Increased Platelet Activation in the Chronic Phase After Cerebral Ischemia and Intracerebral Hemorrhage

Abstract

Background and Purpose-Enhanced thromboxane (TX) biosynthesis has previously been reported in the acute phase after ischemic stroke. We investigated whether enhanced urinary excretion of 11-dehydro-TXB 2 , a noninvasive index of platelet activation, was present in the chronic phase after a transient ischemic attack (TIA) or stroke, including intracerebral hemorrhage. Methods-We obtained a single urinary sample from 92 patients between 3 and 9 months after onset of stroke or TIA. The urinary excretion of the major enzymatic metabolite of TXA 2 , 11-dehydro-TXB 2 , was measured by a previously validated radioimmunoassay. The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases. Results-Urinary 11-dehydro-TXB 2 averaged 294Ϯ139, 413Ϯ419, and 557Ϯ432 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracerebral hemorrhage, respectively; the values were higher in all subgroups (PϽ0.01) than that in control patients (119Ϯ66 pmol/mmol). Increased 11-dehydro-TXB 2 excretion was present in 59% of all patients, in 60% (PϽ0.001) of patients with TIA, in 56% (PϽ0.001) of patients with ischemic stroke, and in 73% (PϽ0.001) of patients with intracerebral hemorrhage. Atrial fibrillation, no aspirin use, and severity of symptoms at follow-up contributed independently to the level of 11-dehydro-TXB 2 excretion in a multiple linear regression analysis. Conclusions-Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persistent platelet activation, which is associated with atrial fibrillation and poor stroke outcome, can be substantially suppressed by aspirin treatment. (Stroke. 1999;30:546-549.)

The Increase of The Mean Platelet Volume in Patients With Intracerebral Haemorrhage

“…Bizim çalışmamızda ise İSK'lı hastaların OTH değeri sağlıklı kontrollere göre istatistiksel olarak anlamlı derecede yüksekti. İSK'nın etiyolojisinde yer alan HT, ateroskeroz, DM, gibi vasküler hastalıklarda OTH artışı bilinmektedir (14). Çalışmamız kanamayı takiben hastaların ilk 24 saatteki OTH değerini gösterdiğinden ve trombositlerin ömrü 8-10 gün arasında değiştiğinden İSK'lı hastalardaki OTH artışı bu hastalarda zeminde var olan vasküler bozukluğa ve trombosit fonksiyon bozukluğuna bağlı olabilir.…”

Platelet activation and inhibition in polycythemia vera and essential thrombocythemia

“…11 As shown in Figure 1, the urinary excretion rates of 11-dehydro-TXB 2 reported in untreated ET 7 and PV 8 patients are at least comparable to unstable angina 12 and higher than a variety of clinical settings at increased cardiovascular risk. [13][14][15][16][17][18][19] Moreover, a role for circulating immature platelets as contributors to cardiovascular events and/or poor antiplatelet drug response has been emerging in both ET 10 and non-MPN diseases. 20,21 Interestingly, immature platelets are increased in ET and have been associated with a higher rate of thrombosis independently of thrombocythosis.…”

Changes in platelet functional parameters and CD62 P expression in liver cirrhosis

“…Granula protein on the platelet surface (CD62P) has very high sensitivity and specificity to platelet activation; thus, it is regarded as a special index of platelet activation [10][11][12] . Platelets are formed by fragments of macrophage kytoplasm, and interact with mono-macrophages in the spleen.…”