Hashimoto Junichiro, Ito Sadayoshi
aMedical Center, Miyagi University of Education, Sendai bDivision of Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
J Hypertens. 2017 Oct;35(10):2034-2043. doi: 10.1097/HJH.0000000000001436.
Stiffening of the aorta often precedes coronary events, but little is known about the aetiological mechanism. We hypothesized that the predisposition to myocardial ischemia could be attributable to aortosclerosis-induced alterations in the central haemodynamics during diastole.
Using noninvasive tonometry and ultrasonography, we investigated the arterial pressure pulse waveforms, pulse wave velocities (PWVs) and compliance in 222 patients with hypertension. The diastolic pressure decay was quantified by fitting a mono-exponential curve as P(t) = P0e [λ: decay index; P0: end-systolic pressure; t: time from end-systole]. The myocardial oxygen supply/demand balance was estimated from the subendocardial viability index (SVI).
The aortic pressure decay fit to an exponential curve significantly (R = 0.98 ± 0.02) and more closely than the radial pressure decay (P < 0.001). The aortic decay index (median, 0.59 s) was associated with the aortic PWV and compliance (but not with the peripheral PWV or resistance), even after controlling for age, sex, renal function, diabetes and hypercholesterolemia (P < 0.001). Also, both the aortic PWV and compliance (together with the augmentation index) were related to the SVI, although these relationships were no longer significant after accounting for the decay index. Mediation analysis revealed substantial mediating effects of the decay index on the relationship between aortic PWV or compliance and SVI (75-100%), despite the lack of similar effects of the augmentation index.
Aortic stiffening with reduced compliance potentially impairs myocardial viability by accelerating the diastolic exponential decay (rather than through enhancing late-systolic augmentation) of the central blood pressure, thus predisposing hypertensive patients to ischemic heart disease.
主动脉僵硬度增加通常先于冠状动脉事件发生，但病因机制尚不清楚。我们推测，心肌缺血的易感性可能归因于主动脉硬化引起的舒张期中心血流动力学改变。
我们使用无创眼压测量法和超声检查，对222例高血压患者的动脉压力脉搏波形、脉搏波速度（PWV）和顺应性进行了研究。通过拟合单指数曲线P(t) = P0e [λ：衰减指数；P0：收缩末期压力；t：从收缩末期开始的时间] 来量化舒张压衰减。根据心内膜下存活指数（SVI）评估心肌氧供/需求平衡。
主动脉压力衰减与指数曲线的拟合度显著更高（R = 0.98 ± 0.02），且比桡动脉压力衰减更紧密（P < 0.001）。即使在控制了年龄、性别、肾功能、糖尿病和高胆固醇血症后，主动脉衰减指数（中位数，0.59 s）仍与主动脉PWV和顺应性相关（但与外周PWV或阻力无关）（P < 0.001）。此外，主动脉PWV和顺应性（连同增强指数）均与SVI相关，尽管在考虑衰减指数后这些关系不再显著。中介分析显示，衰减指数对主动脉PWV或顺应性与SVI之间的关系具有显著的中介作用（75 - 100%），尽管增强指数没有类似作用。
顺应性降低的主动脉僵硬度可能通过加速中心血压的舒张期指数衰减（而非通过增强收缩末期晚期增强）损害心肌活力，从而使高血压患者易患缺血性心脏病。
