Key result
Acute coronary syndromes were associated with a nearly 50-fold lower EC50 of epinephrine for primary platelet aggregation compared to healthy controls (P<0.001).
Why the study?
Does a laser light scattering aggregometer detect differences in platelet aggregability between patients with acute coronary syndromes and healthy controls?
Case-Control (n=53)
Does a laser light scattering aggregometer detect differences in platelet aggregability between patients with acute coronary syndromes and healthy controls?
Effect estimate: nearly 50 times lower
p-value: p=<0.001
A novel laser light scattering aggregometer reveals that platelet hyperaggregability and hypersensitivity in acute coronary syndromes primarily occur in the formation of small aggregates (primary aggregation).
May indicate need for adjusted antiplatelet monitoring in ACS; hypothesis-generating, requiring randomized validation before practice change.
OBJECTIVE: Platelet aggregation has been implicated in the pathogenesis of acute coronary syndromes. Small aggregates consisting of < or = 100 platelets cannot be quantified with a conventional aggregometer employing optical density. Using a recently developed aggregometer based on laser light scattering, we studied platelet aggregability in patients with acute coronary syndromes. METHODS: Peripheral blood samples were obtained from 39 patients with acute myocardial infarction or unstable angina who had received no prior antiplatelet or anticoagulant therapy, to be assayed immediately using a PA-100 platelet aggregometer. Blood samples from 14 healthy volunteers were used as controls. RESULTS: Spontaneous formation of platelet aggregates was observed only in patients with acute coronary syndromes. The size of these aggregates was small, consisting of < or = 100 platelets (primary aggregation). Agonist-induced aggregation consisted of two phases. In the first few minutes, the number of small aggregates increased markedly (primary aggregation), followed by an increase in larger aggregates (secondary aggregation). The EC50 of epinephrine for primary aggregation was nearly 50 times lower in acute coronary patients than in controls (P < 0.001), while the EC50 for secondary aggregation was only 2 times lower (P < 0.001). CONCLUSIONS: Aggregometry using light scattering suggests that platelet hyperaggregability and hypersensitivity in acute coronary syndromes may occur in primary but not secondary aggregation.
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Eto et al. (1998) conducted a case-control in Acute coronary syndromes (n=53). Acute coronary syndromes vs. Healthy volunteers was evaluated on EC50 of epinephrine for primary platelet aggregation (nearly 50 times lower, p=<0.001). Acute coronary syndromes were associated with a nearly 50-fold lower EC50 of epinephrine for primary platelet aggregation compared to healthy controls (P<0.001).
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