Chung Charles S, Strunc Audrey, Oliver Rachel, Kovács Sándor J
Cardiovascular Biophysics Laboratory, Washington Univ. Medical Center, 660 South Euclid Ave., Box 8086, St. Louis, MO 63110, USA.
Am J Physiol Heart Circ Physiol. 2006 Nov;291(5):H2415-23. doi: 10.1152/ajpheart.00257.2006. Epub 2006 May 26.
Because systole and diastole are coupled and systolic ventricular-vascular coupling has been characterized, we hypothesize that diastolic ventricular-vascular coupling (DVVC) exists and can be characterized in terms of relaxation and stiffness. To characterize and elucidate DVVC mechanisms, we introduce time derivative of pressure (dP/dt) vs. time-varying pressure [P(t)] (pressure phase plane, PPP)-derived analogs of ventricular and vascular "stiffness" and relaxation parameters. Although volume change (dV) = 0 during isovolumic periods, and time-varying left ventricular (LV) stiffness, typically expressed as change in pressure per unit change in volume (dP/dV), is undefined, our formulation allows determination of a PPP-derived stiffness analog during isovolumic contraction and relaxation. Similarly, an aortic stiffness analog is also derivable from the PPP. LV relaxation was characterized via tau, the time constant of isovolumic relaxation, and vascular (aortic pressure decay) relaxation was characterized in terms of its equivalent (windkessel) exponential decay time constant kappa. The results show that PPP-derived systolic and diastolic ventricular and vascular stiffness are strongly coupled [K(Ao)(+)=1.71(K(LV)(+)) +154, r=0.86; K(Ao)(-)=0.677(K(LV)(-))-5.53, r=0.86]. In support of the DVVC hypothesis, a strong linear correlation between relaxation (rate of pressure decay) indexes kappa and tau (kappa = 9.89tau - 90.3, r = 0.81) was also observed. The correlations observed underscore the role of long-term, steady-state DVVC as a diastolic function determinant. Awareness of the PPP-derived DVVC parameters provides insight into mechanisms and facilitates quantification of arterial stiffening and associated increase in diastolic chamber stiffness. The PPP method provides a tool for quantitative assessment and determination of the functional coupling of the vasculature to diastolic function.
由于心脏收缩和舒张相互关联，且收缩期心室 - 血管耦合已得到表征，我们推测舒张期心室 - 血管耦合（DVVC）存在，并且可以从舒张和僵硬度方面进行表征。为了表征和阐明DVVC机制，我们引入压力的时间导数（dP/dt）与随时间变化的压力[P(t)]（压力相平面，PPP）导出的心室和血管“僵硬度”及舒张参数的类似物。尽管在等容期容积变化（dV）= 0，且通常表示为单位容积变化的压力变化（dP/dV）的随时间变化的左心室（LV）僵硬度未定义，但我们的公式允许在等容收缩和舒张期间确定PPP导出的僵硬度类似物。同样，主动脉僵硬度类似物也可从PPP导出。LV舒张通过等容舒张时间常数tau来表征，血管（主动脉压力衰减）舒张通过其等效（风箱）指数衰减时间常数kappa来表征。结果表明，PPP导出的收缩期和舒张期心室及血管僵硬度紧密耦合[K(Ao)(+)=1.71(K(LV)(+)) +154，r = 0.86；K(Ao)(-)=0.677(K(LV)(-)) - 5.53，r = 0.86]。为支持DVVC假说，还观察到舒张（压力衰减率）指标kappa和tau之间存在强线性相关性（kappa = 9.89tau - 90.3，r = 0.81）。观察到的这些相关性强调了长期稳态DVVC作为舒张功能决定因素的作用。认识到PPP导出的DVVC参数有助于深入了解机制，并便于量化动脉僵硬度及舒张期心室僵硬度的相关增加。PPP方法为定量评估和确定脉管系统与舒张功能的功能耦合提供了一种工具。
