“…Following aortic intimal tear, platelets are the initially recruited cellular components to adhere to the damaged vessel walls, followed by leukocyte adhesion [10,23], which forms thrombosis in the false lumen [11,24]. By bridging thrombosis and inflammation, activated platelets represent the thrombo-inflammatory status in the setting of aortic dissection [10,23,25].…”
Type A acute aortic dissection is a life-threatening vascular emergency because of its high morbidity and mortality. Platelet is a pivotal ingredient involved in the development of acute aortic dissection. In this study, we aimed to investigate whether mean platelet volume (MPV)/platelet count ratio predicts in-hospital complications and long-term mortality in type A acute aortic dissection. In this single-center and prospective cohort study, 106 consecutive patients with Stanford type A acute aortic dissection admitted to the hospital within 12 h after onset were recruited. The best cut-off value of MPV/platelet count ratio predicting all-cause mortality was determined by the receiver operator characteristic analysis. Patients were divided into high (H-MPV/platelet count) and low (L-MPV/platelet count) groups based on the cut-off value of 7.49 (10 fl/10/l). Patients were followed up for 3.5 years. Of the 106 acute aortic dissection patients, 71 (67.0%) died during the study period, with a median follow-up duration of 570 days. Compared to the L-MPV/platelet count group, patients with H-MPV/platelet count had a higher risk of in-hospital complications including hypotension, hypoxemia, myocardial ischemia/infarction, conscious disturbance, pericardial tamponade, paraplegia, and poor survival (all P < 0.05). In multivariable Cox regression models adjusted for potential confounders, MPV/platelet count ratio was positively associated with the hazard of all-cause mortality, irrespective of interventions either with medication only or urgent surgery, and the hazard ratios were 2.81 (95% confidence interval 1.28-4.48) for the H-MPV/platelet count group when taking L-MPV/platelet count group as the reference (P = 0.005). The MPV/platelet count ratio was a strong independent predictor for in-hospital complications and long-term mortality in patients with type A acute aortic dissection.
“…Following aortic intimal tear, platelets are the initially recruited cellular components to adhere to the damaged vessel walls, followed by leukocyte adhesion [10,23], which forms thrombosis in the false lumen [11,24]. By bridging thrombosis and inflammation, activated platelets represent the thrombo-inflammatory status in the setting of aortic dissection [10,23,25].…”
Type A acute aortic dissection is a life-threatening vascular emergency because of its high morbidity and mortality. Platelet is a pivotal ingredient involved in the development of acute aortic dissection. In this study, we aimed to investigate whether mean platelet volume (MPV)/platelet count ratio predicts in-hospital complications and long-term mortality in type A acute aortic dissection. In this single-center and prospective cohort study, 106 consecutive patients with Stanford type A acute aortic dissection admitted to the hospital within 12 h after onset were recruited. The best cut-off value of MPV/platelet count ratio predicting all-cause mortality was determined by the receiver operator characteristic analysis. Patients were divided into high (H-MPV/platelet count) and low (L-MPV/platelet count) groups based on the cut-off value of 7.49 (10 fl/10/l). Patients were followed up for 3.5 years. Of the 106 acute aortic dissection patients, 71 (67.0%) died during the study period, with a median follow-up duration of 570 days. Compared to the L-MPV/platelet count group, patients with H-MPV/platelet count had a higher risk of in-hospital complications including hypotension, hypoxemia, myocardial ischemia/infarction, conscious disturbance, pericardial tamponade, paraplegia, and poor survival (all P < 0.05). In multivariable Cox regression models adjusted for potential confounders, MPV/platelet count ratio was positively associated with the hazard of all-cause mortality, irrespective of interventions either with medication only or urgent surgery, and the hazard ratios were 2.81 (95% confidence interval 1.28-4.48) for the H-MPV/platelet count group when taking L-MPV/platelet count group as the reference (P = 0.005). The MPV/platelet count ratio was a strong independent predictor for in-hospital complications and long-term mortality in patients with type A acute aortic dissection.
“…AD is associated with platelet activation and coagulopathy, which may mark disease severity and could possibly lead to increased risk of bleeding [51]. Indeed, independent groups have reported that patients with AD presenting more extensive platelet activation and/or consumption show increased mortality.…”
Aortic dissection (AD) is a severe vascular disease associated with major morbidity and mortality. The diagnosis of AD requires the performance of urgent aortic imaging exams such as computed tomography angiography, but the decision to perform these exams now essentially relies on clinical judgment. Several studies have identified a range of potential biomarkers stemming from the aortic extracellular matrix (matrix metalloproteinases, TGF-β, soluble elastin fragments), vascular smooth muscle cells (smooth muscle myosin heavy chain, creatine kinase, calponin), coagulation (D-dimer, platelets) and inflammation (C-reactive protein), whose circulating levels increase in patients affected by AD. Biomarkers of AD could be potentially used to screen patients with compatible symptoms, to identify patients at higher risk of AD, to rule out AD in patients with non-high clinical probability of AD and/or to obtain prognostic stratification of affected patients. This review will summarize available data and discuss present and future perspectives of circulating biomarkers for the diagnosis and prognostic stratification of AD.
“…Patients with aortic aneurysms often show silent disseminated intravascular coagulation preoperatively
[1]. Impairment of coagulation may be caused by CPB and be further aggravated by hypothermic circulatory arrest
[2]. For example, the baseline plasma fibrinogen levels have been reported to decrease by 34% to 58% during CPB
[3,4].…”
BackgroundRepair of thoracic aortic aneurysm (TAA) is often associated with massive hemorrhage aggravated by dilutional coagulopathy with severe hypofibrinogenemia. Although only fresh frozen plasma (FFP) is available for acquired hypofibrinogenemia in Japan, the hemostatic effect of FFP has not been enough for dilutional coagulopathy in TAA surgery. There are increasing reports suggesting that fibrinogen concentrate may be effective in controlling perioperative bleeding and reducing transfusion requirements.MethodsWe retrospectively analyzed the hemostatic effect of fibrinogen concentrate compared with FFP in total 49 cases of elective TAA surgery. In 25 patients, fibrinogen concentrate was administered when the fibrinogen level was below 150 mg/dL at the cardiopulmonary bypass (CPB) termination. The recovery of fibrinogen level, blood loss, and transfused units during surgery were compared between cases of this agent and FFP (n = 24).ResultsWe observed rapid increases in plasma fibrinogen level and subsequent improvement in hemostasis by administration of fibrinogen concentrate after CPB termination. The average volume of total blood loss decreased by 64% and the average number of transfused units was reduced by 58% in cases of fibrinogen concentrate given, in comparison with cases of only FFP transfused for fibrinogen supplementation.ConclusionsIn patients showing severe hypofibrinogenemia during TAA surgery, timely administration of fibrinogen concentrate just after removal from CPB is effective for hemostasis, and therefore in reducing blood loss and transfused volumes.
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