Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets
Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets
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DOI：
10.1016/j.ijcard.2007.04.074
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发表时间：
2008-06-23
影响因子：
3.5
通讯作者：
Wojciechowski, Dariusz
中科院分区：
文献类型：
--
作者：
Maczewski, Michal;Borys, Marcin;Wojciechowski, Dariusz
背景：心肌梗死（MI）后心室重构在很大程度上依赖于肾素-血管紧张素系统活性，而肾素-血管紧张素系统活性是由靶组织中血管紧张素II浓度和血管紧张素II 1型受体（AT(1)R）密度决定的。我们最近的研究表明，心肌梗死急性期AT(1)R密度决定心肌梗死后出院时（8天）的心室重构。本研究的目的是测试在同一组患者中，这种相关性是否在更长时间的随访（6个月）中保持不变。方法：在48例未接受再灌注治疗的首次急性心肌梗死患者中，在心肌梗死发病13 +/- 5小时后，使用放射配体结合试验评估血小板上血管紧张素AT(1)R密度（可能是心血管AT(1)R密度的标记物）。超声心动图左心室功能和尺寸指标作为心室重构的指标。结果：梗死6个月后，基线at (1)R密度高于中位数（N=17）的患者与at (1)R密度低于中位数（N=20）的患者相比，左室收缩末期容积指数更高（LVESVI, 41.3 +/- 2.7 vs. 33.2 +/- 2.3），射血分数更低（LVEF 48.1 +/- 1.8 vs. 54.7 +/- 2.0）。此外，LVESVI和LVEF与AT(1)R密度呈正相关，但相关强度弱于放电时。单次肌钙蛋白T测量和心肌梗死后治疗所反映的梗死面积在高和低at (1)R组之间没有差异：超过85%的患者接受了ace抑制剂、β受体阻滞剂和他汀类药物。结论：心肌梗死急性期血小板AT(1)R密度高（可能是心血管AT(1)R密度的标志）预示6个月随访时左心室收缩功能较差。这表明，在心肌梗死的情况下，现代疗法对肾素-血管紧张素系统活性的阻断作用不是最佳的(C)。版权所有。
Background: Ventricular remodeling after myocardial infarction (MI) is largely dependent on renin-angiotensin system activity, which is determined by angiotensin II concentration and angiotensin II type 1 receptor (AT(1)R) density in target tissues. We have recently shown that AT(1)R density in the acute phase of MI determines post-MI ventricular remodeling at discharge (8 days). The aim of this study was to test whether this correlation is retained in a longer follow-up (6 months), in the same group of patients.Methods: In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT(1)R density on blood platelets (a presumable marker of cardiovascular AT(1)R density) was assessed 13 +/- 5 h after the onset of MI, using radioligand binding assay. Echocardiographic indices of left ventricular function and dimensions were used as measures of ventricular remodeling.Results: 6 months after the infarction patients who at baseline had AT(1)R density above median (N=17) as compared to those with AT(1)R density below median (N=20) had higher left ventricular end-systolic volume index (LVESVI, 41.3 +/- 2.7 vs. 33.2 +/- 2.3) and lower ejection fraction (LVEF 48.1 +/- 1.8 vs. 54.7 +/- 2.0). Moreover LVESVI positively and LVEF negatively correlated with AT(1)R density although the strength of these correlations was weaker than at discharge. Infarct size as reflected by a single troponin T measurement and post-MI therapy did not differ between high-and low-AT(1)R groups: over 85% patients received ACE-inhibitor, beta-blocker and statin.Conclusions: High AT(1)R density on blood platelets (a presumable marker of cardiovascular AT(1)R density) drawn in the acute phase of MI predicts poorer left ventricular systolic function in 6-month follow up. This suggests that modern therapy offers suboptimal blockade of renin-angiotensin system activity in the setting of MI. (C) 2007 Elsevier Ireland Ltd. All rights reserved.