Breithardt Ole A, Sinha Anil M, Schwammenthal Ehud, Bidaoui Nadim, Markus Kai U, Franke Andreas, Stellbrink Christoph
Department of Cardiology, University Hospital, Aachen, Germany.
J Am Coll Cardiol. 2003 Mar 5;41(5):765-70. doi: 10.1016/s0735-1097(02)02937-6.
We studied the acute effects of cardiac resynchronization therapy (CRT) on functional mitral regurgitation in heart failure (HF) patients with left bundle branch block (LBBB).
Both an decrease [corrected] in left ventricular (LV) closing force and mitral valve tethering have been implicated as mechanisms for functional mitral regurgitation (FMR) in dilated hearts. We hypothesized that an increase in LV closing force achieved by CRT could act to reduce FMR.
Twenty-four HF patients with LBBB and FMR were studied after implantation of a biventricular CRT system. Acute changes in FMR severity between intrinsic conduction (OFF) and CRT were quantified according to the proximal isovelocity surface area method by measuring the effective regurgitant orifice area (EROA). Results were compared with the changes in estimated maximal rate of left ventricular systolic pressure rise (LV+dP/dt(max)) and transmitral pressure gradients (TMP), both measured by Doppler echocardiography.
Cardiac resynchronization therapy was associated with a significant reduction in FMR severity. Effective regurgitant orifice area decreased from 25 +/- 19 mm(2) (OFF) to 13 +/- 8 mm(2) (CRT). The change in EROA was directly related to the increase in LV+dP/dt(max) (r = -0.83, p < 0.0001). Compared with OFF, TMP increased more rapidly during CRT, and a higher maximal TMP was observed (OFF 73 +/- 24 mm Hg vs. CRT 85 +/- 26 mm Hg, p < 0.01).
Functional mitral regurgitation is reduced by CRT in patients with HF and LBBB. This effect is directly related to the increased closing force (LV+dP/dt(max)). The results support the hypothesis that an increase in TMP, mediated by a rise in LV+dP/dt(max) due to more coordinated LV contraction, may facilitate effective mitral valve closure.
我们研究了心脏再同步治疗（CRT）对左束支传导阻滞（LBBB）的心力衰竭（HF）患者功能性二尖瓣反流的急性影响。
左心室（LV）关闭力降低和二尖瓣瓣叶牵拉均被认为是扩张型心脏中功能性二尖瓣反流（FMR）的机制。我们假设CRT实现的LV关闭力增加可起到减少FMR的作用。
对24例LBBB和FMR的HF患者植入双心室CRT系统后进行研究。根据近端等速表面积法，通过测量有效反流口面积（EROA），对固有传导（关闭）和CRT之间FMR严重程度的急性变化进行量化。将结果与通过多普勒超声心动图测量的估计左心室收缩压最大上升速率（LV + dP/dt(max)）和跨二尖瓣压力梯度（TMP）的变化进行比较。
心脏再同步治疗与FMR严重程度的显著降低相关。有效反流口面积从（关闭时）25±19 mm²降至（CRT时）13±8 mm²。EROA的变化与LV + dP/dt(max)的增加直接相关（r = -0.83，p < 0.0001）。与关闭时相比，CRT期间TMP上升更快，并且观察到更高的最大TMP（关闭时73±24 mmHg vs. CRT时85±26 mmHg，p < 0.01）。
CRT可降低HF和LBBB患者的功能性二尖瓣反流。这种效应与关闭力增加（LV + dP/dt(max)）直接相关。结果支持以下假设：由于LV收缩更协调导致LV + dP/dt(max)升高介导的TMP增加可能有助于二尖瓣有效关闭。
