LOAD-DEPENDENCY OF CARDIAC RELAXATION HEARTS

在与慢性左心室(LV)肥厚相关的疾病中， 心肌松弛减慢是一种典型的发现； 造成这种异常的机制尚不清楚。这项研究将 对心肌松弛减慢的假设进行检验 压力超负荷性左心室肥厚部分与 后负荷不匹配(收缩期壁应力过高) 潜在心肌缺血的设定。正常人和病人 伴主动脉狭窄的患者在没有冠状动脉疾病的情况下 同步微量压力计测量左心室压力的研究 LV内径和壁厚的记录和测量 (超声波)。这一假说将通过解决5个具体问题来检验 问题：(1)收缩期室壁应力与 正常人左室壁变薄的峰值速度(负荷-松弛关系) 受试者在静息状态和药物施加期间 负荷增加了吗？我希望能找到一种相反的关系 收缩期室壁应力和舒张期室壁减薄率峰值 载荷越大，松弛速率越慢。(2)有没有 高血压患者的可比性反向负荷-松弛关系 主动脉狭窄所致的压力超负荷肥厚 静息状态和输注硝普钠以降低负荷？这个 需要检验的假设是，心脏收缩期壁应力的降低 主动脉瓣狭窄的患者将伴随着主动脉瓣的重建 心肌松弛趋于正常。(3)瞬变的影响是什么？ 起搏诱发的心肌缺血对负荷-松弛关系的影响 在压力超负荷肥厚的患者中？(4)什么是 高血压性心脏病患者心肌松弛功能的关系 压力超负荷性肥厚和肥厚本身的程度？(5) 心肌松弛与心肌纤维的关系是什么？ 正常受试者和正常受试者的刚度(径向应力-应变分析) 压力超负荷肥大的患者？这些研究将有助于 确定正常人心肌松弛的决定因素，以及 将阐明高收缩期壁应力对 慢性阻塞性肺疾病患者心肌舒张性减慢 压力超负荷性左心室肥厚。

In diseases associated with chronic left ventricular (LV) hypertrophy, slowing of myocardial relaxation has been a characteristic finding; the mechanisms responsible for this abnormality are unknown. This study will test the hypothesis that slowing of myocardial relaxation in pressure-overload left ventricular hypertrophy is related in part to afterload mismatch (inappropriately high systolic wall stress) in the setting of potential myocardial ischemia. Normal subjects and patients with aortic stenosis in the absence of coronary artery disease will be studied using simultaneous micromanometer left ventricular pressure recordings and measurement of LV dimensions and wall thickness (ultrasound). The hypothesis will be tested by addressing 5 specific questions: (1) Is there a relationship between systolic wall stress and the peak rate of LV wall thinning (load-relaxation relationship) in normal subjects during the resting state and during pharmacologically imposed increases in load? I expect to find an inverse relationship between systolic LV wall stress and the peak rate of diastolic wall thinning; that is, the greater the load, the slower the relaxation rate. (2) Is there a comparable inverse load-relaxation relationship in patients with pressure-overload hypertrophy due to aortic stenosis, assessed in the resting state and during infusion of nitroprusside to decrease load? The hypothesis to be tested is that reduction of systolic wall stress in patients with aortic stenosis will be accompanied by restoration of myocardial relaxation towards normal. (3) What is the effect of transient ischemia induced by pacing tachycardia on the load-relaxation relationship in patients with pressure-overload hypertrophy? (4) What is the relationship between myocardial relaxation in patients with pressure-overload hypertrophy and the extent of hypertrophy per se? (5) What is the relationship between myocardial relaxation and myocardial fiber stiffness (radial stress-strain analysis) in normal subjects and in patients with pressure-overload hypertrophy? These studies will help to identify the determinants of myocardial relaxation in normal humans, and will clarify the contribution (if any) of high systolic wall stress to the slowing of myocardial relaxation characteristic of patients with chronic pressure-overload LV hypertrophy.