Loss of left ventricular rotation is a significant determinant of functional mitral regurgitation

Aim: To evaluate insufficient rotational movement of the left ventricle (LV) as a potential novel mechanism for functional regurgitation of the mitral valve (FMR). Methods and results: We compared reference subjects and patients with LV dysfunction (LVD, ejection fraction EF < 50%) with and without FMR (regurgitant volume RVol>10 ml). Subjects without structural mitral valve pathology undergoing cardiac MRI were evaluated. Delayed enhancement, global LV remodeling parameters, systolic twist and torsion were measured (using manual and novel automated cardiac MRI tissue-tracking). The study included 117 subjects with mean +/- SD age 50.4 +/- 17.8 years, of which 30.8% were female. Compared to subjects with LVD without FMR (n = 31), those with FMR (n = 37) had similar clinical characteristics, diagnoses, delayed enhancement, EF, and longitudinal strain. Subjects with FMR had significantly larger left ventricles (EDVi:136.6 +/- 41.8 vs 97.5 +/- 26.2 ml/m, p < 0.0001) with wider separation between papillary muscles (21.1 +/- 7.6 vs 17.2 +/- 5.7 mm, p = 0.023). Notably, they had lower apical (p < 0.0001) but not basal rotation and lower peak systolic twist (3.1 +/- 2.4 degrees vs 5.5 +/- 2.5 degrees, p < 0.0001) and torsion (0.56 +/- 0.38 degrees /cm vs 0.88 +/- 0.52 degrees /cm, p = 0.004). In a multivariate model for RVol including age, gender, twist, LV end-diastolic volume, sphericity index and separation between papillary muscles, only gender, volume and twist were significant. Twist was the most powerful correlate (beta 2.23, CI -3.26 to 1.23 p < 0.001). In patients with FMR, peak systolic twist negatively correlates with RVol (r = 0.73, p < 0.0001). Conclusion: Reduced rotational systolic LV motion is significantly and independently associated with RVol among patients with FMR, suggesting a novel pathophysiological mechanism and a potential therapeutic target.