Di Pasquale P, Valdes L, Albano V, Bucca V, Scalzo S, Pieri D, Maringhini G, Paterna S
Coronary Care Unit, GF Ingrassia Hospital, Palermo, Italy.
J Cardiovasc Pharmacol. 1997 Feb;29(2):202-8. doi: 10.1097/00005344-199702000-00008.
It has been reported that endothelin-1 (ET-1) increases in acute myocardial infarction (AMI). Experimental studies showed that captopril administration reduces ET-1 secretion. In addition, it was reported that the increased ET-1 levels are a negative prognostic index. The study sought to verify whether captopril can reduce plasma ET levels in the acute and subacute phases of reperfused anterior AMI. Forty-five patients, hospitalized for suspected anterior AMI within 4 h from the onset of symptoms, suitable for thrombolysis (first episode), Killip class I-2, were randomized (double blind) into two groups: group A (23; seven women/16 men) received captopril (as first dose) 2-4 h after starting thrombolysis (the dose was then increased up to 25 mg every 8 h). Group B (22; five women/17 men) received placebo after thrombolysis. All the patients met the reperfusion criteria. The two groups were similar with regard to age, sex, CK peak, ejection fraction, end-systolic volume and risk factors. Plasma ET levels were measured at entry, and 2, 12, 24, 48, and 72 h after starting thrombolysis. Mean concentrations of ET +/- SD: Group A basal, 1.50 +/- 0.67; at 2h, 2.31 +/- 1.24; 12 h, 1.84 +/- 1.45; 24 h, 1.30 +/- 0.72; 48 h, o.95 +/- 0.50; 72 h, 0.60 +/- 0.15 fmol/ml; p < 0.001. Group B basal, 1.58 +/- 0.83; at 2 h, 2.38 +/- 1.35; 12 h, 2.33 +/- 1.71; 24 h, 1.80 +/- 1.41; 48h, 1.46 +/- 0.88; 72 h, 0.93 +/- 0.44 fmol/ml; p < 0.001. Difference between the two groups was significant at the beginning of the test (between 2 and 12 h, p[=]0.002). After that, the values of the plasma endothelin decreased in parallel, p < 0.001. Our data suggest that captopril affects plasma ET levels in the acute and subacute phases of AMI. Moreover, these results provide additional evidence for a beneficial effect of early captopril treatment.
据报道，急性心肌梗死（AMI）时内皮素-1（ET-1）水平会升高。实验研究表明，给予卡托普利可减少ET-1的分泌。此外，有报道称ET-1水平升高是一个负面预后指标。本研究旨在验证卡托普利是否能降低再灌注性前壁AMI急性期和亚急性期的血浆ET水平。45例因症状发作后4小时内疑似前壁AMI入院、适合溶栓治疗（首次发作）、Killip分级为I - 2级的患者，被随机（双盲）分为两组：A组（23例；7名女性/16名男性）在开始溶栓治疗后2 - 4小时接受卡托普利（首剂）治疗（随后剂量每8小时增加至25毫克）。B组（22例；5名女性/17名男性）在溶栓治疗后接受安慰剂。所有患者均符合再灌注标准。两组在年龄、性别、肌酸激酶峰值、射血分数、收缩末期容积和危险因素方面相似。在入院时以及开始溶栓治疗后2、12、24、48和72小时测量血浆ET水平。ET的平均浓度±标准差：A组基础值为1.50±0.67；2小时时为2.31±1.24；12小时时为1.84±1.45；24小时时为1.30±0.72；48小时时为0.95±0.50；72小时时为0.60±0.15飞摩尔/毫升；p<0.001。B组基础值为1.58±0.83；2小时时为2.38±1.35；12小时时为2.33±1.71；24小时时为1.80±1.41；48小时时为1.46±0.88；72小时时为0.93±0.44飞摩尔/毫升；p<0.001。两组之间的差异在试验开始时显著（2至12小时之间，p = 0.002）。此后，血浆内皮素值平行下降，p<0.001。我们的数据表明，卡托普利可影响AMI急性期和亚急性期的血浆ET水平。此外，这些结果为早期卡托普利治疗的有益效果提供了额外证据。
