Kass D A, Wolff M R, Ting C T, Liu C P, Chang M S, Lawrence W, Maughan W L
Johns Hopkins Medical Institutions, Baltimore, Maryland.
Ann Intern Med. 1993 Sep 15;119(6):466-73. doi: 10.7326/0003-4819-119-6-199309150-00004.
To test, by studying the acute effects of drugs that influence active processes, the hypothesis that in humans with marked ventricular hypertrophy, reduced chamber compliance is primarily caused by passive structural changes.
An uncontrolled (before-after) study.
University Medical Center.
Fourteen patients with ventricular hypertrophy (19 +/- 4.5-mm diastolic-wall thickness) and normal resting systolic function were studied while they had invasive cardiac catheterization.
Intravenous beta-blocker (esmolol) or calcium channel blocker (verapamil) or both.
Left ventricular function was determined by pressure-volume relations. Volume was measured using conductance catheter, providing a continuous voltage signal proportional to chamber volume. Pressure was measured by micromanometer. Cardiac-specific assessment of change in chamber contractility and diastolic compliance due to each drug was determined.
Both drugs lowered contractility by approximately 30% (P < 0.01). Esmolol slowed relaxation and reduced early peak filling rate, whereas verapamil delayed the time to peak filling (all P < 0.05). In contrast to the effects of both drugs on active contraction and early diastole, late-diastolic compliance was unaltered, and end-diastolic pressure-volume relations were almost identical.
Neither beta-receptor nor calcium channel blockade acutely alters left ventricular compliance despite substantial active effects manifest in systole and early diastole. This supports the notion that chamber compliance is principally determined by passive structural elements in the heart rather than by active processes.
通过研究影响主动过程的药物的急性效应,来检验以下假设:在有明显心室肥厚的人类中,心室顺应性降低主要是由被动结构改变引起的。
一项非对照(前后对照)研究。
大学医学中心。
14例心室肥厚患者(舒张期壁厚19±4.5毫米),静息收缩功能正常,在进行有创心脏导管插入术时接受研究。
静脉注射β受体阻滞剂(艾司洛尔)或钙通道阻滞剂(维拉帕米)或两者联用。
通过压力-容积关系测定左心室功能。使用电导导管测量容积,该导管可提供与心室容积成比例的连续电压信号。通过微测压计测量压力。确定每种药物对心室收缩性和舒张顺应性变化的心脏特异性评估。
两种药物均使收缩性降低约30%(P<0.01)。艾司洛尔减慢了舒张速度并降低了早期峰值充盈率,而维拉帕米延迟了达到峰值充盈的时间(均P<0.05)。与两种药物对主动收缩和舒张早期的影响相反,舒张晚期顺应性未改变,舒张末期压力-容积关系几乎相同。
尽管在收缩期和舒张早期有明显的主动效应,但β受体阻滞剂和钙通道阻滞剂均未急性改变左心室顺应性。这支持了心室顺应性主要由心脏中的被动结构成分而非主动过程决定的观点。