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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Tissue plasminogen activator activity and inhibition in acute myocardial infarction and angiographically normal coronary arteries.

Parameters of blood coagulation, blood platelet reactivity and fibrinolysis were analyzed in 18 patients with acute myocardial infarction (AMI) and angiographically normal coronary arteries. This study group was compared with a patient control group of 18 AMI patients with 1-vessel obstructive coronary artery disease. Patients were matched for sex, age and AMI date. A healthy control group consisted of 18 sex- and age-matched volunteers. Blood coagulation measurements and platelet reactivity were similar in the 3 groups, except for fibrinogen, which was significantly higher in the patient control group. Plasma activity of tissue plasminogen activator (tPA) was detectable in only 2 patients in the study group, 9 in the patient control group (p less than 0.02) and 12 in the healthy control group (p less than 0.0001). Median plasma tPA inhibitory activity was higher in the study group (10.3 IU/ml) and the patient control group (8.1 IU/ml) than in the healthy control group (2.7 IU/ml, p less than 0.0001 and p less than 0.03). 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.[1]

References

  1. Tissue plasminogen activator activity and inhibition in acute myocardial infarction and angiographically normal coronary arteries. Verheugt, F.W., ten Cate, J.W., Sturk, A., Imandt, L., Verhorst, P.M., van Eenige, M.J., Verwey, W., Roos, J.P. Am. J. Cardiol. (1987) [Pubmed]
 
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