SUMMARY Plasma concentration of thromboglobulin was used as an index of in vivo platelet activation in 36 patients after acute myocardial infarction. Twelve patients had diabetes, seven had pulmonary oedema or cardiogenic shock (pump failure) or both, and 17 had uncomplicated infarcts. On the first day of admission, concentrations of P thromboglobulin were higher in the patients with diabetes and those with pump failure than in those with uncomplicated infarcts.Concentrations of fl thromboglobulin in the non-diabetic patients were studied by multiple regression analysis and were significantly associated with plasma concentrations of adrenaline, pump failure, and glucose but not with noradrenaline or infarct size. When all subjects were considered together, glucose, adrenaline, and pump failure were associated with the thromboglobulin concentration but diabetes was without significant effect. Hyperglycaemia and raised plasma adrenaline concentration after myocardial infarction may activate platelets, and this could contribute to poor outcome in such patients.Case fatality rates are higher in diabetic patients admitted to hospital with acute myocardial infarction than in non-diabetic patients, with the principal causes of death being refractory heart failure or cardiogenic shock (pump failure) or both.'2 The excess risk of pump failure in diabetic subjects does not result from more extensive necrosis,2'5 nor is there evidence that more widespread atheroma restricts the perfusion of non-infarcted myocardium in these patients.6 The role of hyperglycaemia remains controversial.7"The primary cause of myocardial infarction is thrombosis of a coronary vessel and the fate of this thrombus is an important determinant of outcome after myocardial infarction.'2 Reperfusion of the infarcted myocardium preserves myocardial func-

We have used high-performance liquid chromatography with electrochemical detection to measure content of adrenaline and noradrenaline in platelets in 13 normal subjects at rest. Subjects were exercised to raise plasma catecholamine levels and promote the platelet release reaction. There was a significant positive correlation between plasma noradrenaline concentrations and platelet noradrenaline content. Platelet/plasma concentration ratios were 1855 for noradrenaline and 268 for adrenaline at rest and 473 and 152 respectively after exercise. Plasma noradrenaline levels positively correlated with age. Determination of platelet factors released to the plasma showed increases of beta-thromboglobulin and platelet factor 4 with exercise, whereas thromboxane B2 remained unchanged. No change in platelet catecholamine levels occurred with exercise and no correlations were observed between platelet catecholamines and released platelet factors. These data suggest that plasma catecholamine levels influence platelet content and that noradrenaline and adrenaline are concentrated in platelets.

Platelet function has been studied in diabetic subjects using a new electronic platelet aggregometer which enables platelet aggregation to be studied in whole blood. This may be a more physiological approach to the assessment of platelet behaviour as centrifugation is avoided and platelets are studied in the presence of other blood elements which may be important modulators of platelet function in vivo. Twenty insulin-dependent diabetic subjects were studied along with 20 age and sex-matched controls. Platelet aggregation to collagen (1 microgram/ml) and arachidonic acid (1 mM) was significantly increased in the diabetic group. In addition the sensitivity of diabetic platelets to the antiaggregatory effects of prostacyclin was significantly reduced. A significant inverse correlation was found between platelet sensitivity to prostacyclin and glycosylated haemoglobin concentration in the diabetic group. It is unlikely that the platelet abnormalities in this diabetic group are due to underlying vascular disease as none of the patients had evidence of diabetic complications. These findings may have important implications for the development of vascular disease in diabetics.

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