Browsing by Subject "CLOPIDOGREL"

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  • Metra, Marco; Mentz, Robert J.; Hernandez, Adrian F.; Heizer, Gretchen M.; Armstrong, Paul W.; Clausell, Nadine; Corbalan, Ramon; Costanzo, Maria Rosa; Dickstein, Kenneth; Dunlap, Mark E.; Ezekowitz, Justin A.; Howlett, Jonathan G.; Komajda, Michel; Krum, Henry; Lombardi, Carlo; Fonarow, Gregg C.; McMurray, John J. V.; Nieminen, Markku S.; Swedberg, Karl; Voors, Adriaan A.; Starling, Randall C.; Teerlink, John R.; O'Connor, Christopher M. (2016)
    A growing number of countries and geographical regions are involved in major clinical trials. Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure is the largest trial in acutely decompensated heart failure (HF) with patients from 5 geographical regions: North America (NA), Latin America (LA), Western Europe (WE), Central Europe (CE), and Asia-Pacific (AP). Data from the 5 geographical, areas were compared including baseline characteristics, medications, 30-day outcomes (mortality and mortality or HF hospitalization), and 180-day mortality. Of the 7,141 study patients, 3,243 (45.4%) were from NA (average of 15.2 patients/site), 1,762 (24.7%) from AP (28.4 patients/site), 967 (13.5%) from CE (20.2 patients/site), 665 (9.3%) from LA (17.1 patients/site), and 504 (7.1%) from WE (14.4 patients/site). There were marked differences in co-morbidities, clinical profile, medication use, length of stay, 30-day event rates, and 180-day mortality by region. Compared with NA, the adjusted risk for death or HF hospitalization at 30 days was significantly lower in CE (odds ratio [OR] 0.46, 95% CI 0.33 to 0.64), WE (OR 0.52 95% CI 0.35 to 0.75), and AP (OR 0.62 95% CI 0.48 to 0:79) and numerically lower in LA (OR 0.77, 95% CI 0.57 to 1.04) with similar results for 180-day mortality. In conclusion, in patients with acutely decompensated HF, major differences in baseline characteristics, treatments, length of the hospital stay, and 30-day HF rehospitalization rates, and 180-day mortality were found in patients enrolled from different, geographical areas. (C) 2016 Elsevier Inc. All rights reserved.
  • CENTER-TBI Participants Investigat; Böhm, Julia K.; Maegele, Marc; Palotie, Aarno; Pirinen, Matti; Ripatti, Samuli; Piippo-Karjalainen, Anna; Raj, Rahul (2021)
    Background Trauma-induced coagulopathy in patients with traumatic brain injury (TBI) is associated with high rates of complications, unfavourable outcomes and mortality. The mechanism of the development of TBI-associated coagulopathy is poorly understood. Methods This analysis, embedded in the prospective, multi-centred, observational Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study, aimed to characterise the coagulopathy of TBI. Emphasis was placed on the acute phase following TBI, primary on subgroups of patients with abnormal coagulation profile within 4 h of admission, and the impact of pre-injury anticoagulant and/or antiplatelet therapy. In order to minimise confounding factors, patients with isolated TBI (iTBI) (n = 598) were selected for this analysis. Results Haemostatic disorders were observed in approximately 20% of iTBI patients. In a subgroup analysis, patients with pre-injury anticoagulant and/or antiplatelet therapy had a twice exacerbated coagulation profile as likely as those without premedication. This was in turn associated with increased rates of mortality and unfavourable outcome post-injury. A multivariate analysis of iTBI patients without pre-injury anticoagulant therapy identified several independent risk factors for coagulopathy which were present at hospital admission. Glasgow Coma Scale (GCS) less than or equal to 8, base excess (BE) less than or equal to - 6, hypothermia and hypotension increased risk significantly. Conclusion Consideration of these factors enables early prediction and risk stratification of acute coagulopathy after TBI, thus guiding clinical management.
