Abstract
Background: Mitral valve prolapse (MVP) is characterized by an abnormal movement of the valvular apparatus which may affect the papillary muscles (PMs) function and structure. Aim of the study was to investigate abnormal PM signal in MVP by using cardiac magnetic resonance imaging (MRI). Methods and Results: We enrolled 47 consecutive patients with MVP evaluated by cardiac MRI. Additional groups included healthy volunteers, patients with moderate-to-severe mitral regurgitation (not caused by MVP) and patients with hypertrophic cardiomyopathy. Visual assessment of the PM signals was carried out and the signal intensity (SI) of both the antero-lateral and postero-medial PMs was normalized by that of the left ventricular (LV) parietal myocardium. Our results show that in the MVP group only, the PM signal intensity was significantly lower compared to the one of the LV parietal myocardium. This sign did not correlate with either LV late gadolinium enhancement or positive anamnesis for significant arrhythmias. Conclusions: In MVP patients only, PM signal is significantly reduced compared to LV parietal myocardium (“darker appearance”). The described findings are not clearly related to evidence of myocardial fibrosis, as assessed by MRI, and to previous occurrence of complex ventricular arrhythmias.
Highlights
Mitral valve prolapse (MVP) is characterized by an abnormal movement of the valvular apparatus which may affect the papillary muscles (PMs) function and structure
We looked into a possible association of abnormal PM signal with demonstration of myocardial late gadolinium enhancement (LGE) and occurrence of complex ventricular arrhythmias in MVP patients
Bi-leaflets prolapse was observed in the majority (76%) of the MVP population, while isolated anterior or posterior leaflet prolapse was detected in 5% and 19%, respectively
Summary
Mitral valve prolapse (MVP) is characterized by an abnormal movement of the valvular apparatus which may affect the papillary muscles (PMs) function and structure. Aim of the study was to investigate abnormal PM signal in MVP by using cardiac magnetic resonance imaging (MRI). Methods and Results: We enrolled 47 consecutive patients with MVP evaluated by cardiac MRI. Our results show that in the MVP group only, the PM signal intensity was significantly lower compared to the one of the LV parietal myocardium. This sign did not correlate with either LV late gadolinium enhancement or positive anamnesis for significant arrhythmias. Conclusions: In MVP patients only, PM signal is significantly reduced compared to LV parietal myocardium (“darker appearance”). The described findings are not clearly related to evidence of myocardial fibrosis, as assessed by MRI, and to previous occurrence of complex ventricular arrhythmias
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