LOAD-DEPENDENCY OF CARDIAC RELAXATION HEARTS

在与慢性左心室（LV）肥大相关的疾病中， 心肌舒张减慢是一个特征性的发现; 导致这种异常的机制尚不清楚。 本研究将 测试假设，减缓心肌舒张， 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）， 潜在心肌缺血的设置。 正常受试者和患者 在没有冠状动脉疾病的情况下， 使用同步微压计左心室压力研究 记录和测量LV尺寸和壁厚 （超声波）。 将通过解决5个具体问题来检验假设 问题：（1）收缩期室壁应力与 左室壁变薄的峰值速率（负荷-松弛关系） 受试者在休息状态和在施加压力期间 负荷增加？ 我希望能找到一个反比关系 收缩期LV壁应力和舒张期壁变薄的峰值速率; 载荷越大，松弛速率越慢。 (2)有没有 患者的负荷-松弛关系具有可比性 主动脉瓣狭窄引起的压力超负荷性肥大， 静息状态和输注硝普钠期间降低负荷？ 的 待检验假设是收缩期壁应力的降低， 主动脉瓣狭窄的患者将伴随着恢复 心肌松弛趋于正常。 (3)瞬变的影响是什么 起搏心动过速对心肌缺血负荷-舒张关系的影响 压力超负荷性肥大的患者 (4)是什么 冠心病患者心肌舒张功能 压力超负荷肥大和肥大本身的程度？ （五） 心肌舒张与心肌纤维有什么关系 刚度（径向应力应变分析）在正常人和 压力超负荷性肥大的患者 这些研究将有助于 确定正常人心肌舒张的决定因素， 将阐明高收缩期壁应力对 慢性肺心病患者心肌舒张功能减慢 压力超负荷左心室肥大

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.