Abstract
Recent studies have described the occurrence of complex ventricular arrhythmias and sudden cardiac death among patients with mitral valve prolapse (MVP). The reported incidence rate of sudden cardiac death or ventricular tachycardia is about 1–1.5% among patients with MVP. Various imaging markers have been associated with this increased risk, including mitral annular disjunction, replacement fibrosis by late gadolinium enhancement, and mechanical dispersion. In this review, we briefly discuss how multimodality cardiac imaging can be applied to identify MVP patients with high risk of sudden cardiac death and complex ventricular arrhythmias.
Highlights
Mitral valve prolapse (MVP) has received renewed attention due to several studies documenting its association with scar substrate and increased risk of complex ventricular arrhythmias (VA) and sudden cardiac death (SCD) [1,2,3]
The reported prevalence of MVP has been described to be as high as 17– 35% [10, 11]. These discrepancies are related to initial reports which defined MVP as the presence of 2 mm leaflet displacement in any apical echocardiographic view. This led to an overdiagnosis of MVP primarily due to the assumption that the mitral valve is a planar structure, which was later refuted by the pioneering work of Levine et al in the latter half of the 1980s [7, 12]
All 43 of these patients had patchy fibrosis in the region of the posterior papillary muscle and the left ventricular (LV) wall adjacent to it. They further investigated 30 living patients with MVP with evidence of complex VA and found 28 (93%) of these patients had myocardial fibrosis in the region of papillary muscle with or without involvement of the inferobasal region of the LV wall. Considering these findings, the prior theory of an occult MVP cardiomyopathy has evolved into that of a localized mechanical injury of the myocardium such that MVP patients have unique focal fibrosis which is the substrate of SCD and complex VA [38]
Summary
Mitral valve prolapse (MVP) has received renewed attention due to several studies documenting its association with scar substrate and increased risk of complex ventricular arrhythmias (VA) and sudden cardiac death (SCD) [1,2,3]. Five patients had mid-wall or patchy myocardial fibrosis (nonischemic pattern) in the inferobasal region of the LV It is well-documented in the literature that the presence of scar can lead to the genesis of ventricular arrhythmia. They further investigated 30 living patients with MVP with evidence of complex VA and found 28 (93%) of these patients had myocardial fibrosis in the region of papillary muscle with or without involvement of the inferobasal region of the LV wall Considering these findings, the prior theory of an occult MVP cardiomyopathy has evolved into that of a localized mechanical injury of the myocardium such that MVP patients have unique focal fibrosis which is the substrate of SCD and complex VA [38]. It is elucidated that mechanical dyssynchrony is associated with the expression of certain proteins which makes the heart
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