SUMMARY The etiology of cerebrovascular disease (CVD) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an ageand sex-matched control group. The mean plasma beta-thromboglobulin (/3-TG) level of the patients (mean = 54.9 ± 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 ± 6.9 ng/ml, p < 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p < 0.01). However, the 0-TG levels of patients with MVP (n = 13,52.9 ± 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 ± 33.7 ng/ml) significantly (p < 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma /3-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between /3-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.Stroke, Vol 13, No 4, 1982

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Recent studies have demonstrated a sixfold higher incidence of mitral-valve prolapse (MVP) in young patients with cerebral ischemia compared to an age-matched control population. To examine whether there is a pathogenetic relationship between MVP and cerebral ischemia, we studied 47 patients (12 males, 35 females) under 45 (mean age 35.4 ± 6.6) years with transient ischemic attacks (TIA) and stroke who had failed to show a cause from extracranial Doppler examination, cranial computerized tomography and cerebral angiography. In vivo platelet activity was evaluated by measuring the B-thrcmboglobulin (β-TG) concentration in the platelet poor EDTA-theophylline-PGE1-plasma using the Amersham RIA kit.The β-TG levels of the patients (54.9 ± 31.4, x ± SD ng/ml) were significant higher than those of an age- and sex-matched control group (n=40, 19.7 ± 6.4 ng/ml, p<0.001) MVP was demonstrated in 28% of the patients (13 of 47) in contrast to 7.5% of the controls (3 of 40). The difference of the β-TG levels of patients with MVP (n=13, 52.9 ± 25.5 ng/ml) and of patients without MVP (n=34, 55.7 ± 33.7 ng/ml) was not significant (p < 0.40). There was no correlation bet ween duration or extent of the neurological deficit and the individual β-TG level.Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic young people. The significantly elevated plasma β-TG concentrations in the patients' group nay indicate an increased platelet activity in vivo. There was io significant difference between β-TG levels of patients tfith and without MVP. Thus, MVP can not be the cause for the altered platelet activity.

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