Assessment of markers of thrombin generation in patients with acute myocardial infarction complicated by ventricular fibrillation

Abstract

SummaryBackground: 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.

High plasma levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) and interleukin-8 (IL-8) characterize patients prone to ventricular fibrillation complicating myocardial infarction

“…Myocardial ischemia secondary to thrombotic coronary occlusion is more likely associated with malignant ventricular tachycardia than ischemia due to a mechanical occlusion of a coronary artery (3). Recently published data by our laboratory has shown that patients suffering from VF in the course of acute MI are characterized by an intrinsic hypercoagulable state (9). At present, we can show that there is a highly significant correlation between levels of IL-8 and markers of thrombin generation, such as FPA and F1.2, and even between MMP-9 and FPA and TIMP-1 and F1.2.…”

“…A probable link between thrombin and IL-8 synthesis in cardiomyocytes has not yet been reported. Previously, we have shown that survivors of VF in the setting of acute MI have chronically elevated markers of thrombin generation (9).…”

Effect of the administration of n-3 polyunsaturated fatty acids on circulating levels of microparticles in patients with a previous myocardial infarction

“…A marked increase in F1+2 and TAT plasma levels has been reported during the acute phase of myocardial infarction, but such levels usually subsequently decline. 35,36 It has also been reported that such coagulation markers cannot differentiate between control subjects and post-myocardial infarction patients without new ischemic events, while levels are elevated in patients with recurrent ischemia. 35 These differences may be interpreted keeping in mind that in vivo coagulation markers are measures of the ongoing activity of coagulation, while measurements of MP are an index of the potential to activate coagulation in the presence of a thrombogenic trigger.…”

Decreased TSP-1 following percutaneous coronary intervention is associated with major adverse cardiac events in ST-elevation myocardial infarction

“…Thombospondin was isolated from thrombin activated platelets [23]. As our group has shown previously, markers of coagulation and inflammation including thrombin-antithrombin complexes are elevated in complicated myocardial infarction by ventricular fibrillation [8,9]. Therefore, activated platelets might serve as an alternative source for thrombospondin-1.…”