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急性心肌梗死后既往系统性高血压对随后左心室扩张的影响(来自生存与心室扩大试验)

Effect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial).

作者信息

Kenchaiah Satish, Pfeffer Marc A, St John Sutton Martin, Plappert Ted, Rouleau Jean-Lucien, Lamas Gervasio A, Sasson Zion, Parker John O, Geltman Edward M, Solomon Scott D

机构信息

Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Am J Cardiol. 2004 Jul 1;94(1):1-8. doi: 10.1016/j.amjcard.2004.03.020.

Abstract

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean +/- SD 11 +/- 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure > or =140 or baseline diastolic blood pressure > or =90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 +/- 11.9 vs 68.8 +/- 11.2 cm(2), p = 0.33 at end-diastole; 50.1 +/- 11.3 vs 48.8 +/- 10.8 cm(2), p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 +/- 4.3 vs 25.7 +/- 5.0 cm(2), p = 0.043) and wall thickness (1.15 +/- 0.16 vs 1.21 +/- 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p < or =0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 +/- 11.5 vs +2.2 +/- 10.7 cm(2), p = 0.005 at end-diastole; +6.23 +/- 12.75 vs +2.94 +/- 11.4 cm(2), p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.

摘要

急性心肌梗死后出现左心室(LV)收缩功能障碍的患者,既往存在的系统性高血压是否会影响后续LV扩张的风险尚不清楚。在生存与心室扩大超声心动图亚研究中,我们评估了122例高血压患者(定义为有高血压治疗史,基线收缩压≥140或基线舒张压≥90 mmHg)和334例非高血压患者从基线(平均±标准差11±3天)至急性心肌梗死后2年的心室重构超声心动图证据。与非高血压患者相比,基线时心脏大小(定义为舒张末期和收缩末期LV腔平均短轴和长轴面积之和)相似(舒张末期:70.1±11.9 vs 68.8±11.2 cm²,p = 0.33;收缩末期:50.1±11.3 vs 48.8±10.8 cm²,p = 0.31),但高血压患者舒张末期LV心肌短轴面积(24.7±4.3 vs 25.7±5.0 cm²,p = 0.043)和壁厚(1.15±0.16 vs 1.21±0.17 cm,p = 0.004)更大。两组心肌梗死节段长度相似(p = 0.22)。尽管两组从基线至2年LV腔面积均显著增加(p≤0.001),但高血压患者的增加幅度显著大于非高血压患者(舒张末期:+5.6±11.5 vs +2.2±10.7 cm²,p = 0.005;收缩末期:+6.23±12.75 vs +2.94±11.4 cm²,p = 0.012)。两组之间LV心肌面积或LV壁厚的变化无伴随差异(p>0.30)。在调整已知混杂因素后,既往高血压与LV扩张风险加倍相关(50.8% vs 37.7%,优势比2.09,95%置信区间1.27至3.45,p = 0.004)。这种关联不受糖尿病、心肌梗死节段长度或卡托普利使用的影响(所有交互作用p值>0.10)。我们得出结论,急性心肌梗死后出现LV收缩功能障碍的患者,既往高血压与后续LV扩张相关。

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