Key result
Ventricular fibrillation during acute MI was associated with significantly higher levels of thrombin-antithrombin complexes compared to MI without VF (13.4 vs. 3.03 microg/l; p=0.02).
Why the study?
Are markers of thrombin generation elevated in patients with acute myocardial infarction complicated by ventricular fibrillation compared to those without?
Observational (n=50)
Are markers of thrombin generation elevated in patients with acute myocardial infarction complicated by ventricular fibrillation compared to those without?
Absolute Event Rate: 13.4% vs 3.03%
p-value: p=0.02
Markers of thrombin generation are transiently increased in patients who experience ventricular fibrillation during the acute phase of myocardial infarction, suggesting a potential role of coagulation activation in arrhythmogenesis.
Supports exploring coagulation activation in VF complicating acute MI; hypothesis-generating and should not change practice.
BACKGROUND: In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated. METHODS: We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias. Levels of thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2 (F1 + 2), fibrinopeptide A (FPA), plasmin-antiplasmin complexes (PAP), protein C, antithrombin, activated partial thromboplastin time (aPTT), thromboplastin time, D-Dimer, fibrinogen, and high-sensitivity C-reactive protein (hs-CRP) were measured in plasma samples of all patients. Blood collection was obtained sequentially in two separate settings. Patients were studied at a median of 351 days after the acute coronary event. RESULTS: Higher levels of TAT complexes (13.4 +/- 22.2 vs. 3.03 +/- 4.3 microg/l; p = 0.02), FPA (79.7 +/- 132.3 vs. 24.04 +/- 41.3 ng/ml; p = 0.04), and F1+2 (1.89 +/- 1.3 vs. 1.16 +/- 0.5 nmol/l; p = 0.01) were observed in patients with VF compared with patients without ventricular tachyarrhythmias during the acute phase of MI. D-Dimer levels displayed a trend without reaching statistical significance (0.69 +/- 0.48 vs. 0.48 +/- 0.24 mg/l; p = 0.06). No differences were found in hs-CRP (3.25 +/- 4.5 vs. 4.4 +/- 8.8 mg/l; p = 0.5) and fibrinogen (2.8 +/- 0.9 vs. 2.7 +/- 0.9 g/l; p = 0.6) measurements. Repeat assessment of markers of coagulation activation at a median of 847 days revealed a highly significant decrease in patients with VF. CONCLUSIONS: Markers of thrombin generation are transiently increased in patients with VF during the acute phase of MI. These findings have implications for risk assessment and genetic screening of patients prone to VF during acute myocardial ischemia.
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Elmas et al. (2006) conducted an observational in Acute myocardial infarction (n=50). Ventricular fibrillation during acute MI vs. Acute MI without ventricular tachyarrhythmias was evaluated on Levels of thrombin-antithrombin (TAT) complexes (p=0.02). Ventricular fibrillation during acute MI was associated with significantly higher levels of thrombin-antithrombin complexes compared to MI without VF (13.4 vs. 3.03 microg/l; p=0.02).
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