Kim M H, Devlin W H, Das S K, Petrusha J, Montgomery D, Starling M R
University of Michigan and Veterans Affairs Medical Centers, Ann Arbor, MI 48105, USA.
Circulation. 1999 Aug 17;100(7):729-35. doi: 10.1161/01.cir.100.7.729.
The hemodynamic mechanism for the improvement in left ventricle (LV) end-diastolic pressure in cardiomyopathy patients treated with beta-adrenergic blocking agents is controversial. We hypothesized that the salutary effect of this kind of therapy on LV end-diastolic pressure would be indicative of an improvement in late, passive diastolic relaxation properties.
We studied 14 cardiomyopathy patients in normal sinus rhythm with no arteriographic evidence of coronary artery disease and an LV ejection fraction of </=40% by radionuclide angiography both before and after 6 months of metoprolol therapy with simultaneous micromanometry and biplane cineventriculography. Four comparable patients who were not treated with metoprolol were studied in a similar fashion and served as control subjects. In those receiving metoprolol, LV end-diastolic pressure decreased (P=0.001). The isovolumic relaxation index, tau(ln), shortened (P=0.03). In a similar fashion, the LV chamber stiffness constant, kappa, decreased (P=0.02), LV volume elastance improved (P=0.04), and the myocardial stiffness constant, kappa(e), decreased (P=0.02). A multiple regression analysis revealed that the decrease in LV end-diastolic pressure was indicative of significant improvements in tau(ln) and kappa(e) with the relationship: LV end-diastolic pressure=-4.73+0.27 tau(ln)+0.54 kappa(e) (r=0.81, P<0.0001). These LV diastolic relaxation properties did not change or worsened in the control cardiomyopathy patients.
We conclude that the decrease in LV end-diastolic pressure in cardiomyopathy patients treated with metoprolol is an indicator of improvement in LV diastolic properties resulting from more complete myocardial relaxation.
β-肾上腺素能阻滞剂治疗心肌病患者时,左心室(LV)舒张末期压力改善的血流动力学机制存在争议。我们推测,这种治疗对LV舒张末期压力的有益作用将表明晚期被动舒张松弛特性有所改善。
我们研究了14例正常窦性心律的心肌病患者,这些患者无冠状动脉疾病的血管造影证据,且通过放射性核素血管造影术测得LV射血分数≤40%。在接受美托洛尔治疗6个月前后,同时进行微测压和双平面电影心室造影。以类似方式研究了4例未接受美托洛尔治疗的可比患者,并将其作为对照。接受美托洛尔治疗的患者中,LV舒张末期压力降低(P = 0.001)。等容舒张指数tau(ln)缩短(P = 0.03)。同样,LV腔硬度常数kappa降低(P = 0.02),LV容积弹性改善(P = 0.04),心肌硬度常数kappa(e)降低(P = 0.02)。多元回归分析显示,LV舒张末期压力的降低表明tau(ln)和kappa(e)有显著改善,关系为:LV舒张末期压力 = -4.73 + 0.27 tau(ln) + 0.54 kappa(e)(r = 0.81,P < 0.0001)。这些LV舒张松弛特性在对照心肌病患者中未改变或恶化。
我们得出结论,美托洛尔治疗的心肌病患者LV舒张末期压力降低是LV舒张特性改善的指标,这是由于心肌更完全的松弛所致。