Alterations of Coagulation and Fibrinolytic and Kallikrein-Kinin Systems in the Acute and Postacute Phases in Patients With Unstable Angina Pectoris

Hoffmeister, Hans Martin; Jur, M.; Wendel, Hans Peter; Heller, W.; Seipel, L

doi:10.1161/01.cir.91.10.2520

Cited by 124 publications

(69 citation statements)

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“…A level of >500 mg/L had an independent diagnostic value for myocardial infarction and increased the diagnostic sensitivity of the electrocardiogram and history from 73% to 92%. Hoffmeister et al [14] investigated the coagulation profile in UAP and demonstrated a persistently strong trend of elevated D-dimer levels during the first 10 days after admission. Accordingly, Oldgren et al [15] showed that on longterm follow-up (median 29 months) of patients with UAP, higher baseline levels of D-dimer were correlated with increased mortality.…”

Section: Discussionmentioning

confidence: 99%

Role of ELISA D‐dimer test in patients with unstable angina pectoris presenting at the emergency department with a normal electrocardiogram

Shitrit¹,

Shitrit²,

Rudensky³

et al. 2004

American J Hematol

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Patients with unstable angina pectoris and acute myocardial infarction have higher than normal D-dimer levels. The aim of the study was to determine the value of the D-dimer test in patients with unstable angina pectoris and a normal electrocardiogram on presentation at the emergency department. The study sample included 81 patients who met these criteria. Blood samples collected at admission were subjected to ELISA D-dimer. Findings were correlated with coronary risk factors, use of cardiac medications, blood levels of acute phase reactants (fibrinogen and C-reactive protein), cardiac enzymes levels, length of hospital stay, and catheterization findings. ELISA D-dimer levels were statistically significantly correlated with cardiac risk factors, namely male sex, older age, smoking, and hypertension (r = 0.25, P = 0.02; r = 0.43, P = 0.0001; r = 0.26, P = 0.03; r = 0.35, P = 0.002, respectively), in addition to use of cardiac medications (beta blockers, aspirin, nitrates), levels of acute phase reactants, length of stay, and catheterization findings. On multivariate analysis, only D-dimer level, age, and sex were predictors of length of stay (P = 0.018). The study suggests that D-dimer levels at admission to the emergency department may serve as an additional tool to predict the magnitude of unstable angina pectoris in patients with a normal electrocardiogram. Am.

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Section: Discussionmentioning

confidence: 99%

Role of ELISA D‐dimer test in patients with unstable angina pectoris presenting at the emergency department with a normal electrocardiogram

Shitrit¹,

Shitrit²,

Rudensky³

et al. 2004

American J Hematol

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“…Fibrinopeptide A, which reflects thrombin activity, has been analysed in similar studies and may, despite the risk of venipuncture-procedure related variations, allow a more reliable comparison between heparin and a direct thrombin inhibitor [19,[27][28][29][30][31] . Markers for thrombin activity have been shown to increase in patients with unstable coronary artery disease in comparison to control patients or healthy individuals [31][32][33] . In a study by Merlini et al 32 , with up to 6 months of follow-up, a prolonged hypercoagulable state with sustained high levels of prothrombin fragments 1 and 2 was reported.…”

Section: Discussionmentioning

confidence: 99%

“…No such elevation was observed for fibrinopeptide A in the studies by Merlini et al, suggesting that thrombin activity, but not generation, returns to normal levels after the onset of the disease. In the present study, we used ELISA assays for the analysis of prothrombin fragments 1 and 2 and thrombin-antithrombin, which are well established and utilized in trials with similar patient categories [16,17,19,33,34] . Results from previous studies on thrombin inhibitors for unstable coronary artery disease are not totally consistent with our findings.…”

