Influence of Different Anticoagulants on Platelet Aggregation in Whole Blood; A Comparison between Citrate, Low Molecular Mass Heparin and Hirudin

Wallén, N H; Ladjevardi, Mehdi; Albert, Johanna; Bröijersén, Anders

doi:10.1016/s0049-3848(97)00114-x

Cited by 82 publications

(65 citation statements)

References 17 publications

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“…19 All patients presenting with chest pain to the Edinburgh Royal Infirmary with ischemic symptoms at rest and ECG changes of ischemia (Braunwald Class IIIb) or infarction (with or without troponin elevation at presentation) were included in the clinical study. Patients hospitalized for chest pain at rest or MI within 3 months of their present presentation or who had undergone coronary artery bypass grafting or percutaneous coronary intervention within 6 months of their present presentation were excluded, as were patients taking antiplatelet aggregation drugs other than aspirin.…”

Section: Blood Sampling and Patient Inclusion Criteriamentioning

confidence: 99%

Increased Platelet Binding to Circulating Monocytes in Acute Coronary Syndromes

et al. 2002

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Background — Present therapies for acute coronary syndromes aim toward limiting platelet–platelet adhesion and aggregation processes. However, platelet–leukocyte interactions may contribute importantly to disease progression in the arterial wall. Recent studies suggest that prevention of platelet–leukocyte binding via P-selectin glycoprotein ligand-1 (PSGL-1) may be beneficial in animal models of vascular injury. Methods and Results — P-selectin–PSGL-1 interactions were found to account for most platelet–monocyte binding observed in peripheral blood samples from healthy donors. However, a significant component of observed adhesion was calcium independent, involving neither PSGL-1 nor P-selectin. Platelet–monocyte interactions were examined in 52 patients admitted within 14 hours of symptom onset, with acute coronary syndromes defined as unstable angina (n=12) and acute myocardial infarction (n=13) or noncardiac chest pain (n=27). When compared with patients with noncardiac chest pain, significantly elevated levels of platelet–monocyte binding were found in patients with acute myocardial infarction (70.1±15.4% versus 45.4±23.3%; P <0.01) and unstable angina (67.4±12.9% versus 45.4±23.3%; P >0.01). Calcium-independent platelet–monocyte binding was significantly elevated in myocardial infarction patients alone (14.7±7.7% versus 6.1±5.96%; P <0.001). Conclusions — There is evidence for a significant P-selectin–independent molecular component to the platelet–monocyte conjugation observed in peripheral blood. Patients with myocardial infarction and unstable angina demonstrate increased total binding of platelets to monocytes. Additionally, calcium-independent adhesion was significantly elevated in patients with evidence of myocardial infarction. These findings demonstrate that novel cation-independent adhesion mechanisms may mediate platelet–monocyte binding, representing a new therapeutic target after vascular injury associated with myocardial infarction.

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Section: Blood Sampling and Patient Inclusion Criteriamentioning

confidence: 99%

Increased Platelet Binding to Circulating Monocytes in Acute Coronary Syndromes

et al. 2002

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“…The whole population of platelets is evaluated, rather than the less dense population in PRP, which is required for optical systems. These advantages, together with the relative simplicity of the method, have attracted many investigators working with both human and animal blood [6,[13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Whole Blood Platelet Aggregation in Humans and Animals: A Comparative Study

Soloviev

Okazaki

Harasaki

1999

Journal of Surgical Research

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“…In a meta-analysis of 145 randomized studies on patients with coronary artery disease (prior MI, unstable angina pectoris) and cerebrovascular disease, 75-300 mg/d aspirin therapy reduced the risk of non-fatal MI by 35% ( p < 0.00001) and the risk of vascular events by 18% ( p < 0.00001) [1,2]. Aspirin's antiplatelet effect is related to the inhibition of thromboxane formation [3]. However, the antiplatelet effect of aspirin is not uniform in all patients and some patients do not benefit from aspirin.…”

mentioning

confidence: 99%