OBJECTIVE There is a paucity of a biological large animal model of myocardial infarction (MI). We hypothesized that, using autologous-aggregated platelets, we could create an ovine model that was reproducible and more closely mimicked the pathophysiology of MI. METHODS Mepacrine stained autologous platelets from male sheep (n = 7) were used to create a myocardial infarction via catheter injec...

Accumulating evidence indicates that accelerated formation of fibrin clots composed of compact, highly-branched networks with thin fibres which are relatively resistant to plasmin-mediated lysis can be commonly observed in patients with venous or arterial thrombosis. This review discusses characteristics of fibrin clot structure and function in patients with various thromboembolic manifestation...

Left ventricular noncompaction (LVNC) is characterized by left ventricular (LV) hypertrabeculations and is associated with heart failure, arrhythmias and embolism. We report the case of a 67-year-old LVNC patient, under oral anticoagulation (OAC) therapy for apical thrombosis. After she discontinued OAC, the thrombus involved almost the whole of the left ventricle; in a few months her condition...

Myocardial infarction (MI) is defined by the presence of myocardial necrosis in combination with clinical evidence of myocardial ischemia. Cardiac troponins are regulatory proteins within the myocardium that are released into the circulation when damage to the myocyte has occurred. Therefore, serum troponin is an exquisitely sensitive marker of myocardial injury and is necessary for establishin...

Strategies that enhance functional reperfusion and translate into better clinical outcomes for ST-segment elevation myocardial infarction (STEMI) remain the holy grail of reperfusion therapy. In the absence of complete understanding of the vascular and cellular processes that are initiated with plaque rupture and thrombotic coronary artery occlusion, we have had to rely on therapies that shorte...

Myocardial Infarction-Ardlie et al. MDCBOURNAL 891 1959), a finding which we have confirmed in this study. This elevation could either wholly or partly account for the longer and heavier thrombi found in patients with myocardial infarction. We do not know whether the factor or factors responsible for the development of large thrombi were present before infarction or merely reflect the results o...

Since the first intracoronary stent implantation, the design and ease of use of coronary stents have continued to improve, and the indications for their use have continued to expand from bailout procedures to now-routine implantation in patients with myocardial infarction. Coronary stenting reduces the risk of restenosis and the number of revascularizations compared to balloon angioplasty, but,...

Thrombotic occlusion of a coronary artery occurs in most cases of fatal myocardial infarction (Mitchell and Schwartz, 1963; Allison et al., 1963), and it has been suggested that thrombosis is most likely to occur where the lumen is small (Osborn, 1963). Although the size of arterial plaques and the relative narrowing that they produce have been extensively studied, the absolute size of the effe...

Arterial and venous thromboembolic events, including myocardial infarction, ischemic stroke, peripheral arterial thrombosis, deep venous thrombosis, and pulmonary embolism are common potentially life-, organ-, and limb-threatening vascular diseases. Anticoagulant therapy is recommended in these settings to prevent further thrombosis pending gradual clearance of the thrombotic occlusion by the e...