Section: Discussionmentioning

confidence: 99%

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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“…12 Typical procoagulant abnormalities in ACS are increased circulating thrombin marker levels, such as prothrombin fragment 1.2 (F1.2) or thrombin-antithrombin complexes (TAT), with the maximum values seen in subjects with ST-elevation myocardial infarction (STEMI) and markedly elevated cardiac troponin levels, a marker of myocardial necrosis. [13][14][15][16][17] Moreover, enhanced thrombin activity toward fibrinogen within 12 hours of acute myocardial infarction (AMI) has been found to identify patients at an increased risk of cardiac mortality. 18 Patients with ACS who developed in-hospital recurrent ischemia despite at least 72 hours of heparin infusion had significantly higher plasma levels of thrombin markers determined before the coronary event, and heparin was only partially able to antagonize thrombin activity.…”

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confidence: 99%

Systemic blood coagulation activation in acute coronary syndromes

Undas

Szułdrzyński

Brummel‐Ziedins

et al. 2009

Blood

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We evaluated systemic alterations to the blood coagulation system that occur during a coronary thrombotic event. Peripheral blood coagulation in patients with acute coronary thrombosis was compared with that in people with stable coronary artery disease (CAD). Blood coagulation and platelet activation at the microvascular injury site were assessed using immunochemistry in 28 nonanticoagulated patients with acute myocardial infarction (AMI) versus 28 stable CAD patients matched for age, sex, risk factors, and medications. AMI was associated with increased maximum rates of thrombin-antithrombin complex generation (by 93.8%; P < .001), thrombin Bchain formation (by 57.1%; P < .001), prothrombin consumption (by 27.9%; P ‫؍‬ .012), fibrinogen consumption (by 27.0%; P ‫؍‬ .02), factor (f) Va light chain generation (by 44.2%; P ‫؍‬ .003), and accelerated fVa inactivation (by 76.1%; P < .001), and with enhanced release of platelet-derived soluble CD40 ligand (by 44.4%; P < .001). FVa heavy chain availability was similar in both groups because of enhanced formation and IntroductionAfter vascular injury, blood clotting is initiated when plasma factor (f) VIIa gains access to tissue factor (Tf). The resulting complex activates the plasma zymogens fIX and fX. 1 Factor Xa activates small amounts of thrombin, which activates platelets, and the procofactors fV and fVIII to their respective active forms. 2 These reactions result in the formation of the intrinsic fXase (fVIIIa-fIXa) and prothrombinase (fVa-fXa) on the activated platelet surface. 3 The major bolus of thrombin formed by the prothrombinase complex is largely responsible for the ultimate hemostatic process. 4 A potent, synergistic inhibitory system principally composed of tissue factor pathway inhibitor (TFPI), antithrombin (AT), and the thrombin-thrombomodulin (Tm)-catalyzed dynamic protein C (PC) system opposes thrombin generation. 5,6 The formation of fVa and its regulation by activated protein C (APC) are key processes for maintaining blood homeostasis. The fV activation process involves sequential cleavages to first produce a heavy chain (1-709) and subsequently a light chain resulting in the active cofactor. 7 The PC system inactivates fVa in a kinetically controlled series of cleavage reactions in which APC cleaves the heavy chain of fVa at 2 locations (R506 and R306); the resulting fVai can no longer function in the coagulation system. 8,9 The balance between activation and inactivation of fV is critical to the synergistic control of the coagulation process. 10 The activation of the Tf coagulation pathway appears to be central in arterial and venous thrombosis. 11 A major clinical manifestation of arterial thrombosis is represented by the acute coronary syndromes (ACS), which result from platelet-rich thrombus formation on the surface of ruptured or eroded atheromatosus plaque in the coronary artery. 12 Typical procoagulant abnormalities in ACS are increased circulating thrombin marker levels, such as prothrombin fragment 1.2 (F1.2) or thrombin-antithrombi...

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Alterations of Coagulation and Fibrinolytic and Kallikrein-Kinin Systems in the Acute and Postacute Phases in Patients With Unstable Angina Pectoris

Cited by 124 publications

References 42 publications

Role of ELISA D‐dimer test in patients with unstable angina pectoris presenting at the emergency department with a normal electrocardiogram

Role of ELISA D‐dimer test in patients with unstable angina pectoris presenting at the emergency department with a normal electrocardiogram

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

Systemic blood coagulation activation in acute coronary syndromes

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