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.
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http://dx.doi.org/10.1080/14017430902810911 | DOI Listing |
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 PDFAnn Transl Med
December 2024
Department of Cardiovascular Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
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.
Virol J
January 2025
Department of Pharmacotherapy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
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 PDFNat 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 PDFNat 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.
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