Disease relevance of Coronary Thrombosis

• We studied whether cigarette smoking and abnormal cholesterol values may precipitate acute coronary thrombosis and sudden death resulting from either rupture of vulnerable coronary plaques or erosion of plaques [1].
• To assess the contribution of Factor IX/IXa, to intravascular thrombosis, a canine coronary thrombosis model was studied [2].
• Following the occurrence of and survival from an acute occlusive coronary thrombosis, canalization of the thrombus frequently takes place, leading to the formation of a "luminal collateral vascularization." The vessels making up such complexes are prone in turn to hemorrhage and thrombosis [3].
• BACKGROUND: Plasminogen activator inhibitor type 1 (PAI-1), the primary physiological inhibitor of endogenous plasminogen activators, has been implicated as a potentiating factor in atherogenesis as well as in coronary thrombosis [4].
• This property may render brain vasculature vulnerable to attack by serine proteases, thereby predisposing to injury and initiating an underlying subsequent intracerebral hemorrhage in patients given plasminogen activators for treatment of coronary thrombosis [5].

High impact information on Coronary Thrombosis

• A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis [6].
• Endogenous prostaglandin endoperoxides and prostacyclin modulate the thrombolytic activity of tissue plasminogen activator. Effects of simultaneous inhibition of thromboxane A2 synthase and blockade of thromboxane A2/prostaglandin H2 receptors in a canine model of coronary thrombosis [7].
• Prostaglandin endoperoxides modulate the response to thromboxane synthase inhibition during coronary thrombosis [8].
• The blood of 30 patients who received recombinant tissue-type plasminogen activator for lysis of acute coronary thrombosis was examined to identify the effects of this enzyme on the fibrinolytic and coagulation systems [9].
• For these reasons, elevated PAI-1 activities are associated both with coronary thrombosis and with a poor prognosis in many cancers [10].

Chemical compound and disease context of Coronary Thrombosis

• Interaction between plasma potassium and epinephrine in coronary thrombosis in dogs [11].
• The effect of tissue-type plasminogen activator (t-PA) alone or in combination with heparin, the Arg-Gly-Asp-containing peptide bitistatin, or both heparin and bitistatin was evaluated on thrombolysis time and acute reocclusion in a canine model of coronary thrombosis [12].
• Mediation of reocclusion by thromboxane A2 and serotonin after thrombolysis with tissue-type plasminogen activator in a canine preparation of coronary thrombosis [13].
• In addition, the inhibitory effect of norepinephrine on coronary thrombosis is independent of increases in coronary arterial pressure [14].
• In vivo in dogs, intravenous amrinone 2 mg/kg plus infusion at 20 microg x kg(1) x min(-1) completely abolished coronary thrombosis [15].

Biological context of Coronary Thrombosis

• CONCLUSIONS: The fact that amrinone inhibited human platelet activation at the cellular level and protected against experimental coronary thrombosis in vivo in dogs suggests a potentially advantageous antithrombotic action for this inotropic and vasodilator drug [15].
• OBJECTIVES: This study was designed to identify potential predictors of vascular access site (VAS) complications in the large-scale Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis (IMPACT) II trial, which studied angioplasty with versus without a new glycoprotein (GP) IIb/IIIa receptor inhibitor (eptifibatide) [16].
• Endothelin-1 production in coronary circulation in a new canine model of coronary thrombosis [17].
• The mean area of complicated lesions of three major coronaries and the presence of coronary thrombosis were significantly associated with the ESR1 genotype in men aged 53 years or older (median age as a cut off point) [18].
• The authors describe a patient with MHA who had no history of hemorrhage but who developed complete coronary thrombosis after attempted angioplasty despite an apparent platelet count of 24,000 per mm3 [19].

Anatomical context of Coronary Thrombosis

• Thus, reduced activity and enhanced inhibition of plasma tPA may be important factors in the origin of coronary thrombosis, especially in the absence of coronary artery disease [20].
• Lysis of the coronary thrombosis with intravenous or intracoronary administration of streptokinase or intravenous administration of one of the newer, currently experimental agents, such as tissue plasminogen activation or prourokinase, can directly restore oxygen and substrate delivery to potentially salvageable myocardium [21].

Gene context of Coronary Thrombosis

• Plasminogen activator inhibitor-1 (PAI-1) is the major inhibitor of plasminogen activation and likely plays important roles in coronary thrombosis and arteriosclerosis [22].
• Comparison of desulfatohirudin (REVASC) and heparin as adjuncts to thrombolytic therapy with reteplase in a canine model of coronary thrombosis [23].
• OBJECTIVE: Matrix metalloproteinases 3 and 9 (MMP3 and MMP9) are present in atherosclerotic plaques and co-operate in the degradation of the fibrous cap of the atheroma, leading to fissuring and ultimately to acute coronary thrombosis [24].
• Our findings support previous results on the role of this GPVI polymorphism, or another linked polymorphism, as a possible predictor of the risk of coronary thrombosis [25].
• Simultaneous administration of thromboxane A2- and serotonin S2-receptor antagonists markedly enhances thrombolysis and prevents or delays reocclusion after tissue-type plasminogen activator in a canine model of coronary thrombosis [26].

Analytical, diagnostic and therapeutic context of Coronary Thrombosis

• Influence of heparin and systemic lysis on coronary blood flow after reperfusion induced by the novel recombinant plasminogen activator BM 06.022 in a canine model of coronary thrombosis [27].
• The effects of intraventricular infusion of prostacyclin (PGI2; 50, 100 ng/kg/min) on hemodynamics, the ECG, coronary thrombosis and myocardial ischemia were studied in chronically equipped, resting conscious dogs and compared to those of intracardiac administration of Tris-HCl as vehicle [28].

References