Electrical dyssynchrony induced by biventricular pacing: Implications for patient selection and therapy improvement

被引:115
作者
Ploux, Sylvain [1 ]
Eschalier, Romain [1 ]
Whinnett, Zachary I. [2 ]
Lumens, Joost [1 ,3 ]
Derval, Nicolas [1 ]
Sacher, Frederic [1 ]
Hocini, Meleze [1 ]
Jais, Pierre [1 ]
Dubois, Remi [1 ]
Ritter, Philippe [1 ]
Haissaguerre, Michel [1 ]
Wilkoff, Bruce L. [4 ]
Francis, Darrel P. [2 ]
Bordachar, Pierre [1 ]
机构
[1] Univ Bordeaux, IHU LIRYC, CHU Bordeaux, Hop Cardiol Haut Leveque, F-33604 Bordeaux, France
[2] Univ London Imperial Coll Sci Technol & Med, London, England
[3] Maastricht Univ, Cardiovasc Res Inst Maastricht CARIM, NL-6200 MD Maastricht, Netherlands
[4] Cleveland Clin, Inst Heart & Vasc, Cleveland, OH 44106 USA
关键词
Cardiac resynchronization therapy; Electrocardiographic mapping; Hemodynamic; Heart failure; Pacing; Left bundle branch block; Nonspecific intraventricular conduction disturbance; CARDIAC-RESYNCHRONIZATION THERAPY; BUNDLE-BRANCH BLOCK; RANDOMIZED-CONTROLLED-TRIALS; ACUTE HEMODYNAMIC-RESPONSE; CLINICAL EVENT REDUCTION; CANINE PULMONARY CONUS; HEART-FAILURE PATIENTS; QRS DURATION; VENTRICULAR ACTIVATION; CONDUCTION DELAY;
D O I
10.1016/j.hrthm.2014.12.031
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND Biventricular pacing (BVP) may not achieve complete electrical resynchronization. OBJECTIVE The purpose of this study was to assess whether the resynchronizing effect of BVP varies among patients depending on the underlying electrical substrate. METHODS High-resolution electrocardiographic mapping with invasive measurement of the maximal rate of systolic left ventricular (LV) pressure rise (LVdP/dt(max)) was performed during baseline activation and during BVP in 61 patients with heart failure with various conduction delays: 13 with narrow QRS duration (<120 ms), 22 with nonspecific intraventricular conduction disturbance, and 26 with Left bundle branch block. Electrical dyssynchrony, both during baseline activation and BVP, was quantified by total and LV activation times (TAT and LVTAT) and by ventricular electrical uncoupling (VEU = mean LVTAT - mean right ventricular activation time). Response to BVP was defined as a >= 10% increase in LVdP/dt(max). RESULTS The electrical activation pattern during BVP was similar for all patient groups and, hence, not dependent on baseline conduction disturbance. During BVP, TAT, LVTAT, and VEU were similar for all groups and were either not correlated or weakly correlated with the change in LVdP/dt(max). In contrast, changes in electrical dyssynchrony correlated significantly with the change in LVdP/d(max): r=0.71, 0.69, and 0.69 for Delta TAT, Delta LVTAT, and Delta VEU, respectively (all P < .001). Responders showed higher baseline dyssynchrony levels and BVP-induced dyssynchrony reduction than did nonresponders (all P < .001); in nonresponders, BVP worsened activation times than did baseline activation. CONCLUSION BVP does not eliminate electrical dyssynchrony, but rather brings it to a common Level independent of the patient's underlying electrical substrate. Therefore, BVP is of benefit to patients with dyssynchrony but not to patients with insufficient electrical dyssynchrony in whom it induces an iatrogenic electropathy.
引用
收藏
页码:782 / 791
页数:10
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