Imaging characteristics of papillary muscle site of origin of ventricular arrhythmias in patients with mitral valve prolapse

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Mitral valve prolapse (MVP) is a relatively common valvular abnormality that affects approximately 1–3% of the population.1 In general, outcomes are favorable and the condition is largely benign.2 However, recent studies have suggested that some patients with MVP are at increased risk for ventricular arrhythmias that may precipitate sudden cardiac death, which was reported to occur at rates up to 0.2–0.4% per year.4 The “malignant MVP syndrome” tends to affect younger patients without typical cardiovascular comorbidities such as hypertension, diabetes mellitus, and coronary artery disease.7 Additionally, certain echocardiographic characteristics may be associated with an increased risk of ventricular arrhythmias in these patients, such as bileaflet prolapse, increased anterior mitral leaflet thickness, and moderate to severe mitral regurgitation.8
Fibrosis of the papillary muscles and inferobasal left ventricular wall may provide substrate for ventricular ectopy in patients with MVP, and several studies have included data obtained during electrophysiologic (EP) mapping to implicate these regions as arrhythmogenic origins in these patients.6 Other studies have utilized cardiac magnetic resonance imaging (CMR) to demonstrate late gadolinium enhancement (LGE) in the papillary muscle region, suggestive of fibrosis.13
No studies to date have demonstrated the relationship of leaflet characteristics, papillary muscle fibrosis, and in vivo EP mapping data.6 In the present study, we retrospectively analyzed transthoracic echocardiograms (TTEs) and CMRs with in vivo EP mapping data for patients at our center with MVP and ventricular ectopy to better define the imaging characteristics in understanding the involvement of papillary muscles in ventricular arrhythmogenesis in these patients.
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