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.
Repeated episodes of focal cerebral ischemia in a patient with mitral valve prolapse and migraine headache