Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum antithrombin activity (AA) was correlated with coronary angiographic findings in 69 patients with documented angina. There was excellent correlation between normal values and normal coronary circulation or only one-vessel stenosis in 30 of 35 patients (86%). When AA was above 90%, 90% of patients (20 of 22) had normal circulation or one-vessel occlusion. In 24 patients AA values were significantly decreased. Coronary angiography in this group revealed three with normal circulation or only one-vessel involvement (10%); 21 of 24 had two or three vessels occluded (90%). The correlation between severe CAD and low AA is probably coincidental to a "triggered" or "turned-on" clotting system. The most practical clinical contribution of AA estimation relates to this capacity to identify angina patients in whom clot-preventive measures (aspirin; dipyridamole; anticoagulants) might prove beneficial.
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PMID:Serum antithrombin in coronary-artery disease. 5 72

In 4 well-controlled clinical trials, aspirin reduced the incidence of coronary events in unstable angina. The benefits were present during the acute, subacute and more chronic phases of the disease and were independent of the doses and of other protocol differences. This benefit of aspirin can be extended to some, but not all, other antiplatelet drugs. In 4 clinical trials, heparin used acutely added substantial benefit to the management of unstable angina, reducing the event rate and also the incidence of refractory angina more than aspirin. The long-term benefit of antithrombin therapy remains to be more thoroughly investigated. Despite these successes, the failure rate of aspirin and of heparin remains high, justifying a continuing search for more potent and safe antiplatelet and antithrombotic drugs.
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PMID:Antiplatelet and antithrombotic therapy in unstable angina. 189 73

A comparative study of activity of the progressively acting antithrombin and their heparin-cofactor activity was undertaken in 27 patients with angina pectoris and 46 with macrofocal myocardial infarction. It was established that the count of thrombin inactivation during 5 minutes (Abiligaard method) shows no disorders in the majority of patients. Only in 3 patients with the primary antithrombin III and 3 (40% of patients with acute myocardial infarction showed a marked decrease of this parameter. Inactivation count of the endogenous thrombin according to the "self-coagulogram" during one hour enabled one to show decrease of activity of antithrombin in of 80% of patients. The heparin-cofactor activity in the serial heparin-thrombin test is markedly disrupted, which was used to compute the indices of activity of antithrombin and of the antithrombin plasma reserve. This disorder did not depend much on the increase of the antiheparin factor of thrombocytes in plasma.
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PMID:[Progressively acting antithrombins and plasma heparin resistance in ischemic heart disease]. 728 82

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

The aim of this study was to evaluate the clinical effect of urokinase (UK) in unstable angina (UA). This study was a multicenter, single-blind, heparin-controlled, randomized clinical trial. Entry criteria was that effort angina was significantly aggravated within 96 hours and angina attack at rest within 24 hours. In addition to the control group, thrombolytic therapy was divided into two groups according to the dose of UK. The high-dose group was 18,000 IU/kg, and the total dose was no more than 1.5 million IU (no bolus of heparin in this dose). The low-dose group was 14,000 IU/kg, and the total dose was no more than 1 million IU. All patients were treated by aspirin 300 mg/day and heparin 3000 U IV bolus before thrombolytic therapy (except for the high-dose group), then subcutaneous heparin 7,500 U q12h. The primary endpoint for the comparison between the thrombolytic and control groups was death and AMI (cardiac event) within 30 days of enrollment. Five hundred and fifty-six patients with UA were selected, and 272 and 284 patients were enrolled in thrombolytic group and control groups, respectively. The 30-day incidence of cardiac events was a little higher, but not significantly, in the thrombolytic group than in the control group (7.0% vs. 5.3%, ns), but the rate for cardiac events was much lower in the low-dose UK group than in the high-dose UK group. The difference was significant (3.3% vs. 10.0%, P < 0.05). Even if the rate was also lower than in the control group, this difference was not significant (3.3% vs. 5.3%, P > 0.05). The time interval between enrollment and the AMIs was quite different in these two groups. The majority of AMIs (73.7%) occurred within 24 hours, including 37% of AMIs that occurred within 2 hours after the beginning of thrombolytic therapy in the UK group. However, only small number of AMIs (20%) occurred within 24 hours of enrollment in the control group. The increase in AMI risk on the first day of thrombolytic therapy in this study might be closely related to thrombolysis and to the lack of strong antithrombin therapy. The risk of AMI might be remarkably reduced by using low-dose UK in combination with antithrombin therapy before thrombolytic therapy.
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PMID:Randomized clinical trial of urokinase versus heparin in unstable angina. 1050 Mar 12

