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Platelet Function in Patients Admitted with a Diagnosis of Myocardial Infarction

Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England

M.A. Barradas, B.Sc.

Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England

A. Mier, M.B., MRCP

From the Department of Endocrinology, Royal Free Hospital and School of Medicine, London, England

F. Boag, M.B.

From the Department of Endocrinology, Royal Free Hospital and School of Medicine, London, England

J.Y. Jeremy, M.Sc.

Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England

C.W.H. Havard, M.D.

From the Department of Endocrinology, Royal Free Hospital and School of Medicine, London, England

P. Dandona, M.B.B.S., F.I.C.A.

Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England

Platelet function and thromboxane A₂ release were measured in 71 patients admitted to a coronary care unit with a provisional diagnosis of acute myocardial infarction (AMI). All measurements were carried out within twenty-four hours of admission. Of these, 35 patients had the diagnosis of AMI confirmed. The remainder (n=36), who did not have AMI (NMI), were divided into two groups: (a) those (n = 18) with an unequivocal history of previous vascular disease and (b) those without vascular disease (n=18). Platelet aggregation and thromboxane A₂ (TXA₂) release were significantly increased in the AMI group when compared with those in the NMI without vascular disease group or a healthy control group with similar age and sex distribution. Aggregation and TXA ₂ release in the NMI patients with vascular disease were greater than those in controls and did not differ significantly from those in the AMI group. Patients in the AMI or NMI with vascular disease groups who were taking ß-blockers or calcium channel antagonists at the time of admission showed significantly less platelet aggregation than those who were not taking these drugs. Heparin, added in vitro at therapeutic concentrations, induced significantly more aggregation in patients in the AMI and NMI with vascular disease groups than in the NMI without vascular disease group. We conclude that: (1) platelets obtained from patients with AMI are hyperaggregable and release more TXA₂; (2) platelets from patients with significant vascular disease are hyperaggregable, even in the absence of AMI, although they are not as hyperaggregable as those from AMI; (3) treatment with nifedipine and ß-blockers protects these patients from platelet hyperaggregability; (4) heparin induces significant aggregation of platelets from patients with AMI and NMI with vascular disease. These observations are of importance in considering the pathogenesis and treatment of AMI and ischemic heart disease.

Angiology, Vol. 38, No. 1, 36-45 (1987)
DOI: 10.1177/000331978703800105


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