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在愈合与早期后负荷降低试验(HEART)中,局部室壁应力可预测前间隔心肌梗死后的心室重构:一项基于超声心动图的结构分析。

Regional wall stress predicts ventricular remodeling after anteroseptal myocardial infarction in the Healing and Early Afterload Reducing Trial (HEART): an echocardiography-based structural analysis.

作者信息

Aikawa Y, Rohde L, Plehn J, Greaves S C, Menapace F, Arnold M O, Rouleau J L, Pfeffer M A, Lee R T, Solomon S D

机构信息

Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115, USA.

出版信息

Am Heart J. 2001 Feb;141(2):234-42. doi: 10.1067/mhj.2001.112237.

Abstract

BACKGROUND

Increased left ventricular (LV) wall stress after myocardial infarction (MI) has been implicated in LV remodeling. However, the relationship between LV wall stress and LV remodeling is incompletely defined.

METHOD

We prospectively studied the relationship between regional wall stress and LV remodeling by application of the finite element method to end-systolic LV models from patients enrolled in the Healing and Early Afterload Reducing Therapy (HEART) Trial. Individual LV models were constructed from orthogonal apical echocardiographic views obtained at day 14 after anteroseptal MI in 64 patients. Of these, 31 patients received low-dose (0.625 mg) ramipril and 33 patients received full-dose (10 mg) ramipril. LV wall stress was calculated by the finite element method and correlated with change in LV volume from day 14 to day 90 after MI.

RESULTS

Among all patients, increases in apical regional wall stress were associated with LV volume changes (P -trend =.015). The relationship between apical regional wall stress and change in LV volume was strongest in the low-dose ramipril group (r = 0.53, P =.002) and remained significant after adjustment for end-diastolic volume, infarct size, ejection fraction, and systolic blood pressure yet was attenuated in the full-dose ramipril group.

CONCLUSIONS

Apical regional wall stress is an independent predictor of subsequent LV remodeling after MI. The relationship between increased apical wall stress and LV dilatation appears to be attenuated by full-dose angiotensin-converting enzyme inhibition.

摘要

背景

心肌梗死(MI)后左心室(LV)壁应力增加与LV重塑有关。然而,LV壁应力与LV重塑之间的关系尚未完全明确。

方法

我们通过将有限元方法应用于参加愈合与早期负荷减轻治疗(HEART)试验的患者的收缩末期LV模型,前瞻性地研究了局部壁应力与LV重塑之间的关系。从64例患者前间隔心肌梗死后第14天获得的正交心尖超声心动图视图构建个体LV模型。其中,31例患者接受低剂量(0.625mg)雷米普利,33例患者接受全剂量(10mg)雷米普利。通过有限元方法计算LV壁应力,并将其与心肌梗死后第14天至第90天LV体积的变化相关联。

结果

在所有患者中,心尖局部壁应力的增加与LV体积变化相关(P趋势=0.015)。心尖局部壁应力与LV体积变化之间的关系在低剂量雷米普利组中最强(r=0.53,P=0.002),在调整舒张末期容积、梗死面积、射血分数和收缩压后仍具有显著性,但在全剂量雷米普利组中减弱。

结论

心尖局部壁应力是心肌梗死后随后LV重塑的独立预测因子。全剂量血管紧张素转换酶抑制似乎减弱了心尖壁应力增加与LV扩张之间的关系。

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