To evaluate the suitability of two anticoagulants (heparin vs. argatroban) as adjunctive drugs during and after elective conventional percutaneous transluminal coronary angioplasty, we compared the changes in inflammatory, hemostatic, and endothelium-derived markers in groups of patients with stable angina treated with the two drugs during percutaneous transluminal coronary angioplasty. Twenty-seven patients were randomly allocated to either group 1 (15 patients who received an empiric dose of heparin and aspirin as anticoagulant), or group 2 (12 patients who received an alternative regimen of argatroban and aspirin). Both drugs were administered as a bolus followed by continuous infusion for 96 hours during and after percutaneous transluminal coronary angioplasty. There were no differences in the inflammatory response induced by percutaneous transluminal coronary angioplasty in both groups, but the fibrinogen concentration significantly decreased during percutaneous transluminal coronary angioplasty in group 2. Decreased platelet counts and increased mean platelet volume were observed during percutaneous transluminal coronary angioplasty in both groups. The levels of prothrombin fragment 1+2 and thrombin antithrombin III complex increased markedly during percutaneous transluminal coronary angioplasty. Group 2 showed a more rapid return to the baseline levels of these two markers than group 1. Secondary fibrinolysis was evidenced by a steep increase of D-dimer after percutaneous transluminal coronary angioplasty in both groups. In contrast to the significant decrease in antithrombin activities during percutaneous transluminal coronary angioplasty in group 1, no marked change in these markers was found in group 2. Although the levels of von Willebrand factor and plasminogen activator inhibitor-1 showed essentially the same changes in both groups during and after percutaneous transluminal coronary angioplasty, more markedly increased levels of tissue type plasminogen activator and type plasminogen activator-plasminogen activator inhibitor-1 complex after percutaneous transluminal coronary angioplasty were found in group 1 than in group 2. While neither drug had any effect on the percutaneous transluminal coronary angioplasty-induced inflammatory response, argatroban may more effectively inhibit the generated thrombin and prevent antithrombin consumption during and after percutaneous transluminal coronary angioplasty.
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PMID:Antithrombotic treatment (argatroban vs. heparin) in coronary angioplasty in angina pectoris: effects on inflammatory, hemostatic, and endothelium-derived parameters. 1082 73

The recent availability of novel antiplatelet and antithrombin agents has revolutionized the therapeutic options for intermediate- and high-risk unstable angina (UA). Current guidelines recommend aspirin, unfractionated heparin (UFH), and antianginal therapy. Low-molecular-weight heparin (LMWH) and direct thrombin inhibitors have significant theoretical advantages and apparent clinical benefits compared with UFH and are good alternatives in selected patients. Glycoprotein (GP) IIb/IIIa receptor inhibition reduces the future risk of myocardial infarction (MI) and may reduce the incidence of death in patients with unstable angina. In particular, these drugs should be considered for use in combination with aspirin and UFH in patients undergoing an "early invasive" approach. Coronary revascularization plays an important role in high-risk patients and in those with refractory angina, but its routine application continues to be controversial. Issues regarding the use of LMWH in combination with GP IIb/IIIa inhibitors and during percutaneous transluminal coronary angioplasty (PTCA) are being addressed in clinical trials. Ideally, the incidence of serious cardiac events in patients with UA will continue to decrease with the ongoing search for potent drug combinations that achieve early control of intracoronary thrombosis.
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PMID:Unstable Angina. 1109 9

In the current study, we investigated molecular markers of coagulation activity, ie, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin (TAT) complex, soluble fibrin (SF), and D-dimer, and their relation to death, myocardial infarction, and refractory angina during and after anticoagulant treatment in unstable coronary artery disease. Patients with unstable coronary artery disease (N=320) were randomized to a 72-hour infusion with either inogatran, a low-molecular-mass direct thrombin inhibitor, or unfractionated heparin. During the 30-day follow-up, a 40% lower event rate was seen in patients with high compared with low baseline levels of TAT or SF. High baseline levels of coagulation activity were correlated with a larger decrease during treatment. Patients with decreased compared with raised F1+2 or TAT levels after 6 hours of treatment had a 50% lower event rate at 30 days (F1+2, P=0.04; TAT, P=0.02). At the cessation of antithrombin treatment, there was a clustering of cardiac events that tended to be related to a rise in the levels of TAT and the other markers. During long-term follow-up (median, 29 months), there was a relation between higher baseline levels of D-dimer (P=0.003) and increased mortality. High baseline levels of molecular markers of coagulation activity might identify patients with a thrombotic condition (as the major cause of instability) who are good responders to anticoagulant therapy, with a larger decrease in coagulation activity during treatment and a decreased risk of ischemic events. However, this early benefit is lost during long-term follow-up when high baseline levels of coagulation activity are associated with a raised risk of early reactivation and increased mortality.
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PMID:Coagulation activity and clinical outcome in unstable coronary artery disease. 1139 20


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