261 research outputs found
New Clinical Classification for Ventricular Free Wall Rupture following Acute Myocardial Infarction
No full textVentricular free wall rupture (FWR) is a catastrophic complication after acute myocardial infarction (AMI). However, patients with FWR die of cardiac tamponade secondary to intrapericardial hemorrhage that can be treated if properly diagnosed. Unfortunately, FWR was still not diagnosed and classified quickly and accurately. The aim of this study was to present a new clinical classification for FWR. Seventy-eight patients with FWR after STEMI were enrolled in the study. We classified FWR, according to clinical situations after onset, into the cardiac arrest type, unstable type, and stable type. The cardiac arrest type was the most common type, accounting for about 83.3%. 90.8% of patients of this type were complicated with electromechanical dissociation at the time of FWR onset, and 100% of patients of this type died in the hospital. The unstable type was characterized by sudden clinical condition changes with moderate/massive pericardial effusion. In this study, 9.0% of patients were diagnosed as the unstable type. The average time from onset to death was 4.5 hours. This period was the “golden time” to rescue such patients. The stable types usually have stable hemodynamics, but may worsen, requiring rigorous detection of pericardial effusion and vital signs. In this study, 7.7% of patients were diagnosed as the stable type, and 83.5% of them survived in the hospital. The new clinical classification provides a basis for clinical diagnosis and treatment of FWR. The clinical application of the new classification is expected to improve the prognosis of FWR patients
GW28-e1058 Trimetazidine Prevents Cardiac Rupture in Mice with Myocardial Infarction by Suppressing Oxidative Stress
No full textRationale and design of the RIGHT trial: A multicenter, randomized, double-blind, placebo-controlled trial of anticoagulation prolongation versus no anticoagulation after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction
No full textInternational audienceFull text linksfull-text provider logoActionsFavoritesSharePage navigation Title & authors Abstract Similar articles Publication types MeSH terms Substances Related information LinkOut - more resourcesComparative StudyAm Heart J. 2020 Sep;227:19-30.doi: 10.1016/j.ahj.2020.06.005. Epub 2020 Jun 20.Rationale and design of the RIGHT trial: A multicenter, randomized, double-blind, placebo-controlled trial of anticoagulation prolongation versus no anticoagulation after primary percutaneous coronary intervention for ST-segment elevation myocardial infarctionYan Yan 1 , Xiao Wang 2 , Jincheng Guo 3 , Yongjun Li 4 , Hui Ai 5 , Wei Gong 6 , Bin Que 7 , Lei Zhen 8 , Jiapeng Lu 9 , Changsheng Ma 10 , Gilles Montalescot 11 , Shaoping Nie 12Affiliations PMID: 32663660 DOI: 10.1016/j.ahj.2020.06.005 AbstractBackground: Current guidelines recommend anticoagulation therapy during primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI). However, whether anticoagulation should be continued after pPCI has not been well investigated.Methods/design: The RIGHT trial is a prospective, multicenter, randomized, double-blind, placebo-controlled trial in STEMI patients treated with pPCI evaluating the prolongation of anticoagulation after the procedure. Patients are randomized in a 1:1 fashion to receive either prolonged anticoagulant or matching placebo (no anticoagulation) for at least 48 hours after the procedure. When randomized to anticoagulation prolongation, the patient is assigned to intravenous unfractionated heparin (UFH) or subcutaneous enoxaparin or intravenous bivalirudin (same drug and same regimen at each center). The primary efficacy endpoint is the composite of all-cause death, non-fatal myocardial infarction, non-fatal stroke, stent thrombosis (definite) or urgent revascularization (any vessel) at 30 days. The primary safety endpoint is major bleeding (BARC 3-5) at 30 days. Based on a superiority design and assuming a 35% relative risk reduction (from 7% to 4.5%), 2856 patients will be enrolled, accounting for a 5% drop-out rate (α = 0.05 and power = 80%).Conclusion: The RIGHT trial tests the hypothesis that post-procedural anticoagulation is superior to no anticoagulation in reducing ischemic events in STEMI patients undergoing pPCI
Deletion of vitamin D receptor leads to premature emphysema/COPD by increased matrix metalloproteinases and lymphoid aggregates formation
No full textDeficiency of vitamin D is associated with accelerated decline in lung function. Vitamin D is a ligand for nuclear hormone vitamin D receptor (VDR), and upon binding it modulates various cellular functions. The level of VDR is reduced in lungs of patients with chronic obstructive pulmonary disease (COPD) which led us to hypothesize that deficiency of VDR leads to significant alterations in lung phenotype that are characteristics of COPD/emphysema associated with increased inflammatory response. We found that VDR knock-out (VDR(-/-)) mice had increased influx of inflammatory cells, phospho-acetylation of nuclear factor-kappaB (NF-κB) associated with increased proinflammatory mediators, and up-regulation of matrix metalloproteinases (MMPs) MMP-2, MMP-9, and MMP-12 in the lung. This was associated with emphysema and decline in lung function associated with lymphoid aggregates formation compared to WT mice. These findings suggest that deficiency of VDR in mouse lung can lead to an early onset of emphysema/COPD because of chronic inflammation, immune dysregulation, and lung destruction
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