Origin and pathophysiological role of increased plasma endothelin-1 in patients with acute myocardial infarction.

Abstract

To investigate the origin and pathophysiological role of increased plasma endothelin-1 (endothelin-1) concentration in patients with acute myocardial infarction (AMI), the authors measured plasma endothelin-1 sequentially after the onset of AMI and analyzed the origin by the simultaneously obtained blood samples from the radial artery, right atrium, and pulmonary artery in 28 patients with AMI. The data were correlated with cardiovascular hemodynamics, infarct size, and coronary arteriographic findings. Arterial endothelin-1 at twenty-four and seventy-two hours significantly correlated with mean pulmonary arterial pressure (r = 0.48, r = 0.46, P < 0.05, respectively), central venous pressure (r = 0.42 and 0.51, P < 0.05, respectively), and pulmonary vascular resistance (r = 0.42, r = 0.42, P < 0.05), and endothelin-1 at one hundred twenty hour significantly correlated with peak creatine kinase (r = 0.53, P < 0.05) and creatine kinase isozyme MB (r = 0.58, P < 0.01). Simultaneous blood samples showed no significant difference in endothelin-1 concentrations among them. However, a subgroup of patients with endothelin-1 concenration higher in the radial artery than that in the right atrium showed a significantly higher mean pulmonary arterial pressure (25.2 +/- 6.5 vs 17.0 +/- 1.6 mmHg, P < 0.05), peak creatine kinase (3594 +/- 1597 vs 865 +/- 495 IU/L, P < 0.05), and peak creatine kinase MB (214 +/- 91 vs 69 +/- 22 IU/L, P < 0.05) as compared with those in patients in whom endothelin-1 was higher in the right atrium than in the radial artery. Increased plasma endothelin-1 concentration in the early stage of AMI reflects higher pulmonary artery pressure and elevated pulmonary vascular resistance, while that in the later stage is related to the infarct size. The production of endothelin-1 in patients with severe pump failure may be accerelated in the pulmonary vascular bed, left ventricle, or systemic arterial trees, and the main origin in the later stage is possibly coronary vasculature in the infarcted area.