Myocardial endothelin-1 release and indices of inflammation during angioplasty for acute myocardial infarction and stable coronary artery disease.

Background: Elevations in endothelin-1 (ET-1) and inflammatory cytokines may impair myocardial reperfusion through the induction of microvascular constriction or obstruction; however, the generation of these factors close to the site of lesion rupture is unknown.

Methods And Results: Coronary sinus (CS) and aortic blood was sampled during angioplasty for acute myocardial infarction (AMI) or stable angina to assess the local release of ET-1, interleukin-1beta, interleukin-6, tumor necrosis factor-alpha and C-reactive protein following atherosclerotic plaque rupture. Transthoracic echocardiography documented left ventricular function in AMI. ET-1 levels were higher in CS than in aortic blood in AMI (3.0 +/- 0.3 pmol/L vs 2.6 +/- 0.3 pmol/L, P =.04), but not in stable angina (1.7 +/- 0.2 pmol/L vs 1.5 +/- 0.3 pmol/L, P = NS). CS ET-1 levels were also higher in AMI than in stable angina (3.0 +/- 0.3 pmol/L vs 1.7 +/- 0.2 pmol/L, P =.002), and correlated with left ventricular dysfunction (R(2) = 0.51, P =.02). In contrast, C-reactive protein levels were higher in CS than in aortic blood only in stable angina (2.3 +/- 0.4 mg/L vs 1.8 +/- 0.3 mg/L, P =.01). Similarly, CS tumor necrosis factor-alpha was higher in stable angina than in AMI (6.0 +/- 1.4 pg/mL vs 2.5 +/- 0.9 pg/mL, P =.02).

Conclusions: Local myocardial release of ET-1 is highest in AMI, where it relates to the extent of myocardial dysfunction. Although local inflammation is a component of stable coronary artery disease, it does not appear acutely enhanced in AMI.