Association between bleeding and mortality among women and men with high-risk acute coronary syndromes: Insights from the Early versus Delayed, Provisional Eptifibatide in Acute Coronary Syndromes (EARLY ACS) trial
Kaul P.,University of Alberta |
Tanguay J.-F.,Montreal Heart Institute |
Newby L.K.,Duke Clinical Research Institute |
Hochman J.S.,New York University |
And 8 more authors.
American Heart Journal | Year: 2013
Background Female sex is an established risk factor for bleeding, which is an important safety end point in patients presenting with non-ST-segment elevation acute coronary syndromes (NSTE ACS). However, it is unknown whether the association between bleeding and mortality is modulated by sex in this patient population. Methods We examined the interaction between sex and bleeding and 30-day mortality outcomes among 2,975 women and 6,431 men with high-risk NSTE ACS enrolled in the EARLY ACS trial. The Global Utilization of Strategies to Open Occluded Arteries (GUSTO) criteria were used to identify moderate or severe bleeds. Results Women were older and had more comorbid disease compared with men. Bleeding rates were higher among women (8.2%) than among men (5.5%; P <.01). However, the association of bleeding and 30-day mortality was stronger among men (odds ratio 5.8, 95% CI 3.9-8.8) than among women (odds ratio 1.5, 95% CI 0.8-2.9; sex* bleeding interaction P <.01). Sex differences in the association of bleeding and mortality persisted in a landmark analysis of 120-hour survivors. Conclusions In a contemporary high-risk NSTE ACS cohort, women had higher bleeding rates than did men. Paradoxically, the association between bleeding and mortality was worse among men than among women. © 2013 Mosby, Inc.
Bogaert J.,Gasthuisberg University Hospitals Leuven |
Olivotto I.,Referral Center for Myocardial Diseases
Radiology | Year: 2014
Hypertrophic cardiomyopathy (HCM), the most common genetically transmitted cardiac disorder, has been the focus of extensive research over the past 50 years. HCM is a multifaceted disease with highly heterogeneous genetic background, phenotypic expression, clinical presentation, and long-term outcome. Though most patients have an indolent course with a life expectancy comparable to that of the general population, early diagnosis and accurate risk profiling are essential to identify the sizeable subset at increased risk of sudden cardiac death or disease progression and heart failure-related complications, requiring aggressive management options. Imaging has a central role in the diagnosis and prognostic assessment of HCM patients, as well as screening of potentially affected family members. In this context, magnetic resonance (MR) imaging has recently emerged as an ideal complement to transthoracic echocardiography. Its multiparametric approach, fusing spatial, contrast, and temporal resolution, provides the clinician with detailed characterization of the HCM phenotype and assessment of its functional consequences including causes and site of dynamic obstruction, presence and extent of myocardial perfusion abnormalities, and fibrosis. Moreover, MR is key in differentiating HCM from "phenocopies"-that is, hearts with similar morphology but profoundly different etiology, such as amyloid or Anderson-Fabry disease. Long term, the incremental information provided by MR is relevant to planning of septal reduction therapies, identification of the early stages of end-stage progression, and stratification of arrhythmic risk. The aim of this review is to depict the increasingly important role of MR imaging in relation to the complexity of HCM, highlighting its role in clinical decision making. © RSNA, 2014.
Dubois C.,Gasthuisberg University Hospitals Leuven |
Liu X.,Vlaams Institute for Biotechnology |
Claus P.,Gasthuisberg University Hospitals Leuven |
Marsboom G.,Vlaams Institute for Biotechnology |
And 19 more authors.
