SERIAL PLASMA-CATECHOLAMINE RESPONSE EARLY IN THE COURSE OF CLINICAL ACUTE MYOCARDIAL-INFARCTION - RELATIONSHIP TO INFARCT EXTENT AND MORTALITY
SERIAL PLASMA-CATECHOLAMINE RESPONSE EARLY IN THE COURSE OF CLINICAL ACUTE MYOCARDIAL-INFARCTION - RELATIONSHIP TO INFARCT EXTENT AND MORTALITY
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DOI：
10.1016/0002-8703(81)90408-7
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发表时间：
1981-01-01
影响因子：
4.8
通讯作者：
ROBERTS, R
中科院分区：
文献类型：
--
作者：
KARLSBERG, RP;CRYER, PE;ROBERTS, R
临床和实验证据表明，交感肾上腺激活导致缺血性心脏病患者死亡。为确定急性心肌梗死（AMI）极早期交感肾上腺激活的水平，并确定梗死部位（前壁与下壁）是否与交感肾上腺激活相关，在症状发作后4小时内和血浆肌酸激酶（CK）升高之前研究了去甲肾上腺素（NE）和肾上腺素（E）。平均初始值（NE = 591 . ±. 111 pg/ml，E = 73 ±。19 pg/ml），峰值（NE = 1356 ± 0.001 μ g/ml）。178和E .+-。1098 .+-. 608)和平均值（NE = 815 . ±. 142和E = 252。68)血浆儿茶酚胺浓度明显高于正常值（NE = 228 ± 0.001）。10和E = 34。2 pg/ml，n = 60），下壁和前壁梗死的数值相似。在18个月内。随访中3例死亡，其NE、E均值及CK峰值均高于8例晚期存活者。3例EP峰值> 1000的AMI患者死亡。8例EP峰值< 1000的AMI患者存活（P < 0.01）。临床AMI早期交感肾上腺激活的程度似乎与心肌损伤的程度和晚期死亡率有关。
Clinical and experimental evidence suggest that sympathoadrenal activation contributes to mortality in patients with ischemic heart disease. To determine the level of sympathoadrenal activation in the very early phase of acute myocardial infarction (AMI) and to determine if location of infarction (anterior vs. inferior) was related to sympathoadrenal activation, norepinephrine (NE) and epinephrine (E) were studied within 4 h after the onset of symptoms and prior to any rise in plasma creatine kinase (CK). Mean initial (NE = 591 .+-. 111 pg/ml and E = 73 .+-. 19 pg/ml), peak (NE = 1356 .+-. 178 and E .+-. 1098 .+-. 608) and average (NE = 815 .+-. 142 and E = 252 .+-. 68) plasma catecholamine concentrations were considerably above normal (NE = 228 .+-. 10 and E = 34 .+-. 2 pg/ml, n = 60) and values were similar for inferior and anterior infarctions. During an 18-mo. follow-up, 3 patients died in whom the AMI mean NE and E and peak CK were higher than in the 8 late survivors. The 3 AMI patients with peak EP values > 1000 died. The 8 AMI patients with peak EP values < 1000 survived (P < 0.01). The magnitude of sympathoadrenal activation early in the course of clinical AMI appeared related to the extent of myocardial damage and late mortality.