Division of Cardiovascular Medicine, University of Wisconsin, Madison, Wisconsin, USA.
Am J Hypertens. 2013 Jul;26(7):866-71. doi: 10.1093/ajh/hpt043. Epub 2013 Mar 28.
Changes in the cardiovascular system with age may predispose older persons to development of heart failure with preserved ejection fraction. Vascular stiffening, aortic pressure augmentation, and ventricular-vascular coupling have been implicated. We explored the potential for acute reductions in late systolic pressure augmentation to impact left ventricular relaxation in older persons without heart failure.
Sixteen older persons free of known cardiovascular disease with the exception of hypertension had noninvasive tonometry and cardiac ultrasound to evaluate central augmentation index (AI) and diastolic function at baseline and after randomized, blinded administration of intravenous B-type natriuretic peptide (BNP) and hydralazine in a crossover design.
AI was significantly reduced after BNP (11.4±8.9 to -0.2±14.7%; P = 0.02) and nonsignificantly reduced after hydralazine (14.7±8.4% to 11.5±8.8%; P = 0.39). With decreased AI during BNP, a trend toward worsened myocardial relaxation by tissue Doppler imaging occurred (E' velocity pre- and post-BNP: 10.0±2.5 and 8.8±2.0cm/s, respectively; P = 0.06). There was a significant fall in stroke volume with BNP (68.5±18.3 to 60.9±18.1ml; P = 0.02), suggesting that changes in preload overwhelmed effects of afterload reduction on ventricular performance. With hydralazine, neither relaxation nor stroke volume changed.
Acute changes in late systolic aortic pressure augmentation do not necessarily lead to improved systolic or diastolic function in older people. Preload may be a more important determinant of cardiac performance than afterload in older people with compensated ventricular function. The potential for changes in preload to impair rather than enhance left ventricular systolic and diastolic function in older people warrants further study.
This study is registered at clinicaltrials.gov as NCT00204984.
随着年龄的增长,心血管系统的变化可能使老年人易患射血分数保留型心力衰竭。血管僵硬、主动脉压力增强和心室血管耦联已被涉及。我们探讨了急性降低收缩期末压力增强对无心力衰竭的老年人左心室舒张功能的潜在影响。
16 名无已知心血管疾病(除高血压外)的老年人进行了无创张力测量和心脏超声检查,以评估中心增强指数(AI)和舒张功能,基线时和随机、盲法静脉内给予 B 型利钠肽(BNP)和肼屈嗪后进行交叉设计。
BNP 后 AI 显著降低(11.4±8.9 至-0.2±14.7%;P = 0.02),肼屈嗪后略有降低(14.7±8.4%至 11.5±8.8%;P = 0.39)。随着 BNP 期间 AI 的降低,组织多普勒成像显示心肌松弛趋势恶化(E'速度在 BNP 前后分别为 10.0±2.5 和 8.8±2.0cm/s,P = 0.06)。BNP 后心排量显著下降(68.5±18.3 至 60.9±18.1ml;P = 0.02),表明前负荷的变化超过了后负荷降低对心室功能的影响。肼屈嗪治疗后,舒张功能和心排量均无变化。
急性收缩期末主动脉压力增强变化不一定导致老年人收缩或舒张功能改善。在心室功能代偿的老年人中,前负荷可能比后负荷更能决定心脏功能。前负荷变化可能会损害而不是增强老年人的左心室收缩和舒张功能,这需要进一步研究。
本研究在 clinicaltrials.gov 注册,注册号为 NCT00204984。