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Mechanical dispersion and arrhythmic mitral valve prolapse: substrate and trigger in electrical instability
  1. Martina Perazzolo Marra1,
  2. Cristina Basso2
  1. 1Cardiology Unit, Department of Cardiac-Thoracic-Vascular Sciences and Public Health, University of Padua Medical School, Padova, Italy, University of Padua, Padova, Italy
  2. 2Cardiovascular Pathology Unit, Department of Cardiac-Thoracic-Vascular Sciences and Public Health, University of Padua Medical School, Padova, Italy
  1. Correspondence to Prof Martina Perazzolo Marra, Department of Cardia-Thoracic-Vascular Sciences and Public Health, University of Padua, Padua 35128, Italy; martina.perazzolomarra{at}unipd.it

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Mitral valve prolapse (MVP) represents the most common degenerative valve disease, mainly characterised by the onset of significant mitral regurgitation. However, a small cohort of patients with MVP presents a potentially ‘malignant’ MVP–ventricular arrhythmia phenotype’.1 Traditionally, the ‘arrhythmic profile’ is that of young women with bileaflet MVP, biphasic or inverted T waves in the inferior leads, and frequent complex ventricular ectopic beats with documented ventricular bigeminy or ventricular tachycardia as well as polymorphic premature ventricular beats. Imaging techniques such as contrast-enhanced cardiac magnetic resonance provided further tissue characterisation features of arrhythmic MVP, identifying myocadial replacement-type fibrosis at the level of the left ventricular (LV) inferobasal wall and of papillary muscles.2 Further, there has been a revival of mitral annular disjunction (MAD) in MVP, considered as a ‘primum movens’ of arrhythmias.3–5

On this basis, arrhythmic MVP consists of MAD, myxomatous mitral leaflets and myocardial fibrosis, but the clinical challenge in MVP is to identify the concealed ‘high-risk patient’ within a large population of low-risk patients with MVP with a benign behaviour. Electrophysiological studies demonstrated that ventricular ectopies originate not only from the LV papillary muscles and inferolateral basal wall but also from right ventricular outflow tracts and the anterolateral LV base. These preliminary observations open to the existence of a diffuse myocardial process, with interstitial or replacement-type fibrosis that is under the action of a trigger able to initiate arrhythmias. In order to better understand the physiopathological mechanism of ventricular arrhythmias in MVP, Ermakov et al investigated the possible role of mechanical dispersion by strain echocardiography for arrhythmic risk stratification in MVP.6 The finding that patients with arrhythmic …

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