Cerebral ischemia in young patients: it is associated with mitral valve prolapse and abnormal platelet activity in vivo?
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Young patients experiencing stroke or TIA show increased platelet activity and higher rates of mitral valve prolapse (MVP). However, MVP itself does not appear to cause the elevated platelet markers in these cerebrovascular disease cases.
Area of Science:
- Neurology
- Cardiology
- Hematology
Background:
- Cerebrovascular disease (CVD) in young patients often presents an unknown etiology.
- Mitral valve prolapse (MVP) and altered platelet function have been anecdotally linked to cerebral ischemic events.
Purpose of the Study:
- To investigate the in vivo platelet release reaction and the incidence of MVP in young patients with cryptogenic TIA or stroke.
- To determine if MVP is associated with increased platelet activity in this patient cohort.
Main Methods:
- Studied 47 patients under 45 with TIA/stroke of unknown cause and an age/sex-matched control group.
- Measured plasma beta-thromboglobulin (beta-TG) levels to assess in vivo platelet release.
- Assessed the incidence of mitral valve prolapse (MVP) in both patients and controls.
Main Results:
- Patients exhibited significantly higher mean plasma beta-TG levels (54.9 ng/ml) compared to controls (20.6 ng/ml).
- MVP was found in 13/47 patients, significantly more than in 4/4 controls.
- Beta-TG levels did not significantly differ between patients with MVP and those without MVP.
Conclusions:
- Young patients with cryptogenic cerebrovascular events show increased platelet activity.
- The incidence of MVP is higher in young patients with unexplained TIA or stroke.
- Mitral valve prolapse is unlikely to be the direct cause of the observed heightened platelet activity in these patients.
Abstract:
The etiology of cerebrovascular disease (CDV) 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 age- and sex-matched control group. The mean plasma beta-thromboglobulin (beta-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 less than 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p less than 0.01). However, the beta-T 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 less than 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 beta-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between beta-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.