  • PLATO Investigators; Franchi, Francesco; James, Stefan K.; Lakic, Tatevik Ghukasyan; Lassila, Riitta (2019)
    Background-There are limited data on how the combination of diabetes mellitus (DM) and chronic kidney disease (CKD) affects cardiovascular outcomes as well as response to different P2Y(12) receptor antagonists, which represented the aim of the present investigation. Methods and Results-In this post hoc analysis of the PLATO (Platelet Inhibition and Patient Outcomes) trial, which randomized acute coronary syndrome patients to ticagrelor versus clopidogrel, patients (n=15 108) with available DM and CKD status were classified into 4 groups: DM+/CKD+ (n=1058), DM+/CKD- (n=2748), DM-/CKD+ (n=2160), and DM-/CKD- (n=9142). The primary efficacy end point was a composite of cardiovascular death, myocardial infarction, or stroke at 12 months. The primary safety end point was PLATO major bleeding. DM+/CKD+ patients had a higher incidence of the primary end point compared with DM-/CKD- patients (23.3% versus 7.1%; adjusted hazard ratio 2.22; 95% CI 1.88-2.63; P Conclusions-In acute coronary syndrome patients, a gradient of risk was observed according to the presence or absence of DM and CKD, with patients having both risk factors at the highest risk. Although the ischemic benefit of ticagrelor over clopidogrel was consistent in all subgroups, the absolute risk reduction was greatest in patients with both DM and CKD.
  • Song, Yun-Qing; Weng, Zi-Miao; Dou, Tong-Yi; Finel, Moshe; Wang, Ya-Qiao; Ding, Le-Le; Jin, Qiang; Wang, Dan-Dan; Fang, Sheng-Quan; Cao, Yun-Feng; Hou, Jie; Ge, Guang-Bo (2019)
    Magnolol, the most abundant bioactive constituent of the Chinese herb Magnolia officinalis, has been found with multiple biological activities, including anti-oxidative, anti-inflammatory and enzyme-regulatory activities. In this study, the inhibitory effects and inhibition mechanism of magnolol on human carboxylesterases (hCEs), the key enzymes responsible for the hydrolytic metabolism of a variety of endogenous esters as well as ester-bearing drugs, have been well-investigated. The results demonstrate that magnolol strongly inhibits hCE1-mediated hydrolysis of various substrates, whereas the inhibition of hCE2 by magnolol is substrate-dependent, ranging from strong to moderate. Inhibition of intracellular hCE1 and hCE2 by magnolol was also investigated in living HepG2 cells, and the results showed that magnolol could strongly inhibit intracellular hCE1, while the inhibition of intracellular hCE2 was weak. Inhibition kinetic analyses and docking simulations revealed that magnolol inhibited both hCE1 and hCE2 in a mixed manner, which could be partially attributed to its binding at two distinct ligand-binding sites in each carboxylesterase, including the catalytic cavity and the regulatory domain. In addition, the potential risk of the metabolic interactions of magnolol via hCE1 inhibition was predicted on the basis of a series of available pharmacokinetic data and the inhibition constants. All these findings are very helpful in deciphering the metabolic interactions between magnolol and hCEs, and also very useful for avoiding deleterious interactions via inhibition of hCEs.
  • Tornio, Aleksi; Palmer, Colin N. A.; Doney, Alex S. F. (2018)
  • Viikila, Juho; Nieminen, Tuomo; Tierala, Ilkka; Laine , Mika (2016)
    Backround: The optimal antithrombotic treatment during a primary percutaneous coronary intervention (pPCI) is not known. This single center registry study aims to assess the safety of a novel antithrombotic regimen combining enoxaparine and prasugrel at presentation, followed by bivalirudin at the catheterisation laboratory. Methods: All consecutive patients who underwent a pPCI were collected prospectively. The primary endpoint was major bleeding within 30 days. The secondary endpoints were a composite of major adverse cardiovascular events (MACE) consisting of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, a new target vessel revascularisation and all-cause mortality at 30 days. Results: Ninety-nine out of the total of 390 patients were treated according to the new regimen (protocol-treated group). The rest received other antithrombotic treatment (non-protocol-treated group). The protocol-treated group had a lower risk than the non-protocol-treated group according to the GRACE ischaemic (112 vs. 124, p = 0.002) and CRUSADE bleeding scores (21 vs. 28, p <0.0001). The incidences of bleeding were similar: severe GUSTO or TIMI bleeding occurred in 0 % of the protocol-treated group and in 1.0 and 0.3 %, respectively, of the other group (p = 0.311 for GUSTO and p = 0.559 for TIMI). The incidence of MACE in the groups was 6.1 and 10.7 %, respectively (p = 0.178). The respective incidences of all-cause mortality were 5.1 and 9.6 % (p = 0.158). Conclusions: Administration of the novel antithrombotic regimen seems to be safe.