Background: Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion. In addition increased levels of ET-1 were reported as a negative prognostic index. The study was aimed to verify whether captopril was able to reduce plasma ET-1 levels in the acute and subacute phases of AMI.
Methods: Forty five patients, hospitalized for suspected anterior AMI within 4 h since the onset of symptoms, suitable for thrombolysis (first episode), in Killip class 1-2, were randomized (double blind) into two groups: Group A (23 patients, pts), 7 females and 16 males, received captopril 6.25 mg orally (as first dose) 2-4 h after starting thrombolysis, and the doses of captopril were successively increased up to 25 mg every 8 h. Group B: (22 pts), 5 females and 17 males, received placebo after thrombolysis. All the patients met the reperfusion criteria.
Results: The two groups were similar for age, sex, CK peak, ejection fraction, end systolic volume and risk factors. Plasma ET levels were checked on admission, and 2, 12, 24, 48, 72 hours, after starting thrombolysis. Mean concentrations of ET +/- SD: Group A: basal 1.50 +/- 0.67, at 2 h 2.31 +/- 1.24, 12 h 1.84 +/- 1.45, 24 h 1.30 +/- 0.72, 48 h 0.95 +/- 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, 48 h 1.46 +/- 0.88, 72 h 0.93 +/- 0.44 fmol/ml (p < 0.001). Difference between the two groups was significant at 48 h (p < 0.05), and 72 h (p < 0.001).
Conclusions: Our data suggest that captopril affects plasma endothelin levels in the acute and subacute phases of AMI. In addition, our results seem to be an additional support to the beneficial effects of early captopril treatment in patients with AMI.