red triangle), and annular-papillary distance (yellow line). (B) Bulging of inferior wall (orange line). The PPM attachment was outwardly displaced because of bulging of the inferior wall after necrosis. (C) Convexity of the AML toward the left atrium in mid-systole (pink star). (D) AML diastolic normal motion. The AML (pink line) in diastole moves forward the green line connecting PPM head and intervalvular fibrosa.

Figure 2

Relationship between MR severity at baseline and after 1 and 20 months and each 1-cm² increase in baseline tenting area.

Figure 3

Receiver operating characteristic (ROC) curve analysis showing the tenting area cutoff level distinguishing worsening MR of at least one degree from unchanged or improved MR during follow-up (A, red line) and moderate to severe MR from none to mild MR at 20 months (B, blue line).

Figure 4

(A) A patient with mild MR at baseline and a tenting area of 3.7 cm² who experienced no MR progression during follow-up. (B) A patient with mild MR at baseline and a tenting area of 4.5 cm² who worsened to moderate MR at 20 months.