Relationship between platelet aggregation and stroke risk after percutaneous coronary intervention: a PENDULUM analysis.

In patients undergoing percutaneous coronary intervention (PCI) with a stent, high on-treatment platelet reactivity may be associated with an increased risk of stroke. This post hoc analysis of the PENDULUM registry compared the risk of post-PCI stroke according to on-treatment P2Y12 reaction unit (PRU) values. Patients aged ≥ 20 years who underwent PCI were stratified by baseline PRU (at 12 and 48 h post-PCI) as either high (HPR, > 208), optimal (OPR, > 85 to ≤ 208), or low on-treatment platelet reactivity (LPR, ≤ 85). The incidences of non-fatal ischemic and non-ischemic stroke through to 12 months post-PCI were recorded. Almost all enrolled patients (6102/6267 [97.4%]) had a risk factor for ischemic stroke, and most were receiving dual antiplatelet therapy. Of the 5906 patients with PRU data (HPR, n = 2227; OPR, n = 3002; LPR, n = 677), 47 had a non-fatal stroke post-PCI (cumulative incidence: 0.68%, ischemic; 0.18%, non-ischemic stroke). Patients with a non-fatal ischemic stroke event had statistically significantly higher post-PCI PRU values versus those without an event (P = 0.037). The incidence of non-fatal non-ischemic stroke was not related to PRU value. When the patients were stratified by PRU ≤ 153 versus > 153 at 12-48 h post-PCI, a significant difference was observed in the cumulative incidence of non-fatal stroke at 12 months (P = 0.044). We found that patients with ischemic stroke tended to have higher PRU values at 12-48 h after PCI versus those without ischemic stroke.Clinical trial registration: UMIN000020332.

Study on coagulation profiles and platelet function in trauma-induced coagulopathy caused by three types of injury.

BACKGROUND: Traumatic coagulopathy is a major public health issue globally with undefined mechanisms. We established rat models of hemorrhagic shock (HS), multiple injury (MI) and traumatic brain injury (TBI) to investigate the diversity of traumatic coagulopathy, especially platelet dysfunction. METHODS: Seventy male SD rats were divided randomly into seven groups(n = 10): control, HS30min, HS3h, MI30min, MI3h, TBI30min and TBI3h. Plasma or whole blood was collected for conventional coagulation tests, thromboelastography and platelet mapping. X-ray, 7T magnetic resonance imaging and hematoxylin-eosin staining of injured tissues were conducted to confirm the injuries of rats model. RESULTS: The activated partial thromboplastin time (aPTT) prolonged significantly in HS30min and MI3h groups, compared with those in control (P = 0.0403 and P = 0.0076, respectively). R values decreased in HS30min and HS3h groups, compared with those in control (P < 0.0001 and P < 0.0001, respectively). The maximum amplitude (MA) were 71.8 ± 0.6 mm, 71.9 ± 0.5 mm, 71.8 ± 0.7 mm, 70.0 ± 0.7 mm, 72.6 ± 0.9 mm, 70.4 ± 0.9 mm in HS30min, HS3h, MI30min, MI3h, TBI30min and TBI3h groups respectively, which were lower than those in control (P = 0.0304, P = 0.0205, P = 0.0431, P = 0.0007 and P = 0.0066, respectively). The platelet counts were 539±46 × 109/L, 523±31 × 109/L, 629 ± 18 × 109/L and 636±20 × 109/L in HS30min, HS3h, MI3h and TBI3h groups respectively, which were lower than those in control (P = 0.0040, P = 0.0001, P = 0.0127 and P = 0.0232, respectively). The adenosine diphosphate (ADP) inhibition rate decreased in HS30min group, compared with that in control (P = 0.0355). While, ADP inhibition rate increased in HS3h and TBI3h groups (P = 0.0041 and P = 0.0433 vs. control, respectively). The arachidonic acid (AA) inhibition rate increased in MI30min and MI3h groups, compared with control (P = 0.0029 and P = 0.0185, respectively). CONCLUSION: These results demonstrated that it might be the failure of forming a strong clot instead of the prolonged clot time, which contributed to traumatic coagulopathy. The platelet dysfunctions might contribute to trauma-induced coagulopathy in different ways. The loss of platelets might be the main reason for HS-induced coagulopathy. While, AA-dependent pathway inhibition might account for MI-induced coagulopathy. ADP-dependent pathway inhibition might be the major contributor for TBI-induced coagulopathy.

Platelet-function analyzer closure times indicate shear stress-induced hemostatic abnormalities in patients with aortic valve stenosis and correlate with perioperative transfusion requirements.

BACKGROUND: Shear stress-induced hemostatic abnormalities are highly prevalent in patients with aortic valve stenosis. In this study, we determined closure times with a platelet-function analyzer (PFA-100, Dade Behring, Marburg, Germany) in patients admitted for aortic valve replacement to assess the correlation with the severity of aortic valve stenosis, blood loss, perioperative transfusion requirements, and need for re-thoracotomy. PATIENTS AND METHODS: Fifty consecutive patients (mean age [+/- SD] 68 +/- 9 years) were enrolled. Closure times of epinephrin/collagen and adenosine diphosphate (ADP)/collagen cartridges were determined at least ten days after discontinuation of antiplatelet medication and compared to those of healthy control subjects without medication. RESULTS: Closure times of epinephrin/collagen (210 +/- 69 sec vs. 140 +/- 50 sec, p < 0.0001) and ADP/collagen (145 +/- 58 sec vs. 108 +/- 45 sec, p < 0.0001) cartridges were prolonged in patients with aortic valve stenosis. Intraoperative transfusion of red blood cell units was associated with the closure times of epinephrin/collagen (r = 0.28, p = 0.04) and ADP/ collagen cartridges (r = 0.28, p = 0.04). Total transfusion of red blood cell units was associated with ADP/ collagen closure times (r = 0.31, p = 0.02), but not epinephrin/collagen closure times (r = 0.26, p = 0.07). No significant association of closure times with intraoperative, postoperative and total transfusion of fresh frozen plasma units was observed. CONCLUSIONS: Prolongation of closure times determined with a platelet-function analyzer is highly prevalent in patients with aortic valve stenosis and appears to reflect shear stress-induced hemostatic abnormalities. Since prolonged closure times are associated with increased perioperative transfusion of red blood cell units, the assay could significantly contribute to the identification of individuals at risk.