Intracoronary artery thrombus formation in unstable angina: A clinical, biochemical and angiographic correlation

Wilensky, Robert L.; Bourdillon, Patrick D.V.; Vix, Vernon A.; Zeller, Jack A.

doi:10.1016/0735-1097(93)90102-7

Cited by 47 publications

(13 citation statements)

References 37 publications

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“…The decrease in thrombin-antithrombin during infusion, observed in both groups, may well be interpreted as a reduction in thrombin generation, but according to the explanation, a comparison between inogatran and heparin on the basis of this marker is questionable. 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] .…”

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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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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“…The findings of haziness and filling defect are angiographic criteria for the presence of intracoronary thrombi [13,14,15], though angiography has been shown to be less sensitive than angioscopy for detection of thrombi [6,7]. Angio-A B graphy can probably recognize only the thrombi under conditions of stasis.…”

Section: Methodsmentioning

confidence: 99%

Angioscopic Evaluation of Thrombi in the Culprit Coronary Lesions in Patients With Acute Myocardial Infarction

Morio

Fujimori

Terasawa

et al. 2000

Diagnostic and Therapeutic Endoscopy

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The purpose of this study was to evaluate intracoronary thrombi in the culprit lesions in patients with acute myocardial infarction (AMI) by angioscopy, and to compare them with clinical and angiographic features. We angioscopically observed the culprit coronary lesions in 66 patients with AMI (55 males and 11 females, 63.9 + 15.4 years old) just before interventional therapy. Thrombi were observed in 42 of 66 lesions (64%), namely, red thrombi in 16, mixed thrombi in 15, white thrombi in 11. In patients with complete obstruction (TIMI grade 0 and I), red thrombi were more frequently observed than mixed or white thrombi. On the other hand, in patients with incomplete obstruction (TIMI grade II and III), white thrombi were more frequently observed than the others. Angiographically, haziness and filling defect were significantly more frequently observed in patients with red thrombi than the others (p < 0.05). The distance from proximal side branch to thrombi tended to be longer in patients with red thrombi than the others. The time from onset of AMI tended to be longer in patients with white thrombi than the others. These results suggest that blood flow may be an important determinant of thrombi characterization.

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“…A 12-lead ECG was obtained at presentation (0 hours), 4 hours later, and for recurrent chest pain. Blood specimens for creatine kinase (CK) and CK-MB% were obtained at 0, 8,16, and 24 hours. TnI, Myo, and MLC samples were obtained at 0, 4, and 8 hours and FPA samples at 0 and 4 hours.…”

Section: Methodsmentioning

confidence: 99%

“…FPA was evaluated because elevated levels predict angiographic intracoronary thrombus formation in patients with acute coronary syndromes. 7,8 …”

mentioning

confidence: 99%

Prospective Study Correlating Fibrinopeptide A, Troponin I, Myoglobin, and Myosin Light Chain Levels With Early and Late Ischemic Events in Consecutive Patients Presenting to the Emergency Department With Chest Pain

et al. 2000

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Background-Although thrombus formation plays a major role in acute coronary syndromes, few studies have evaluated a thrombus marker in risk stratification of patients with chest pain. Furthermore, the relation between markers that reflect myocardial injury and thrombus formation that may predict events in a heterogeneous patient population is unknown. This study correlated markers of thrombus and myocardial injury with early and late ischemic events in consecutive patients with chest pain. Methods and Results-Serum troponin I (TnI), myoglobin, and myosin light chain levels were obtained from 247 patients and urinary fibrinopeptide A (FPA) from 178 of the 247. By multivariate analysis, patients with an elevated FPA level were 4.82 times more likely to die or have myocardial infarction, unstable angina, and coronary revascularization at 1 week (Pϭ0.002, 95% CI 1.78, 13.03), whereas those with an elevated TnI (Ͼ0.2 ng/mL) were 9.41 times more likely (PϽ0.001, 95% CI 2.84, 31.17). At 6 months (excluding the index event), an elevated FPA level was an independent predictor of events, with an odds ratio of 9.57 (PϽ0.001, C1 3.29, 27.8), and was the only marker to predict a shorter event-free survival (PϽ0.001). The other markers did not independently correlate with cardiac events, although MLC incrementally increased early predictive accuracy in combination with the FPA and TnI. Conclusions-Elevated FPA and TnI correlated with cardiac events during the initial week in patients presenting to the Emergency Department with chest pain. FPA predicted adverse events and a shorter event-free survival at 6 months.

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Intracoronary artery thrombus formation in unstable angina: A clinical, biochemical and angiographic correlation

Cited by 47 publications

References 37 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

Angioscopic Evaluation of Thrombi in the Culprit Coronary Lesions in Patients With Acute Myocardial Infarction

Prospective Study Correlating Fibrinopeptide A, Troponin I, Myoglobin, and Myosin Light Chain Levels With Early and Late Ischemic Events in Consecutive Patients Presenting to the Emergency Department With Chest Pain

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