Abstract
To clarify the role of platelets in cardiogenic embolism (CE), the authors studied plasma β-thromboglobulin (BTG) levels and computed tomographic (CT) findings in 31 patients with both CE and atrial fibrillation (Af). There were 11 males and 20 females, and their mean age was 77.5 ± 10.3 years. Fifty-three paired blood samples were simultaneously obtained from the internal jugular vein (A) and the antecubital vein (B) for measurement of BTG. The ΔBTG value was defined as A-B/B, which indicates activated platelets in the cerebral circulation, and the BTG (B) level denotes those in the systemic circulation. The data obtained from the 31 patients with CE and Af (CE/Af group) were compared with those of the following four groups; age-matched, healthy volunteers (control group, n=24); non-stroke patients with Af (Af group; n=25); patients with other than stroke (non-stroke group; n=25); and patients with chronic-phase cerebral thrombosis (Th group; n=44). Blood sampling was performed in the early acute phase (<3 days post-ictus), late acute phase (4-7 days post-ictus) or non-acute phase (>8 days post-ictus). The site and extent of infarction were determined by CT. The mean BTG (B) level (± SD) of the CE/Af group (78.7 ± 65.9 ng/ml) was significantly higher than that of the control group (39.9 ± 19.4 ng/ml), although considerable variability was observed. Even in the chronic phase of CE, the BTG (B) level was elevated 75.5 ± 66.3 ng/ml as it was in the Af group (65.7 ± 56.7 ng/ml). These findings suggest that the elevation of BTG (B) in the CE/Af group was due to the presence of Af. The mean ΔBTG values (± SD) in patients were 0.42 ± 0.70 (n=14), 0.14 ± 0.49 (n=7) and 0.22 ± 0.75 (n=28) in the early, late, and non-acute phases, respectively. Only in the early acute phase was the Δ BTG value higher than that of the non-stroke group (-0.04± 0.42), although it was lower than that of the Th group (2.20 ± 4.54). The majority of patients in the early acute phase and those with hemorrhagic infarction had temporarily increased ΔBTG values. No correlation between ΔBTG values and CT findings was observed in any phase of infarction. These findings suggest that in cardiogenic embolism, platelet activation occurs mainly in the heart, but that platelets can be activated in the cerebral circulation when there is a secondary thrombosis in the early acute phase or repair of damaged blood vessels at the site of hemorrhagic infarction is in progress. Therefore, it appears that the pathophysiological role of platelets differs in cardiogenic embolism and cerebral thrombosis.
