title: Incremental value of global systolic dyssynchrony in determining the occurrence of functional mitral regurgitation in patients with left ventricular systolic dysfunction.
abstract: OBJECTIVE
  The aim of this study was to assess the contribution of left ventricular (LV) systolic dyssynchrony to functional mitral regurgitation (MR).
  
  
  RESULTS
  Patients (n = 136) with LV systolic dysfunction (ejection fraction <50%) and at least mild MR were prospectively recruited. The effective regurgitant orifice area (EROA) was assessed by the proximal isovelocity surface area method. Left ventricular global systolic dyssynchrony [the maximal difference in time to peak systolic velocity among the 12 LV segments (Ts-Dif)] and regional systolic dyssynchrony (the delay between the anterolateral and posteromedial papillary muscle attaching sites) were assessed by tissue Doppler imaging. Left ventricular global and regional remodelling, systolic function, indices of mitral valvular and annular deformation were also measured. The size of the EROA correlated with the degrees of mitral deformation, LV remodelling, systolic function, and systolic dyssynchrony. By multivariate logistic regression analysis, the mitral valve tenting area (OR = 1.020, P < 0.001) and the Ts-Dif (OR = 1.011, P = 0.034) were independent determinants of significant functional MR (defined by EROA ≥20 mm(2)). From the receiver-operating characteristic curve, the tenting area of 2.7 cm(2) (sensitivity 83%, specificity 82%, AUC 0.86, P < 0.001) and the Ts-Dif of 85 ms (sensitivity 66%, specificity 72%, AUC 0.74, P < 0.001) were associated with significant functional MR. The assessment of Ts-Dif showed an incremental value over the mitral valve tenting area for determining functional MR (χ(2) = 53.92 vs.49.11, P = 0.028).
  
  
  CONCLUSIONS
  This cross-sectional study showed that LV global, but not regional systolic dyssynchrony, is a determinant of significant functional MR in patients with LV systolic dysfunction, and is incremental to the tenting area that is otherwise the strongest factor for mitral valve deformation.
authors.affiliation: Division of Cardiology, Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, Peoples' Republic of China.
authors.forename: Yu-Jia
authors.initials: YJ
authors.lastname: Liang
authors.forename: Qing
authors.initials: Q
authors.lastname: Zhang
authors.forename: Fang
authors.initials: F
authors.lastname: Fang
authors.forename: Alex Pui-Wai
authors.initials: AP
authors.lastname: Lee
authors.forename: Ming
authors.initials: M
authors.lastname: Liu
authors.forename: Bryan Ping-Yen
authors.initials: BP
authors.lastname: Yan
authors.forename: Yat-Yin
authors.initials: YY
authors.lastname: Lam
authors.forename: Gary Chin-Pang
authors.initials: GC
authors.lastname: Chan
authors.forename: Cheuk-Man
authors.initials: CM
authors.lastname: Yu
mesh_terms: D000368:Aged; D001145:Arrhythmias, Cardiac / Q000150:complications* / Q000503:physiopathology; D003430:Cross-Sectional Studies; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008944:Mitral Valve Insufficiency / Q000209:etiology* / Q000503:physiopathology; D010210:Papillary Muscles / Q000502:physiology; D011446:Prospective Studies; D012372:ROC Curve; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000502:physiology