Mullens Wilfried, Verga Tanya, Grimm Richard A, Starling Randall C, Wilkoff Bruce L, Tang W H Wilson
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
J Am Coll Cardiol. 2009 Feb 17;53(7):600-607. doi: 10.1016/j.jacc.2008.08.079.
Our aim was to determine the potential hemodynamic contributions of cardiac resynchronization therapy (CRT) in patients admitted for advanced decompensated heart failure.
CRT restores synchrony of the heart resulting in hemodynamic support that can facilitate the reversal of left ventricular (LV) remodeling in some patients.
A total of 40 consecutive patients with advanced decompensated heart failure and CRT implanted >3 months, admitted due to hemodynamic derangements, underwent simultaneous comprehensive echocardiographic and invasive hemodynamic evaluation under different CRT settings.
All patients (mean LV ejection fraction 22 +/- 7%, LV end-diastolic volume 323 +/- 140 ml, 40% ischemic) had experienced progressive cardiac remodeling despite adequate LV lead positions and continuous biventricular pacing. A significant worsening of hemodynamics was observed immediately when CRT was programmed OFF in the majority (88%) of patients (systolic blood pressure: 105 +/- 12 mm Hg to 98 +/- 13 mm Hg; pulmonary capillary wedge pressure: 17 +/- 6 mm Hg to 21 +/- 7 mm Hg; cardiac output: 4.6 +/- 1.4 l/min.m(2) to 4.0 +/- 1.1 l/min.m(2); all p < 0.001). Worsening of hemodynamics coincided with reappearance of significant electrical (QRS width 161 +/- 29 ms to 202 +/- 39 ms, p < 0.001) and intraventricular mechanical dyssynchrony (15 +/- 26 ms to 57 +/- 41 ms, p < 0.001), together with a significant reduction in diastolic filling time (377 +/- 138 ms to 300 +/- 118 ms, p < 0.001).
Despite progressive cardiac remodeling and decompensation, chronic CRT continues to provide hemodynamic augmentation in the failing heart in most patients. Our data suggest that disease progression may not be explained by diminished beneficial hemodynamic contributions of successful resynchronization.
我们的目的是确定心脏再同步治疗(CRT)对因晚期失代偿性心力衰竭入院患者潜在的血流动力学影响。
CRT可恢复心脏同步性,从而提供血流动力学支持,这有助于部分患者逆转左心室(LV)重构。
共有40例晚期失代偿性心力衰竭且CRT植入超过3个月的患者,因血流动力学紊乱入院,在不同的CRT设置下同时接受了全面的超声心动图和有创血流动力学评估。
所有患者(平均左心室射血分数22±7%,左心室舒张末期容积323±140ml,40%为缺血性)尽管左心室电极位置合适且持续双心室起搏,但仍经历了进行性心脏重构。大多数(88%)患者在CRT程控关闭时立即观察到血流动力学显著恶化(收缩压:105±12mmHg降至98±13mmHg;肺毛细血管楔压:17±6mmHg升至21±7mmHg;心输出量:4.6±1.4l/min·m²降至4.0±1.1l/min·m²;所有p<0.001)。血流动力学恶化与明显的电活动(QRS波宽度从161±29ms增至202±39ms,p<0.001)和心室内机械不同步(从15±26ms增至57±41ms,p<0.001)再次出现同时发生,同时舒张期充盈时间显著缩短(从377±138ms降至300±118ms,p<0.001)。
尽管存在进行性心脏重构和失代偿,但在大多数患者中,长期CRT仍可继续为衰竭心脏提供血流动力学增强作用。我们的数据表明,疾病进展可能无法用成功再同步化有益的血流动力学作用减弱来解释。