Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with unstable angina pectoris (UAP; n = 20) and acute myocardial infarction (AMI; n = 34) were studied in the acute phase of ischaemic heart disease. We found significantly higher levels of thrombin-antithrombin-III (TAT) complexes, lower levels of systemic tissue plasminogen activator (t-PA) activity, and higher levels of plasminogen activator inhibitor (PAI) activity in the AMI patients compared to the UAP patients. In contrast to these specific changes, general acute phase reactants such as C-reactive protein, fibrinogen and von Willebrand factor did not differ significantly between the two groups. Studies of the relationship between coagulation (TAT-complexes) and fibrinolysis data revealed a significant positive correlation between plasma antigen concentrations of TAT-complexes and t-PA (P less than 0.02), and between TAT-complexes and PAI-I (P less than 0.002). These observations indicate a common pathophysiological mechanism underlying the changes in coagulation and fibrinolysis, suggesting that coagulation activity and t-PA-related fibrinolysis are interrelated processes in vivo, and probably take place at the level of the endothelial cell.
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PMID:Interrelationship between coagulant activity and tissue-type plasminogen activator (t-PA) system in acute ischaemic heart disease. Possible role of the endothelium. 170 58

The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.
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PMID:Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation. 170 56

It has been shown that coagulation factor VII (FVII) has an increased coagulant activity (FVIIc) in cardiovascular high risk patients and that it is a important risk factor for the development of ischaemic heart disease (IHD) and cardiovascular death. In this study, we measured FVII coagulant (FVIIc) and immunological (FVIIag) activities during the acute phase of unstable angina (UA) and acute uncomplicated and complicated myocardial infarction (AMI). We have also studied its changes in relation to thrombin formation and coagulation activation, as assessed by determination of thrombin-antithrombin circulating complexes (T-AT) at the same time. Our results show a marked increase in FVIIc in all patients, with highest significant levels in complicated AMI. In fact, this increase was also different between groups, complicated AMI showing a significant degree of increase in FVIIc in relation to UA and uncomplicated AMI. FVIIag did not vary between groups and controls, implicating a progressive activation of FVII. As expected, we found comparable levels of T-AT in UA and in AMI patients, suggesting that a common thrombotic process is involved in both situations. FVIIc was strongly correlated to T-AT in all patients (r = 0. 750; p less than 0.001) and also within groups. This study underlines the important positive contribution of FVIIc to IHD and to the prognosis of its thrombotic acute events, and shows that the increase in FVII activity is associated with an increase of a thrombotic marker (thrombin-antithrombin). Further studies are needed to evaluate if FVII activation is the cause or the consequence of the thrombotic processes.
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PMID:Factor VII hyperactivity in acute myocardial thrombosis. A relation to the coagulation activation. 318 58

Non-emigrated Greenlanders have a low incidence of acute myocardial infarction (AMI), when compared with age- and sex adjusted death rates for ischemic heart disease in western countries. We find that Greenlanders have plasma lipid levels corresponding to favourable risk factor levels for AMI. This can be attributed to their diet, rich in n-3 polyunsaturated fat. This diet further supplies eicosapentaenoic acid which influence platelet vessel wall function in an antithrombotic direction. A high level of plasma-antithrombin-III, raising the anticoagulant activity of the blood, in combination with a genetically high activation threshold for the complement system may further contribute to the resistancy against thrombo-embolic disorders. Bleeding tendency, and susceptibility to infection disorders may be the possible draw-backs. Our data are framed into a hypothesis combining the indications of genetic predispositions and the evidence of exogenous protective factors, inflicting a coherent enhancement of nonsusceptibility to vascular ischemic catastrophies.
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PMID:A hypothesis on the development of acute myocardial infarction in Greenlanders. 629 41

