Salukhe Tushar V, Francis Darrel P, Morgan Michelle, Clague Jonathan R, Sutton Richard, Poole-Wilson Philip, Henein Michael Y
National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom.
Am J Cardiol. 2006 May 1;97(9):1358-64. doi: 10.1016/j.amjcard.2005.11.053. Epub 2006 Mar 20.
The mechanisms underlying cardiac resynchronization therapy have consistently been studied at rest and remain ill defined. Peak stress total isovolumic time (t-IVT) is a major determinant of cardiac output (CO) in chronic heart failure. In this study, pharmacologic stress was used to assess the effects of atrioventricular (AV) delay shortening and ventricular resynchronization elements of cardiac resynchronization therapy. Thirty patients undergoing cardiac resynchronization therapy were studied <6 months after implantation. t-IVT and CO were measured during native activation (left bundle branch block), AV delay shortening (right ventricular dual-chamber pacing), and full resynchronization (atrio-biventricular pacing). Full resynchronization shortened peak stress t-IVT by 9.4 +/- 6.2 s/min (p <0.001) and increased peak stress CO by 0.9 +/- 0.4 L/min (p <0.001), with the effects in individual patients showing a large correlation (r = -0.64, p <0.001). In contrast, simple AV delay shortening did not shorten peak stress t-IVT nor increase peak stress CO, nor was CO at rest affected by full resynchronization or AV delay shortening. Of all measurements during native activation, the best predictor of gain in peak stress CO from full resynchronization was peak stress t-IVT (r = 0.75, p <0.001), with every 5 s/min increment in peak stress t-IVT during native activation predicting a 6% gain in peak stress CO. No conventional measures during native activation at rest or during stress (including QRS duration, the Tei index, tissue Doppler intraventricular delay, and t-IVT at rest) added significant additional information. In conclusion, only during stress does resynchronization consistently increase CO. Second, little of this increment in CO is achieved by AV delay shortening alone. Third, under native activation, long t-IVT during peak stress is the single best predictor of resynchronization-mediated increment in peak stress CO.
心脏再同步治疗的潜在机制一直是在静息状态下进行研究的，目前仍不清楚。峰值应力总等容时间（t-IVT）是慢性心力衰竭心输出量（CO）的主要决定因素。在本研究中，使用药物负荷试验来评估房室（AV）延迟缩短和心脏再同步治疗的心室再同步元件的效果。对30例接受心脏再同步治疗的患者在植入后<6个月进行研究。在自身激动（左束支传导阻滞）、AV延迟缩短（右心室双腔起搏）和完全再同步（房室双心室起搏）期间测量t-IVT和CO。完全再同步使峰值应力t-IVT缩短9.4±6.2秒/分钟（p<0.001），并使峰值应力CO增加0.9±0.4升/分钟（p<0.001），个体患者的效应显示出高度相关性（r=-0.64，p<0.001）。相比之下，单纯的AV延迟缩短并未缩短峰值应力t-IVT，也未增加峰值应力CO，静息时的CO也不受完全再同步或AV延迟缩短的影响。在自身激动期间的所有测量中，完全再同步导致的峰值应力CO增加的最佳预测指标是峰值应力t-IVT（r=0.75，p<0.001），自身激动期间峰值应力t-IVT每增加5秒/分钟，预测峰值应力CO增加6%。静息或负荷试验期间自身激动时的常规测量指标（包括QRS时限、Tei指数、组织多普勒室内延迟和静息时的t-IVT）均未提供显著的额外信息。总之，只有在负荷试验期间再同步才能持续增加CO。其次，CO的这种增加很少仅通过AV延迟缩短来实现。第三，在自身激动状态下，峰值应力期间较长的t-IVT是再同步介导的峰值应力CO增加的唯一最佳预测指标。
