Inhibitory effect of acetylsalicylic acid on platelet function in patients with completed stroke or reversible ischemic neurologic deficit.

Abstract

The purpose of our study was to investigate the effects of different doses of acetylsalicylic acid on platelet aggregation. Among inpatients of the National Taiwan University Hospital, 236 cases of completed stroke and seven cases of reversible ischemic neurologic deficit that were diagnosed by computed tomography of the brain and that had not ingested acetylsalicylic acid or acetylsalicylic acidlike drugs for > 2 weeks before admission were selected for this study. Thromboxane B 2 and 6-keto-PGF lo were measured by radioimmunoassay, threshold concentration of adenosine diphosphate was measured by Born's method, and circulating platelet aggregates were measured by the method of Wu and Hoak. Various single doses of acetylsalicylic acid (75, 300, or 600 mg) or 300 mg acetylsalicylic acid every 6 hours for four doses or one dose of 300 mg acetylsalicylic acid with 75 mg dipyridamole significantly suppressed the mean plasma thromboxane B, concentrations and elevated the mean adenosine diphosphate threshold concentrations. Abnormal plasma thromboxane B, concentrations, adenosine diphosphate threshold concentrations, or circulating platelet aggregate ratios were significantly normalized after administration of these regimens. The effects were not significantly different among treatment groups. Forty milligrams of acetylsalicylic acid seemed to have less platelet-inhibitory effect. A single dose of 75 mg acetylsalicylic acid significantly inhibited platelet hyperfunction and effectively corrected the abnormal plasma thromboxane B 2 concentrations, adenosine diphosphate threshold concentrations, and circulating platelet aggregate ratios. Higher doses did not enhance the inhibitory effect. In addition, this single dose of acetylsalicylic acid did not significantly suppress plasma 6-keto-PGF lo . We conclude that 75 mg acetylsalicylic acid per day is adequate to inhibit platelet hyperfunction. (Stroke 1988; 19:566-570) I t has been documented that acetylsalicylic acid (ASA) has an inhibitory effect on platelet function through specific blocking of the enzyme cyclooxygenase 1 ; thus, this antiplatelet agent is now widely used for the prevention of ischemic cerebrovascular disease.Treatment with oral administration of 1,000-1,300 mg ASA/day has been reported to have a significantly beneficial effect in male patients with threatened stroke, 2 in patients with a history of multiple transient ischemic attacks (TIAs), 3 and in the secondary prevention of atherothrombotic cerebral infarction 4 or to have no favorable influence in patients with reversible cerebral ischemic attacks. 5 However, an increasing number of studies have documented that high doses of ASA might depress not only thromboxane A 2 (TXA 2 ) but also prostacyclin (PGIJ.6 " 10 Since PGI 2 has an inhibitory effect on platelet activity, suppression of this prostaglandin could possibly have adverse effects on Address for correspondence: Dr. Ti-Kai Lee, Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China...

Evaluation of the clinical utility of platelet aggregation studies in the long‐term follow‐up of patients with atherosclerotic vascular disease

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