BACKGROUND: Alterations in transmitral pressure, valve structure, subvalvular geometry, and abnormal myocardial function have all been implicated in the pathophysiology of functional/progressive mitral valve regurgitation (MR). In this study, we hypothesized that a relatively small structural lesion to the mitral valve apparatus predisposes to severe MR in the setting of progressive left ventricular dilation. While examining this hypothesis, an additional purpose of this study was to determine the extent of papillary muscle (PM) distortion and mitral annular dilation with increasing MR resulting from progressive dilated cardiomyopathy. METHODS AND RESULTS: Mild MR was produced via a limited, fixed structural lesion to the mitral valve apparatus of 8 dogs (20 to 22 kg). Incremental tachypacing induced left ventricular dilation over an 8-month period. The pacer was deactivated and the dogs followed for an additional 6 weeks. Echocardiographic measurements demonstrated significant cardiac remodeling (left ventricular end diastolic diameter) and MR progression with a 54% increase in left ventricular end diastolic diameter and a 44% increase in MR jet area (P < .05). Tachypacing induced decreases in left ventricular ejection fraction recovered nearly to baseline levels by 6 weeks after pacing cessation. Nevertheless, left ventricular dilation persisted and MR remained severe after pacing cessation. There was a significant increase in the short axis PM segment length and PM angular separation from baseline (6.28 +/- 0.83 versus 4.02 +/- 0.56 cm and 99.7 +/- 2.6 versus 90.1 +/- 3.2 deg, respectively, P < .05) with no change in mitral annulus circumference (8.71 +/- 0.70 versus 8.15 +/- 0.35 cm, P = NS). CONCLUSION: Progressive MR severity in nonischemic dilated cardiomyopathy resulted from changes in left ventricular shape and altered papillary muscle geometries and does not require mitral annulus dilation or a reduced left ventricular ejection fraction.
BACKGROUND: Alterations in transmitral pressure, valve structure, subvalvular geometry, and abnormal myocardial function have all been implicated in the pathophysiology of functional/progressive mitral valve regurgitation (MR). In this study, we hypothesized that a relatively small structural lesion to the mitral valve apparatus predisposes to severe MR in the setting of progressive left ventricular dilation. While examining this hypothesis, an additional purpose of this study was to determine the extent of papillary muscle (PM) distortion and mitral annular dilation with increasing MR resulting from progressive dilated cardiomyopathy. METHODS AND RESULTS: Mild MR was produced via a limited, fixed structural lesion to the mitral valve apparatus of 8 dogs (20 to 22 kg). Incremental tachypacing induced left ventricular dilation over an 8-month period. The pacer was deactivated and the dogs followed for an additional 6 weeks. Echocardiographic measurements demonstrated significant cardiac remodeling (left ventricular end diastolic diameter) and MR progression with a 54% increase in left ventricular end diastolic diameter and a 44% increase in MR jet area (P < .05). Tachypacing induced decreases in left ventricular ejection fraction recovered nearly to baseline levels by 6 weeks after pacing cessation. Nevertheless, left ventricular dilation persisted and MR remained severe after pacing cessation. There was a significant increase in the short axis PM segment length and PM angular separation from baseline (6.28 +/- 0.83 versus 4.02 +/- 0.56 cm and 99.7 +/- 2.6 versus 90.1 +/- 3.2 deg, respectively, P < .05) with no change in mitral annulus circumference (8.71 +/- 0.70 versus 8.15 +/- 0.35 cm, P = NS). CONCLUSION: Progressive MR severity in nonischemic dilated cardiomyopathy resulted from changes in left ventricular shape and altered papillary muscle geometries and does not require mitral annulus dilation or a reduced left ventricular ejection fraction.