Ovricenco Eduard, Sinescu Crina, Dinescu Smaranda
Department of Cardiology, Bagdasar-Arseni Clinical Emergency Hospital, 10-12 Berceni str. Bucharest IV, Romania.
J Med Life. 2008 Jul-Sep;1(3):323-33.
Left ventricular (LV) remodeling after acute ST-elevation myocardial infarction (STEMI) is an important predictor of mid and long-term prognosis. Pathological cardiac remodeling is associated with the development of LV systolic dysfunction and of congestive heart failure. The role of angiotensin converting enzyme (ACE) inhibitors in preventing cardiac remodeling and LV function improvement is well-known. The aim of our study was to assess the impact of an angiotensin II type 1 receptor antagonist administration instead of ACE inhibitor, in the standardized therapy of STEMI, on LV remodeling and function.
We have studied 34 consecutive patients with STEMI (91% men, mean age 58.5 +/- 10.2 years, 41% with anterior location of MI, mean GISSI class 4.7 +/- 1.2) within 6 hours of symptom onset, who received standard fibrinolytic therapy with 1.5 million IU of streptokinase, followed by unfractionated heparin for at least 48 hours. These patients also received: aspirin (100%), valsartan (100%), statins (94%), beta-blockers (85%) and other drugs according to the physician's choice. Neither of them received ACE inhibitors. An echocardiography was performed at baseline and 6 months after STEMI. Left ventricular end-diastolic diameter (LVEDD) and left ventricular mass corrected to body surface (LVm_BS) were used to assess the remodeling process. Left ventricular ejection fraction (LVEF) and a wall motion index (WMI) based on the analysis of regional contractility of 17 segments were taken into account for the LV systolic function. Changes in these values from baseline to the end of the study were compared using the Wilcoxon statistical test for paired samples.
After six months follow-up, there were no significant statistical differences from baseline in LVEDD (from 52.1 +/-6.1 to 52.7 +/- 5.6 mm, Z = 0.61, p = 0.53) and in LVm_BS (from 104.8 +/- 27.5 to 105.2 +/- 27.8 g/m2, Z = -0.54, p = 0.54). There was a significant improvement of WMI (from 1.57 +/- 0.29 to 1.43 +/- 0.34, Z = -3.05. p = 0.002) and a significant increase of LVEF (from 41.0 +/- 7.1 to 45.2 +/- 10.0%, Z = 2.96, p = 0.003).
The results of this study suggested that administration of valsartan instead of ACE inhibitor, in consecutive patients with medium-risk STEMI, attenuates pathological LV remodeling and improves LV systolic function. However, as obtained within the first six months after the infarction, these results can not be generalized to the later period after STEMI.
急性ST段抬高型心肌梗死（STEMI）后左心室（LV）重构是中长期预后的重要预测指标。病理性心脏重构与左心室收缩功能障碍和充血性心力衰竭的发生有关。血管紧张素转换酶（ACE）抑制剂在预防心脏重构和改善左心室功能方面的作用已广为人知。我们研究的目的是评估在STEMI的标准化治疗中，使用血管紧张素II 1型受体拮抗剂代替ACE抑制剂对左心室重构和功能的影响。
我们研究了34例症状发作6小时内的连续STEMI患者（男性占91%，平均年龄58.5±10.2岁，41%为前壁心肌梗死，平均GISSI分级4.7±1.2），这些患者接受了150万国际单位链激酶的标准溶栓治疗，随后接受普通肝素治疗至少48小时。这些患者还接受了：阿司匹林（100%）、缬沙坦（100%）、他汀类药物（94%）、β受体阻滞剂（85%）以及医生选择的其他药物。他们均未接受ACE抑制剂。在STEMI基线时和6个月后进行超声心动图检查。左心室舒张末期直径（LVEDD）和校正体表面积后的左心室质量（LVm_BS）用于评估重构过程。基于17节段区域收缩性分析的左心室射血分数（LVEF）和壁运动指数（WMI）用于评估左心室收缩功能。使用配对样本的Wilcoxon统计检验比较这些值从基线到研究结束时的变化。
经过6个月的随访，LVEDD（从52.1±6.1变为52.7±5.6 mm，Z = 0.61，p = 0.及LVm_BS（从104.8±27.5变为105.2±27.8 g/m2，Z = -0.54，p = 0.54）与基线相比无显著统计学差异。WMI有显著改善（从1.57±0.29变为1.43±0.34，Z = -3.05，p = 0.002），LVEF有显著增加（从41.0±7.1变为45.2±10.0%，Z = 2.96，p = 0.003）。
本研究结果表明，在连续的中度风险STEMI患者中，使用缬沙坦代替ACE抑制剂可减轻病理性左心室重构并改善左心室收缩功能。然而，由于这些结果是在梗死后的前6个月内获得的，不能推广到STEMI后的后期。
