SUMMARY Two hundred and three patients, 148 males and 55 females, who during the last month before admission had experienced at least one reversible cerebral ischemic attack of less than 72 hours duration, were randomly assigned to treatment with either acetylsalicylic acid (ASA) 1000 mg daily (101 patients) or placebo (102 patients). The average follow-up period was 25 months. The two treatment groups were comparable with respect to age, sex, associated diseases, risk factors, number and duration of cerebral ischemic attacks.No statistically significant differences were found between the treatment groups as to the primary end point: stroke or death (ASA group 20.8%, placebo group 16.7%). Occurrence of transient ischemic attacks during the treatment period was not reduced by ASA treatment, whereas there was a trend suggesting fewer myocardial infarctions in the ASA group (5.9%) than in the placebo group (13.7%). The difference, however, was not statistically significant (p = 0.10).We were thus unable to demonstrate any favorable influence of ASA 1000 mg daily in patients with reversible ischemic attacks. This study does not, of course, prove that ASA treatment is ineffective in stroke prevention. Stroke Vol 14, No 1, 1983PLATELET-FIBRIN EMBOLI originating from arteriosclerotic lesions in the precerebral arteries are acknowledged to be responsible for a major part of reversible ischemic cerebral attacks. 12 The recognition of the key-role played by platelets in thrombus formation in arteriosclerotic arteries has increased the interest in the use of platelet function inhibiting drugs in the prophylaxis of ischemic cerebrovascular and cardiovascular diseases. 34The results of small scale studies and two large cooperative studies suggest a beneficial effect of acetylsalicylic acid (ASA) and other platelet function inhibiting drugs in patients with transient cerebral ischemic attacks. The present study was begun in 1976, the main objective being to determine if ASA would reduce stroke frequency and mortality in patients with reversible cerebral ischemic attacks. The study was conducted as a cooperative, multicenter, double-blind, randomized clinical trial.

The present study was performed in 34 patients with transient cerebral ischemia, TCI. Twenty-four of the patients were examined angiographically. Atherosclerotic abnormalities were demonstrated in 13 and a total occlusion of the interior carotid artery was found in one patient. The angiograms were normal in 10 patients. One patient suffered from hyperlipoproteinemia, type IV, and one from diabetes mellitus. The platelet aggregation in vitro was increased significantly, as more patients than normal controls showed secondary aggregation with low ADP-concentration: less than or equal to 1 mumol (p less than 0.001). The fibrinolytic capacity was significantly reduced (p less than 0.01) but not particularly in the patients with increased tendency for platelet aggregation. No correlation found between changes in platelet aggregation, the fibrinolytic activity and the angiographic findings. The results described may favor the concept that a prophylactic use of drug excerting an antiaggregation effect on platelets might be useful in patients suffering from TCI.

The threshold concentrations of ADP and adrenaline inducing platelet aggregation in vitro were determined in a Payton aggregometer in 90 normal controls, 30 patients with ischemic heart disease (IHS), in 34 with transient cerebral ischemia (TCI) and 22 with peripheral thrombo-atherosclerosis (PTA). The threshold concentrations were significantly lower in normal women ≥ 50 years old than in normal women < 50 years old.Compared with the corresponding control groups significantly lower threshold concentrations were found in following groups of patients: men and women ≥ 50 years with IHS (p < 0.005 and p < 0.001 respectively), men + women < 50 years with IHS (p < 0.05), men + women with TCI (p < 0.01), men + women ≥ 50 years with PTA (p < O.002 and p < 0.001 respectively), men + women < 50 years with PTA (p < 0.005).

ADP‐induced platelet aggregation in vitro has been studied in 90 normal controls and in 30 patients with ischemic heart disease (IHD) and 22 with peripheral thromboatherosclerosis (PTA). The sensitivity to ADP was defined by the threshold concentration which produced secondary aggregation with an amplitude corresponding to not less than 80% of the transmission obtained by platelet‐poor plasma. In the normal controls the threshold concentration was significantly lower in women aged 50 or more than in women under that age. The geometric means were lower in the patients than in the controls. Significantly lower threshold concentrations than in the corresponding age groups of controls were found in the following age groups of patients: Men and women ≥50 years with IHD (p<0.005 and p<0.001, respectively), men and women under 50 with IHD (p<0.05). Men and women ≥50 years with PTA (p<0.002 and p<0.01, respectively), men and women under 50 with PTA (p<0.005).