Usefulness of the measurement of plasma beta-thromboglobulin (beta-TG) in cerebrovascular disease.

Abstract

The plasma concentration of the platelet-specific protein beta-thromboglobulin (beta-TG) was measured in 39 normal subjects and 568 patients of neurological diseases. The beta-TG RIA commercially available KIT was also evaluated. Abnormally high plasma levels of beta-TG were demonstrated in groups of ischemic or obstructive cerebrovascular diseases as compared with that of normal subjects. The highest concentrations were found in 8 patients with Moya-Moya disease, (mean concentration of beta-TG was 204.4 ng/ml), completed stroke at an acute stage was next (mean beta-TG level was 194.8 +/- 70.8 ng/ml). On the other hand, many hemorrhagic cerebro-vascular diseases or other neurological diseases such as brain tumors, hydrocephalus, etc. do not show elevated beta-TG levels. In many patients with ischemic or obstructive cerebro-vascular diseases treated with anti-platelet drugs such as Aspirin, Dipyridamole, Bencyclane or Ticlopidine, a significant fall in plasma concentration of beta-TG was chronologically demonstrated. The measurement of plasma beta-TG concentration may be useful not only in the diagnosis of ischemic or obstructive cerebro-vascular disorders but also in judging the efficacy of anti-platelet therapies and prognosis.

Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation.

“…31 The high concentrations of vWF:Ag and factor VIII:C and low concentrations of prekallikrein in the NVAF groups are consistent with the findings in previous studies of ischemic cerebrovascular disease. 32^3 The fibrinolytic system seemed to be less involved in this elderly population with stroke than in young patients with stroke or myocardial infarction.…”

Platelet reactivity is not associated with recurrent cardiovascular events in men with a history of myocardial infarction: a cohort study

“…Our findings in a cohort of men who survived a first MI do not confirm the notion that increased basal platelet reactivity increases the risk of recurrent cardiovascular events. This important negative finding contradicts previous studies which suggested that these inflammatory markers play a role in the development of first and recurrent cardiovascular events [12][13][14][15][16][17]. Regarding the beta-thromboglobulin NAP-2, our findings are in line with the recent study of Berent et al [20], in which no difference in the recurrence of cardiovascular events was found between patients with low and high beta-thromboglobulin levels.…”

“…Regarding the beta-thromboglobulin NAP-2, our findings are in line with the recent study of Berent et al [20], in which no difference in the recurrence of cardiovascular events was found between patients with low and high beta-thromboglobulin levels. A possible explanation for the absence of an association between platelet reactivity markers and recurrent cardiovascular events in our study is that our study population represented a group of stable patients with chronic cardiovascular disease, whereas patients in previous studies were studied in an acute setting [13][14][15][16][17]. However, platelet inflammatory markers might play a more dominant role in the development of cardiovascular events in stable patients with a low prevalence of classic risk factors [12].…”

“…Three of these chemokines are NAP-2 (neutrophilactivating peptide-2), which is an activation product of CXCL7 (CXC chemokine ligand 7, also known as precursor of beta-thromboglobulin), CXCL4 (CXC chemokine ligand 4, also known as platelet factor 4) and RANTES (regulated on activation, normal T cell expressed and secreted), which modulates monocytes involved in the progression of atherosclerotic plaques [6]. We measured NAP-2, CXCL-4 and RANTES because these markers were studied previously in relation to cardiovascular disease and serve as a marker of basal platelet activity [6][7][8][9][10][11][12][13][14][15][16][17]. We hypothesized that increased basal activity of these platelet markers increase the risk of a recurrent cardiovascular event.…”

Effects of Anticoagulation Intensity on Hemostatic Markers in Patients With Non-Valvular Atrial Fibrillation

“…4 Many studies have shown no significant changes in PF4 or TG with aspirin, [25][26][27] a consistent finding with the present results, but some studies have reported a significant reduction of TG with aspirin. 28,29 A possible explanation for the lack of significant decreases in PF4 and TG by antiplatelet treatment may be that different pathways activate the release of PF4 and TG and the inhibition of one pathway may not be enough to reduce the plasma concentrations of PF4 and TG. 30 In addition to fibrin generation, platelet activation and aggregation have an important role in the process of thrombogenesis.…”