Echocardiographic and biochemical predictors of ventricular arrhythmias in young patients with mitral valve prolapse

Purpose: Ventricular arrhythmias are known to be common in symptomatic patients with Mitral Valve Prolapse (MVP). The aim of our study was to investigate the prevalence, echocardiographic and biochemical predictors, and possible mechanisms of ventricular arrhythmias in young asymptomatic patients with MVP without significant mitral regurgitation. Methods: We studied 78 asymptomatic young subjects (mean age 19.7±1.6, 72% male) in sinus rhythm with MVP in comparison with 80 sex- and age-matched healthy subjects. Transthoracic echocardiography (Vivid 7 Dimension, GE) and 24-hour Holter monitoring were performed. MVP was diagnosed by billowing of 1 or both mitral leaflets >2 mm above the mitral annulus in the long-axis parasternal view. Longitudinal strain were determined from three apical views, using spackle tracking (EchoPAC'08, GE) with grey-scale frame rate 50-55/sec. Concentration of Monocyte Chemoattractant Protein-1 (MCP-1) in serum were determined by enzyme-linked immunosorbent assay. Results: The frequency of isolated Ventricular Premature Contractions (VPCs) was similar in both groups (32.4% and 33.3%; χ2=1.2, p=0.90). Ventricular tachycardias were not found in either MVP nor in control group. However, the ventricular couplets were recorded only in patients with MVP (in 8.1% of MVP group; χ2=5.2, p=0.01). The presence of couplets negatively correlated with Left Ventricular (LV) ejection fraction (r=–0.66; p=0.0001), with a global LV longitudinal strain (r=–0.78; p<0.0001), but positively correlated with the concentration of profibrotic chemokine MCP-1 (r=0.56; p=0.008). In patients with couplets more often were revealed local wall motion abnormalities (z=–2.0, p=0.04). Based on logistic regression analysis for MVP cases, in the case of ventricular couplets, the longitudinal strain (p=0.001) and MCP-1 serum level (p=0.01) were the independent predictors of couplets. Conclusion: In young asymptomatic patients with MVP more often than in the healthy population recorded ventricular couplets, the origin of which may be associated with impaired LV contractility, probably due to fibrosis of the myocardium.