Background: Disturbance of the hemostatic and the inflammatory system plays an important role in the pathophysiology of acute coronary syndromes (ACS). Their markers have been shown to predict further coronary events in patients with ACS. The prognostic value of the admission electrocardiogram (ECG), which is commonly used to evaluate ischemia, was studied previously. We investigated the correlation between serum markers of the hemostatic/inflammatory system and ECG changes in ACS. Methods: A standard 12-lead ECG was obtained from 85 patients with ACS on admission (0d). Markers of the hemostatic and inflammatory system were measured on admission and after 2 days (2d). Results: Patients with ST-T-changes had higher fibrinogen and thrombin-antithrombin III complex (TAT) levels than patients without ECG alterations at both times (fibrinogen: 0d: 492 ± 38 vs. 357 ± 36 mg/dl, p < 0.01; 2d: 633 ± 55 vs. 440 ± 50 mg/dl, p < 0.02; TAT: 0d: 7.2 ± 1.3 vs. 3.6 ± 0.7 µg/l, p < 0.05; 2d: 5.3 ± 0.9 vs. 3.2 ± 0.5 µg/l, p < 0.05). Tissue-type plasminogen activator (TPA) was elevated in patients with ECG changes initially (10.1 ± 0.6 vs. 7.2 ± 0.7 ng/ml, p < 0.02). D-dimers, the acute-phase proteins C-reactive protein, serum amyloid A and the soluble adhesion molecules showed no significance. Conclusions: The data reveal a correlation between electrocardiographic changes and hemostasis in patients with ACS. The association of myocardial damage and a disturbed hemostatic system might stratify patients who are at high risk of suffering further coronary events.

SummaryPatients with acute coronary syndromes (ACS) frequently present with signs of disturbed fibrinolysis. The present study investigates the correlation of alterations in the fibrinolytic system and the amount of myocardial damage characterized by troponin release.In 85 patients with ACS markers of plasmin activation, plasminogen activator system and troponin T (TnT) were measured initially and after 48 h. Patients with TnT release (≥ 0.01 g/l) at admission had higher TPA levels than those without release (10.2 ± 0.7 ng/ml vs. 7.6 ± 0.5 ng/ml; p <0.01). Additionally, patients with positive TnT had higher D-dimer levels initially (457 ± 39 ng/ml vs. 316 ± 22 ng/ml; p < 0.01) and 48 h later (451 ± 42 ng/ml vs. 275 ± 37 ng/ml; p < 0.01). The association of myocardial damage with a prothrombotic state and an enhanced fibrinolysis may explain the high prognostic value of troponin measurements in respect to future coronary events.

The pathophysiologic meaning of elevated circulating endothelin-1 (ET-1) levels in various cardiovascular diseases is not understood. The aim of this study was to measure ET-1 and big ET-1 levels in patients with unstable angina pectoris (UAP) and within 5 days after stabilization. These values were compared to those of patients with stable angina pectoris (SAP) and to healthy controls (Co). In addition, a venous occlusion test was performed as an endothelial provocation test to characterize endothelial function. Big ET-1 levels were increased to 2.6 +/- 1.5 fmol/ml during unstable angina pectoris compared to normal values of 0.52 +/- 0.07 fmol/ml (p < 0.03; n = 14). After stabilization, big ET-1 decreased to 1.5 +/- 0.4 fmol/ml within 5 days (n.s.). ET-1 levels were not increased during UAP and after stabilization. ET-1 and big ET-1 levels from patients with SAP did not differ from those of healthy controls. The venous occlusion test resulted in an increase of ET-1 levels (0.3 +/- 0.02 to 0.46 +/- 0.02 fmol/mg, p = 0.008; SAP 0.3 +/- 0.04 to 0.39 +/- 0.05 fmol/ml, p = 0.009) in healthy controls and in patients with SAP. In contrast, patients with UAP showed no significant increase in ET-1 with this test. After stabilization for 5 days, the provocation test induced an increase in circulating ET-1 in patients with UAP comparable to that of controls (0.62 +/- 0.18 fmol/mg vs. 0.95 +/- 0.25 fmol/mg; p < 0.02). In summary, during UAP big ET-1 values are significantly increased and ET-1 values tend to be elevated. In an endothelial provocation test, ET-1 values did not increase. This might reflect a general activation of the endothelium in UAP during the acute stage, because the normal response is recovered 5 days later.