Why the study?
MVP causes LV remodelling even without significant mitral regurgitation, but whether apical papillary muscle insertion influences the pattern and severity of this remodelling is unknown.
Does apical papillary muscle insertion influence left ventricular remodelling and arrhythmogenicity in patients with mitral valve prolapse?
Does apical papillary muscle insertion influence left ventricular remodelling and arrhythmogenicity in patients with mitral valve prolapse?
Apical papillary muscle insertion in patients with mitral valve prolapse is associated with adverse left ventricular remodelling, papillary muscle fibrosis, and increased ventricular arrhythmogenicity.
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Apical PM insertion may refine MVP remodelling assessment; leaves open its prognostic or therapeutic role.
AIMS: Mitral valve prolapse (MVP) causes left ventricular (LV) remodelling even in the absence of significant mitral regurgitation. To evaluate whether apical insertion of the papillary muscle (PM) influences the pattern and severity of MVP-related LV remodelling. METHODS AND RESULTS: All MVP patients who underwent CMR at our institution between December 2008 and December 2019 were included, thoroughly reviewed and grouped according to apical/non-apical PM insertion. Apical PM insertion was found in 53/92 patients (58%) and associated with mitral leaflet thickening (P < 0.01) and a trend towards higher prevalence of mitral annular disjunction (P = 0.05). Whereas no differences in ventricular volumes or ejection fraction were found, patients with apical PM insertion showed more lateral wall remodelling with mid lateral wall thinning [2.1 (1.8-2.5) vs. 4.0 (3.5-5.0) mm, P < 0.01], increased LV eccentricity and a lower GCS at this level (15 ± 3% vs. 20 ± 3%, P < 0.01). In long-axis direction, increased end-diastolic mid lateral wall angulation was found (i.e. angle <155° measured in the thinnest point of the mid lateral wall in four-chamber view) with a higher angle variation during systole (25 ± 11° vs. 17 ± 8°, P < 0.01). Remarkably, PM fibrosis was significantly more frequent in patients with apical PM insertion (i.e. 66% vs. 28%, P < 0.01). Finally, a higher burden of premature ventricular complexes (>5%) and non-sustained ventricular tachyarrhythmias was found in patients with apical PM insertion: 53% vs. 25% (P = 0.04) and 38% vs. 18% (P = 0.04), respectively. CONCLUSION: Apical PM insertion is part of the phenotypic spectrum of MVP, impacts significantly LV remodelling, and potentially may be related to increased ventricular arrhythmogenicity.
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Ferreira et al. (2021) studied this question.
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