Hemostatic Function and Progressing Ischemic Stroke

Abstract

Background and Purpose-Early clinical progression of ischemic stroke is common and is associated with increased risk of death and dependency. We hypothesized that activation of the coagulation system is an important contributor in some cases of deterioration. We aimed to characterize alterations in circulating hemostatic markers in patients with progressing stroke. Methods-Consecutive acute ischemic stroke admissions were recruited. Progressing stroke was defined by deterioration in components of the Scandinavian Stroke Scale.

Correlation between Serum D-Dimer Level and Volume in Acute Ischemic Stroke

“…Barber et al 5) showed D-dimer can help physicians target interventions for preventing early neurological deterioration after acute ischemic stroke. However, some studies postulated that D-dimer assessment cannot be used as an AIS index, with the exception of the cardioembolic subtype 15,41) .…”

“…Plasmin splits the fibrin into FDP and D-dimers when the coagulation and fibrinolytic system is activated. A number of studies have shown that D-dimer, C-reactive protein, and other markers of hemostatic activation associate with a stroke diagnosis 5,18,19,[21][22][23]28,31,35,39) and with progression and death in acute ischemic stroke 5,6,10,30,44) . The report by Laskowitz et al 22) suggests that a biomarker panel may add valuable and time-sensitive diagnostic information to early stroke evaluation and rapid identification of patients with suspected stroke, which would expand the availability of time-limited treatment strategies.…”

“…Many studies have shown elevated D-dimer levels during the acute phase of stroke, which eventually fall 14,26,30,34) . However, previous studies have demonstrated only that plasma D-dimer levels predict a progressing ischemic stroke 4,5) . We studied the relationship between D-dimer level and infarction volume and the relationship between D-dimer change and clinical outcome in AIS.…”

Cytokines Associated with Increased Erythropoiesis in Sprague-Dawley Rats Administered a Novel Hyperglycosylated Analog of Recombinant Human Erythropoietin

“…Increased circulating vWF was identified in the AMG 114 high-dose group only, present 48 hr after a single dose of drug and at each subsequent time point through day 9. vWF is a well-described prothrombotic mediator of endothelial cell and PLTs in clot formation (van Galen et al 2012) and plays a critical role in formation of microvascular thrombosis in animal models of vascular injury (Ogunshola et al 2006;Patel et al 2008;Denis et al 1998). Increased circulating vWF from activated endothelial cells and/or PLTs (Rondaij et al 2006) has been documented in diverse patient populations with thrombotic complications (Tousoulis et al 2007;Adachi et al 2006;Mina, Favaloro, and Koutts 2007) and correlated with clinical deterioration of acute stroke patients (Barber et al 2004). While increased expression of vWF has been detected in vitro on endothelial cells and PLTs incubated with rHu-EPO (Fuste et al 2002), increased circulating vWF was not detected in chronic renal failure patients (Pawlak, Pawlak, and Mysliwiec 2007;Christensson, Danielson, and Lethagen 2001) or healthy human volunteers (Heinisch et al 2012) administered chronic or an acute dose of rHu-EPO, respectively.…”

Thrombin Generation and Atherothrombosis: What Does the Evidence Indicate?

“…In those with cardioembolic stroke, it appeared that F1.2 was minimally elevated ( P =0.03). A subsequent study by Barber et al showed that F1.2 and TAT were elevated in progressive stroke but only D‐dimer and arterial blood pressure appeared to be independent predictors of stroke 56. Furie et al did not find a correlation between the level of F1.2 and type of stroke 57.…”