Mirsky I, Aoyagi T, Ihara T, van Eyll C, Rousseau M F, Pouleur H
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Eur Heart J. 1995 Jun;16(6):808-17. doi: 10.1093/oxfordjournals.eurheartj.a061000.
Large-scale drug trials have focused primarily on mortality and morbidity and less on the functional state of the myocardium. A model was developed to assess myocardial contractile state in patients with left ventricular (LV) dysfunction and to address the questions of differences in function between patients with and without overt heart failure, effects of enalapril, and best predictors of functional outcome. Pressure-angiographic data were obtained from 16 patients with overt heart failure and 47 without heart failure. Repeat studies were conducted in 41 patients following 1 year's treatment with enalapril or placebo. Left ventricular silhouettes were divided into 18 segments to estimate regional ejection fraction, wall stress and myocardial damage (% myocardial damage). Contractile state was assessed and ranked by ejection rate-preload-afterload relationships and by a score method based on 10 myocardial and ventricular function parameters. End-diastolic and end-systolic volumes (EDV, ESV) were significantly greater (P < 0.001), ejection fraction (EF) lower (P < 0.009), % myocardial damage greater (P < 0.008) and contractile state more depressed in patients with overt heart failure. Changes in EDV and ESV (delta placebo vs delta enalapril) were significant (delta EDV, P < 0.003; delta ESV, P < 0.014). Directional shifts in the diastolic pressure-volume relationships with enalapril or placebo depended primarily on the basal contractile state and diastolic volume range. The best single predictors of post-treatment EF were the score index (a surrogate parameter for the contractile state) and ESV. Added benefits of enalapril include the prevention of further dilatation in patients with less depressed contractile state and delay in the onset of heart failure. Asymptomatic patients with LV dysfunction should also be considered for angiotensin converting enzyme (ACE) inhibitor therapy.
大规模药物试验主要关注死亡率和发病率,而较少关注心肌的功能状态。开发了一种模型,用于评估左心室(LV)功能不全患者的心肌收缩状态,并解决有明显心力衰竭和无明显心力衰竭患者之间的功能差异、依那普利的作用以及功能转归的最佳预测因素等问题。从16例有明显心力衰竭的患者和47例无心力衰竭的患者获取了压力-血管造影数据。对41例接受依那普利或安慰剂治疗1年的患者进行了重复研究。将左心室轮廓分为18个节段,以估计局部射血分数、壁应力和心肌损伤(%心肌损伤)。通过射血率-前负荷-后负荷关系以及基于10个心肌和心室功能参数的评分方法评估并对收缩状态进行排序。有明显心力衰竭的患者舒张末期和收缩末期容积(EDV、ESV)显著更大(P<0.001),射血分数(EF)更低(P<0.009),%心肌损伤更大(P<0.008),收缩状态更受抑制。EDV和ESV的变化(安慰剂组与依那普利组的差值)具有显著性(ΔEDV,P<0.003;ΔESV,P<0.014)。依那普利或安慰剂引起的舒张期压力-容积关系的方向性变化主要取决于基础收缩状态和舒张期容积范围。治疗后EF的最佳单一预测因素是评分指数(收缩状态的替代参数)和ESV。依那普利的额外益处包括预防收缩状态受抑制程度较轻的患者进一步扩张以及延缓心力衰竭的发生。左心室功能不全的无症状患者也应考虑接受血管紧张素转换酶(ACE)抑制剂治疗。