Journal of the American College of Cardiology | Year: 2010
Objectives: We compared biological repair after acute myocardial infarction (AMI) with selected porcine progenitor cell populations. Background: Cell types and mechanisms responsible for myocardial repair after AMI remain uncertain. Methods: In a blinded, randomized study, we infused autologous late-outgrowth endothelial progenitor cells (EPC) (n = 10, 34 ± 22 × 106 CD29-31-positive, capable of tube formation), allogeneic green fluorescent peptide-labeled mesenchymal stem cells (MSC) (n = 11, 10 ± 2 × 106 CD29-44-90-positive, capable of adipogenic and osteogenic differentiation), or vehicle (CON) (n = 12) in the circumflex artery 1 week after AMI. Systolic function (ejection fraction), left ventricular (LV) end-diastolic and end-systolic volumes, and infarct size were assessed with magnetic resonance imaging at 1 week and 7 weeks. Cell engraftment and vascular density were evaluated on postmortem sections. Results: Recovery of LV ejection fraction from 1 to 7 weeks was similar between groups, but LV remodeling markedly differed with a greater increase of LV end-systolic volume in MSC and CON (+11 ± 12 ml/m2 and +7 ± 8 ml/m2 vs. -3 ± 11 ml/m2 in EPC, respectively, p = 0.04), and a similar trend was noted for LV end-diastolic volume (p = 0.09). After EPC, infarct size decreased more in segments with >50% infarct transmurality (p = 0.02 vs. MSC and CON) and was associated with a greater vascular density (p = 0.01). Late outgrowth EPCs secrete higher levels of the pro-angiogenic placental growth factor (733 [277 to 1,214] pg/106 vs. 59 [34 to 88] pg/106 cells in MSC, p = 0.03) and incorporate in neovessels in vivo. Conclusions: Infusion of late-outgrowth EPCs after AMI improves myocardial infarction remodeling via enhanced neovascularization but does not mediate cardiomyogenesis. Endothelial progenitor cell transfer might hold promise for heart failure prevention via pro-angiogenic or paracrine matrix-modulating effects. © 2010 American College of Cardiology Foundation.
Dauwe D.F.,Gasthuisberg University Hospitals Leuven |
Nuyens D.,Gasthuisberg University Hospitals Leuven |
De Buck S.,Gasthuisberg University Hospitals Leuven |
Claus P.,Catholic University of Leuven |
And 12 more authors.
European Heart Journal Cardiovascular Imaging | Year: 2014
Aim Biological therapies for ischaemic heart disease require efficient, safe, and affordable intramyocardial delivery. Integration of multiple imaging modalities within the fluoroscopy framework can provide valuable information to guide these procedures. We compared an anatomo-electric method (LARCA) with a non-fluoroscopic electromechanical mapping system (NOGA®). LARCA integrates selective three-dimensional-rotational angiograms with biplane fluoroscopy. To identify the infarct region, we studied LARCA-fusion with pre-procedural magnetic resonance imaging (MRI), dedicated CT, or 18F-FDG-PET/CT. Methods and results We induced myocardial infarction in 20 pigs by 90-min LAD occlusion. Six weeks later, we compared peri-infarct delivery accuracy of coloured fluospheres using sequential NOGA®- and LARCA-MRI-guided vs. LARCA-CT- and LARCA-18F-FDG-PET/CT-guided intramyocardial injections. MRI after 6 weeks revealed significant left ventricular (LV) functional impairment and remodelling (LVEF 31 ± 3%, LVEDV 178 ± 15 mL, infarct size 17 ± 2% LV mass). During NOGA ®-procedures, three of five animals required DC-shock for major ventricular arrhythmias vs. one of ten during LARCA-procedures. Online procedure time was shorter for LARCA than NOGA® (77 ± 6 vs. 130 ± 3 min, P < 0.0001). Absolute distance of injection spots to the infarct border was similar for LARCA-MRI (4.8 ± 0.5 mm) and NOGA ® (5.4 ± 0.5 mm). LARCA-CT-integration allowed closer approximation of the targeted border zone than LARCA-PET (4.0 ± 0.5 mm vs. 6.2 ± 0.6 mm, P < 0.05). Conclusion Three-dimensional -rotational angiography fused with multimodal imaging offers a new, cost-effective, and safe strategy to guide intramyocardial injections. Endoventricular procedure times and arrhythmias compare favourably to NOGA®, without compromising injection accuracy. LARCA-based fusion imaging is a promising enabling technology for cardiac biological therapies. © 2014 Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: firstname.lastname@example.org.