Relationship between hemostatic abnormalities and neuroendocrine activity in heart failure

Sbarouni, Eftihia; Bradshaw, Anne; Andreotti, Felicita; Tuddenham, E G D; Oakley, Celia M.; Cleland, John G.F.

doi:10.1016/0002-8703(94)90670-x

Cited by 154 publications

(86 citation statements)

References 33 publications

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“…Although the causative mechanism remains to be elucidated, our findings may be explained in part by the occurrence of pulmonary congestion secondary to acute myocardial infarction, because it has previously been pointed out that plasma vWF concentrations are increased in patients with heart failure regardless of the underlying heart disease. [27][28][29][30] In accordance with this hypothesis, plasma vWF levels have been shown to be correlated with pulmonary capillary wedge pressure. 31 In the present study, the highest vWF plasma levels were demonstrated in patients with delayed blood flow in the main trunk of the left coronary artery, resulting in severe pulmonary edema.…”

Section: Discussionmentioning

confidence: 84%

Enhanced Shear-Induced Platelet Aggregation in Acute Myocardial Infarction

et al. 1999

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Background-Experiments under controlled flow conditions indicate that the binding of von Willebrand factor (vWF) to platelet glycoprotein (GP) Ib␣ and integrin ␣ IIb ␤ 3 (GP IIb/IIIa complex) is crucial for aggregation at elevated shear rates. We have tested how the plasma of patients with acute myocardial infarction affects this process. Methods and Results-Citrated plasma was obtained from 18 patients with acute myocardial infarction within 6 hours from the onset of symptoms and from 26 control subjects with chest pain syndrome without evidence of ischemia. Aggregation of normal platelets at high shear rates was significantly greater in the presence of patient than control plasma and was inhibited by both anti-GP Ib␣ and anti-␣ IIb ␤ 3 monoclonal antibodies. The observed values (meanϮSD) were 47.6Ϯ17.8% versus 30.1Ϯ9.9% at 10 800 s Ϫ1 (PϽ0.01) and 32.9Ϯ14.1% versus 17.5Ϯ9.5% at 7200 s Ϫ1 (PϽ0.01), respectively, and were positively correlated with plasma vWF antigen levels and ristocetin cofactor activities. In contrast, at the lower shear rate of 1200 s Ϫ1 , aggregation was similar in the presence of control or patient plasma and was not inhibited by the anti-GP Ib␣ antibody. Both vWF antigen and platelet aggregation decreased 2 weeks after the onset of myocardial infarction. Conclusions-Shear-induced platelet aggregation is enhanced in plasma in the presence of acute myocardial infarction, apparently as a result of increased vWF concentration. This may contribute to the onset of acute coronary artery thrombosis and early reocclusion after reperfusion treatment. (Circulation. 1999;99:608-613.)

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Section: Discussionmentioning

confidence: 84%

Enhanced Shear-Induced Platelet Aggregation in Acute Myocardial Infarction

et al. 1999

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“…Patients with CHF have abnormal levels of soluble P-selectin and von Willebrand factor, as well as high plasma viscosity, which contribute to the hypercoagulable state induced by the disease in association with the venous stasis and decreased mobility. 21,23,41 For many years, inpatients with CHF have been considered at increased risk for VTE and prophylaxis is recommended. [42][43][44][45] The recommendations were based on expert opinion, small clinical trials of VTE prophylaxis performed before the routine use of diagnostic testing, and more recent trials of prophylaxis in general medical patients, which often included those with CHF.…”

Section: Discussionmentioning

confidence: 99%

Incidence and Clinical Predictors of Deep Vein Thrombosis in Patients Hospitalized With Heart Failure in Japan

Ota

Yamada

Tsuji

et al. 2009

Circ J

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“…The predisposing conditions are: low cardiac output through dilated chambers, ventricular hypocontractility, abnormalities in the segmental kinetics, endocardial surface modified after myocardial infarction or inflammatory or infiltrative cardiomyopathies, hypercoagulability and the presence of AF 262,263 . Right ventricular dysfunction is present in 50% of cases and it constitutes a marker of poor prognosis, especially in patients with hemodynamic instability.…”

Section: A Pulmonary Thromboembolism (Tables 46 and 47)mentioning

confidence: 99%