Haemostatic variables in patients with unstable angina

Al-Nozha, Mansour M.; Gader, A. M. A.; Al-Momen, Abdul Kareem; Noah, Mohamed S.; Jawaid, Muhammad Moazzam; Arafa, Mohammad

doi:10.1016/0167-5273(94)90207-0

Cited by 29 publications

(10 citation statements)

References 36 publications

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“…Results from previous studies on thrombin inhibitors for unstable coronary artery disease are not totally consistent with our findings. In accordance with the results from our study, one group has reported a reduction in the formation of thrombin-antithrombin during treatment with heparin in patients with unstable angina pectoris [35] . Inogatran has once previously been evaluated in a small study in patients with unstable coronary artery disease, in which a tendency towards a reduction in thrombinantithrombin and prothrombin fragments 1 and 2 was seen [36] .…”

Section: Discussionsupporting

confidence: 82%

The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease

Linder

Oldgren²,

Egberg³

et al. 1999

European Heart Journal

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Aim This study evaluated a novel specific thrombin inhibitor, inogatran, in comparison with unfractionated heparin, with regard to markers for coagulation activity in patients with unstable coronary artery disease. Methods and ResultsIn the Thrombin Inhibition In Myocardial ischaemia (TRIM) study patients were randomized to one of three different doses of inogatran or to unfractionated heparin, given intravenously over 72 h. In a subpopulation of 320 patients, markers for coagulation activity were measured at baseline, during and after the study infusion.Prothrombin fragment 1+2, indicating thrombin generation, decreased in the low, medium and high dose inogatran groups and in the heparin group during the first 6 h of treatment by 12%, 15%, 21% and 26%, respectively. From 6 h to 72 h after the start of infusion the levels changed by 7%, 6%, 4% and +34%, respectively. The increase in the heparin group continued after the infusion was stopped. Thrombin-antithrombin complex, also indicating thrombin generation, decreased by 0%, 2%, 18% and 22%, respectively, during the first 6 h of treatment. During the same period soluble fibrin, an intermediate in fibrin formation, increased both in the low and medium inogatran group by 9%, while a decrease by 4% and 18%, respectively, was seen in the high dose inogatran group and in the heparin group. Fibrin dissolution, as measured by fibrin D-dimer, decreased during the first 24 h of treatment by 20%, 18%, 18% and 20%, respectively. The first 24 h after discontinuation of infusion, fibrin D-dimer increased by 6%, 23%, 25% and 44%, respectively.After 72 h, at the end of infusion, patients treated with inogatran, to a larger extent than those given heparin, had suffered from death, myocardial infarction or refractory angina pectoris. After 7 days this trend was less marked. ConclusionThe more pronounced decrease in thrombin generation and fibrin turnover during the first 6 h of infusion, and the later increase in thrombin generation and fibrin turnover, in the heparin group, as compared to the inogatran groups, may be related to the lower clinical event rate during infusion with heparin compared with inogatran and the recurrence of ischaemic events, early after cessation of heparin infusion. (Eur Heart J 1999; 20: 506-518)

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Section: Discussionsupporting

confidence: 82%

The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease

Linder

Oldgren²,

Egberg³

et al. 1999

European Heart Journal

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“…In some studies concerning the role of haemostatic factors in acute coronary syndrome, the factors of interest have been measured only once after the event [10], or the follow-up has been short [6]. However, because after any acute coronary event haemostatic factors vary greatly in relation to time, the results may depend on the interval between event and measurement.…”

Section: Introductionmentioning

confidence: 98%

“…After transmural AMI, lower PC activity has been correlated with higher risk for recurrent cardiovascular events [3]. AMI patients [4] and unstable angina patients [5,6] have shown low AT values, although other studies reveal no relationship between PC, AT and ischaemic coronary events [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Low normal level of protein C or of antithrombin increases risk for recurrent cardiovascular events

Pelkonen

Wartiovaara‐Kautto²,

Nieminen³

et al. 2005

Blood Coagulation &Amp; Fibrinolysis

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The relationship between haemostatic factors and recurrent cardiovascular events was investigated in patients enrolled with acute coronary syndrome (acute non-Q myocardial infarction or unstable angina pectoris). One hundred and fifteen patients, aged 64 +/- 10 years, were included in the study. Haemostatic parameters [prothrombin time, activities of factor VII, factor VIII, factor X, antithrombin (AT) and protein C (PC), and concentrations of free protein S, fibrinogen, D-dimer, prothrombin fragment 1+2, and thrombin-antithrombin complex] were measured four times: within 48 h of hospitalization, at discharge (days 5-8), at 3 months and after 1 year. Screening for factor V Leiden mutation was also performed. Patients were followed for cardiovascular endpoints (new or refractory unstable angina pectoris, non-fatal myocardial infarction, stroke, or death) for an average of 555 days. Of all patients, 35 had an endpoint during the follow-up ("endpoint" group) and 80 patients did not ("no endpoint" group). Analysing the whole follow-up period, PC (P < 0.01) and AT (P < 0.01) were lower in the "endpoint" than in the "no endpoint" group. With 50% percentiles at enrollment, the odds ratio for getting an endpoint in the low (cut-off value < 100%) versus high PC group was 2.72 (95% confidence interval, 1.18-6.29; P < 0.05). Lower levels of AT (P < 0.05) and PC (P < 0.05) during the whole follow-up were associated with a shorter event-free time. In conclusion, lower PC and AT values, even within the normal range, seem to be associated with elevated risk for recurrent cardiovascular events and shorter event-free time in acute coronary syndrome patients.

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“…Fibrinogen is an acute-phase protein directly involved in the coagulation cascade; increased fi brinogen levels are associated with higher risk of thrombotic events 9 and higher risk of events in ACS patients [10][11][12][13][14] . Finally, factor VIII-c, a procoagulant enzyme cofactor, is also involved in infl amation 15 and is a marker of ischemic heart disease [16][17][18] .…”

mentioning

confidence: 99%

Análise de marcadores de estabilização da placa aterosclerótica após evento coronariano agudo

Mouco¹,

Nicolau²,

Souza³

et al. 2006

Arq. Bras. Cardiol.

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Haemostatic variables in patients with unstable angina

Cited by 29 publications

References 36 publications

The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease

The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease

Low normal level of protein C or of antithrombin increases risk for recurrent cardiovascular events

Análise de marcadores de estabilização da placa aterosclerótica após evento coronariano agudo

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