Objective: Morbid obesity is increasingly observed in patients being evaluated for heart transplantation and represents a relative contraindication. We sought to evaluate the influence of pre-transplant obesity on morbidity and mortality after heart transplantation.

Design: We retrospectively reviewed 90 consecutive patients with preoperative obesity (BMI > or = 30) and 90 age matched patients with normal weight (BMI 19 - 26) who underwent heart transplantation at our institution between January 1997 and December 2005.

Results: Morbidly obese patients experienced higher rates of pre-transplant diabetes (29% vs 15%, p < 0.05) and prolonged waiting time before transplantation (191.4+/-136.1 vs 117.4+/-143.2 days, p < 0.001). There were no significant differences in post-operative complications including rejection and major and minor infections. There was no difference in actuarial survival between the obese and control groups after a mean follow-up of 4.26+/-2.95 years (p = 0.513, log-rank statistic 0.452). Causes of death did not differ. Cox proportional hazard analysis revealed increased association of peripheral vascular disease (HR 31.718, p = 0.001), and pre operative inotropic support (HR 33.725, p = 0.013) with increased mortality in the obese group.

Conclusions: This study suggests morbid obesity does not affect survival or rates of infection and rejection after heart transplantation.

Download full-text PDF

Source
http://dx.doi.org/10.1080/14017430902810911DOI Listing

Publication Analysis

Top Keywords

heart transplantation
16
pre-transplant obesity
8
morbid obesity
8
heart
5
transplantation
5
obesity heart
4
transplantation predictors
4
predictors worse
4
worse outcomes?
4
outcomes? objective
4

Similar Publications

Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.

J Clin Invest

January 2025

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.

The pathogenesis of thoracic aortic aneurysm (TAA) in Marfan syndrome (MFS) is generally attributed to vascular smooth muscle cell (VSMC) pathologies. However, the role of immune cell-mediated inflammation remains elusive. Single-cell RNA sequencing identified a subset of CX3CR1+ macrophages mainly located in the intima in the aortic roots and ascending aortas of Fbn1C1041G/+ mice, further validated in MFS patients.

View Article and Find Full Text PDF

Background: Patients with end-stage kidney disease (ESKD) are at high risk for coronary artery disease. We investigate the trends and outcomes of percutaneous coronary intervention (PCI) for stable ischemic heart disease (SIHD) in patients with ESKD.

Methods: We utilized the United States Renal Data System [2010-2018] to include adult patients with ESKD on dialysis for at least 3 months who underwent PCI for SIHD.

View Article and Find Full Text PDF

Introduction: Organ transplant recipients face a substantial risk of developing posttransplant lymphoproliferative disorders (PTLD). In over 90% of cases with B-cell PTLD following solid organ transplantation, the Epstein-Barr virus (EBV) genome is promptly identified, usually within the initial year. A continuing discussion revolves around the efficacy of antiviral prophylaxis in mitigating the incidence of PTLD in solid organ transplant (SOT) patients.

View Article and Find Full Text PDF

Donor-derived GD2-specific CAR T cells in relapsed or refractory neuroblastoma.

Nat Med

January 2025

Department of Hematology/Oncology, Cell and Gene Therapy, Scientific Institute for Research, Hospitalization and Healthcare (IRCCS), Bambino Gesù Children's Hospital, Rome, Italy.

Allogeneic chimeric antigen receptor (CAR) T cells targeting disialoganglioside-GD2 (ALLO_GD2-CART01) could be a therapeutic option for patients with relapsed or refractory, high-risk neuroblastoma (r/r HR-NB) whose tumors did not respond to autologous GD2-CART01 or who have profound lymphopenia. We present a case series of five children with HR-NB refractory to more than three different lines of therapy who received ALLO_GD2-CART01 in a hospital exemption setting. Four of them had previously received allogeneic hematopoietic stem cell transplantation.

View Article and Find Full Text PDF

The highly conserved PIWI-interacting RNA CRAPIR antagonizes PA2G4-mediated NF110-NF45 disassembly to promote heart regeneration in mice.

Nat Cardiovasc Res

January 2025

Department of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology at College of Pharmacy (The Key Laboratory of Cardiovascular Research, Ministry of Education; National Key Laboratory of Frigid Zone Cardiovascular Diseases), Harbin Medical University, Harbin, China.

Targeting the cardiomyocyte cell cycle is a promising strategy for heart repair following injury. Here, we identify a cardiac-regeneration-associated PIWI-interacting RNA (CRAPIR) as a regulator of cardiomyocyte proliferation. Genetic ablation or antagomir-mediated knockdown of CRAPIR in mice impairs cardiomyocyte proliferation and reduces heart regenerative potential.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!