Plasma prothrombin fragment F 1 + 2 (F1 + 2), thrombin-antithrombin complexes (TAT), fibrinogen and factor VII were related to variables associated with increased cardiovascular risk in 86 plasma donors (49 male and 37 female). F1 + 2 had a log-normal distribution and increased significantly with age and body mass index (BMI). Significantly, higher F1 + 2 levels were found in smoking compared with non-smoking males and in indolent males compared with males taking regular exercise. Higher levels were found in subjects with a parental history of ischaemic heart disease than in those lacking such a history. F1 + 2 correlated strongly with increasing cholesterol in males. Fibrinogen was significantly higher in male smokers than male non-smokers but did not vary with age or BMI. Factor VII correlated strongly with cholesterol and to a lesser extent with fibrinogen, F1 + 2 and BMI, but not with smoking. F1 + 2 correlated more closely with risk factors for cardiovascular disease than fibrinogen and factor VII, and consistently reflected the difference in cardiovascular risk when correlated with risk factors which have markedly different effects between the sexes. It promises to be a useful predictive marker of ischaemic heart disease.
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PMID:Prothrombin fragment F1 + 2: correlations with cardiovascular risk factors. 807 5

Antiphospholipid antibodies (aPL) have been found to be associated with arterial and venous thrombosis. Percutaneous transluminal coronary angioplasty (PTCA) is an established therapy for ischaemic heart disease (IHD), which is still affected by restenosis at a rate of 20-30%. This study was aimed at investigating the possible role of aPL in restenosis after PTCA. In sixty consecutive IHD patients, aPL (lupus anticoagulant -LA- and anticardiolipin antibodies -aCL) and markers of haemostatic activation were investigated before PTCA, and patients were followed up for restenosis. No infections, autoimmune disease or treatment by drugs that may alter aPL levels occurred in any of the patients. aPL were found in 15/60 patients: aCL in 7/60, LA in 5/60 and aCL and LA in 3/60. No statistically significant difference was found between aPL negative and aPL positive patients in pre PTCA plasma levels of prothrombin activation fragment (F1+2) 1.4 nmol/l (0.3-5.71) vs 1.4 nmol/l (0.9-4.0), thrombin-antithrombin complex (TAT) 4.0 microg/l (1.1-34.2) vs 5.2 microg/l (2.1-60.0), D-dimer (DD) 25 ng/ml (2-515) vs 44 ng/ml (2-160) or plasminogen activator inhibitor activity (PAI) 4.8 IU/ml (2.5-36.4) vs 4.4 IU/ml (2.5-13.4). Restenosis was observed in 13/60 patients (7/45-15% - aPL negative and 6/15-40% - aPL positive patients) who underwent angiographic tests after PTCA because of recurring angina or positive exercise test. Restenosis occurred after 2.2 months (0.5-3) in aPL positive patients and after 3.5 months (1-12.8) in aPL negative. These results suggest that 1) restenosis with recurrent ischaemia occurs more frequently in aPL positive than in aPL negative patients, 2) in aPL positive patients restenosis occurs earlier, and 3) the presence of aPL is not associated with hypercoagulability.
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PMID:Antiphospholipid antibodies: a new risk factor for restenosis after percutaneous transluminal coronary angioplasty? 960 31

Contrast baths effects on hemostasis were studied in 72 patients with postinfarction cardiosclerosis and stable angina pectoris. Hemostasis was assessed by recalcification time, blood plasma tolerance to heparin, fibrinolytic activity, functional activity of antithrombin, soluble fibrin-monomeric complex, platelet count and aggregation. The results were compared to those in patients exposed to laser irradiation. Hydrotherapy with contrast baths was hemostatically effective in 70.9% of patients. Blood coagulation and platelet aggregation improved, the risk of intravascular microthrombogenesis diminished. Contrast baths had more pronounced beneficial effects on coagulation in ischemic heart disease of NYHA functional class II.
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PMID:[The effect of contrast baths on the hemostatic function of patients with ischemic heart disease]. 977 Nov 41

