Key result
Prior thrombosis linked to ~5-fold higher rate of platelet aggregating activity.
Why the study?
The incidence and significance of novel plasma derived platelet aggregating activity in patients with thrombosis and thrombotic tendencies were not well characterized.
Is plasma derived platelet aggregating activity associated with a history of thrombosis in hospitalized patients?
Cross-Sectional (n=262)
Is plasma derived platelet aggregating activity associated with a history of thrombosis in hospitalized patients?
Absolute Event Rate: 52% vs 10%
Plasma derived platelet aggregating activity is highly associated with a history of thrombosis and may serve as a marker for vascular thrombosis.
May mark thrombosis risk in hospitalized patients; hypothesis-generating and requires prospective validation before clinical use.
This study examines the incidence and significance of novel plasma derived platelet aggregating activity (PAA) in 190 consecutive patients admitted to the medical wards of a general hospital. Seventy five patients (39%) demonstrated this activity. The incidence was highest in patients with a history of thrombosis (52%) or in those with a heightened thrombotic tendency, for example, patients with diabetes or hypertension. In contrast, platelet aggregating activity was observed in six out of 62 patients (approximately 10%) in whom a current or past medical history of thrombosis could not be elicited and in only two out of 72 healthy volunteers examined (3%). A high frequency of PAA was also noted in a small group of patients with idiopathic thrombocytopenia and patients who had previously received platelet transfusions. In these patients, this activity presumably reflects the presence of antiplatelet antibodies. A good correlation between the presence of plasma derived platelet aggregating activity and the phenomenon of spontaneous platelet aggregation was observed. The platelet aggregating activity was not heparin dependent, but was completely abolished by EDTA (5 mM) and benzamidine (8 mM), or by pretreating the platelets with aspirin. A synergistic response was observed with subaggregatory concentrations of thrombin and adrenalin. Our results suggest that the presence of this platelet aggregating activity may provide a marker for vascular thrombosis. Furthermore we postulate that this plasma derived activity may be partly responsible for platelet hyperactivity previously observed in patients with thromboembolic disorders.
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Jackson et al. (1989) conducted a cross-sectional in Thrombosis (n=262). History of thrombosis vs. No history of thrombosis was evaluated on Presence of plasma derived platelet aggregating activity (PAA). A history of thrombosis was associated with a 52% incidence of plasma derived platelet aggregating activity, compared to 10% in patients without such history and 3% in healthy volunteers.
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