Shapiro Brian P, Lam Carolyn S P, Patel Jeetendra B, Mohammed Selma F, Kruger Martina, Meyer Donna M, Linke Wolfgang A, Redfield Margaret M
Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
Hypertension. 2007 Sep;50(3):503-11. doi: 10.1161/HYPERTENSIONAHA.107.090092. Epub 2007 Jul 9.
Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV(200)) and diastolic (EDV(20)) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV(200) and EDV(20). However, at any load, OHT had lower ESV(200) and EDV(20), associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV(20) were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.
衰老和高血压会导致动脉重塑，并使动脉（Ea）和心室（LV）的收缩期硬度呈串联增加（心室-动脉[VA]耦合）。衰老和高血压还易引发射血分数正常的心力衰竭（HFnlEF），在高血压急症或运动期间出现症状很常见。我们假设：（1）慢性VA耦合在舒张期也会发生；（2）Ea的急性变化与舒张期和收缩期压力-容积关系（PVR）的改变相关联；（3）舒张期VA耦合反映的是LV舒张期硬度的变化，而非外力或舒张功能的变化。对老年慢性高血压（OHT，n = 8）和年轻正常（YNL，n = 7）犬在基线以及后负荷和前负荷变化期间进行了PVR（腔静脉闭塞）、主动脉压力、尺寸和血流的评估。通过计算在相同压力下的收缩期（ESV(200)）和舒张期（EDV(20)）容积（顺应性）来解释PVR斜率/位置的伴随变化。OHT表现出明显的血管重塑。反映Ea搏动成分的指标（主动脉硬度和全身动脉顺应性）在OHT中，在任何扩张压力下都受损更严重。在两组中，Ea的急性增加均与ESV(200)和EDV(20)的降低相关。然而，在任何负荷下，OHT的ESV(200)和EDV(20)均较低，这与LV重塑和心肌内皮素激活有关。EDV(20)的急性变化并非由舒张功能或外力的变化介导。这些观察结果为动脉重塑以及收缩期和舒张期急慢性VA耦合可能导致负荷增加并与之相互作用从而引发HFnlEF的机制提供了深入见解。