Several prospective studies have demonstrated that high plasma fibrinogen levels are associated with an increased risk of ischemic heart disease. Since in most patients an increased thrombin generation has been reported, we investigated whether the control of thrombin generation could affect plasma fibrinogen levels. Forty male outpatients (20 asymptomatic with previous myocardial infarction and 20 with stable effort angina) were enrolled in a randomized medium-term (6 months) cross-over study. Clottable fibrinogen, according to Clauss, prothrombin fragment 1 + 2, thrombin-antithrombin complex, and fibrinopeptide A were evaluated in relation to treatment with low-dose heparin. After a 15-day wash-out period, during which patients had been treated only with nitrates if needed, patients were allocated to two sequential periods of treatment with standard heparin (12,500 U, subcutaneously daily) plus antianginal treatment or antianginal treatment alone, separated by a second 15-day wash-out period. At the end of the treatment period with low-dose heparin significant decreases in the plasma fibrinogen (2.5 +/- 0.6 g/l vs. 3.3 +/- 0.5 g/l, P < 0.001), prothrombin fragment 1 + 2 (1.4 +/- 0.5 nmol/l vs. 1.9 +/- 0.7 nmol/l, P < 0.001), thrombinantithrombin (4.5 +/- 2.4 ng/ml vs. 9.7 +/- 3.6 ng/ml, P < 0.001), and fibrinopeptide A (2.1 +/- 1.1 ng/ml vs. 3.5 +/- 2.1 ng/ml, P < 0.001) were observed compared with the period without heparin. The present results indicate that low-dose heparin can effectively control the increased abnormal thrombin generation and elevated fibrinogen levels in patients with ischemic heart disease, possibly decreasing the risk of cardiovascular death.
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PMID:Effect of low-dose heparin on fibrinogen levels in patients with chronic ischemic heart disease. 980 27

We report on a 51-year-old man with severe two-vessel coronary disease and an ejection fraction of 15% who presented with myocardial ischemia and heparin-induced thrombocytopenia after coronary angioplasty. Before coronary bypass surgery, the antithrombin agent argatroban was used for anticoagulation and an intraaortic balloon pump was inserted. Direct coronary bypass surgery was performed to the left anterior descending artery and to the posterior descending artery using the 'Octopus' tissue stabilization device (Manfrotto, Feltre, Italy). The postoperative course was uneventful and associated with normal platelet counts. The patient was discharged on the 6th postoperative day.
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PMID:Heparin-induced thrombocytopenia in coronary bypass surgery. 1047 40

Thrombin and platelets are directly involved in arterial thrombosis, typically occurring at sites of atherosclerotic plaque rupture among patients with acute coronary syndromes. Understanding the dynamic nature of pathologic thrombosis has important clinical implications. Methods: Fibrinopeptide A (FPA), thrombin-antithrombin complexes (TAT), and prothrombin activation fragment 1.2 (F1.2), plasma markers of fibrin formation (thrombin activity) and thrombin generation, and platelet activation, determined by the recognition of a surface-expressed platelet alpha-granule protein, P-selectin, using flow cytometry, were measured in 36 consecutive patients with unstable angina and non-Q-wave myocardial infarction participating in the Thrombolysis In Myocardial Ischemia (TIMI) III B trial. Results: Thrombin generation (TAT 12.1 +/- 17.8 ng/ml vs. 3.4 +/- 1.0 ng/ml; F1.2 0.19 +/- 0.14 nmol/l vs. 0.12 +/- 0.8 nmol/l), fibrin formation (FPA 15.8 +/- 23.5 ng/ml vs. 7.5 +/- 2.3 ng/ml), and platelet activation) 10.6 +/- 2.4% vs. 2.5 +/- 2.0%) were increased significantly in patients compared with healthy, age-matched controls (p < 0.01). Fibrin formation, represented by plasma FPA levels, did not correlate with the percentage of activated platelets (r = -.10, p = 0.69). Thrombin generation and platelet activation also did not correlate. A statistically insignificant trend between TAT and platelet activation was observed (r =.42, p = 0.07); however, even with TAT levels in excess of 20 ng/ml (nearly sixfold greater than normal healthy controls) platelet activation was increased by only 1.7-fold. Conclusions: Thrombin generation, fibrin formation, and platelet activation are increased modestly among patients with unstable angina and non-Q-wave myocardial infarction. Despite the involvement of platelets and coagulation proteins in arterial thrombotic processes, their relative contributions may vary, providing a pathophysiologic basis for the dynamic expression of di sease and response to treatment observed commonly in clinical practice.
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PMID:Dynamic Nature of Thrombin Generation, Fibrin Formation, and Platelet Activation in Unstable Angina and Non-Q-Wave Myocardial Infarction. 1063 14


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