Background: Detecting myocardial ischemia in hemodialysis patients is crucial given the high incidence of silent ischemia and the high cardiovascular mortality rates. Abnormal myocardial fatty acid metabolism as determined by imaging with (123)I-labeled BMIPP (β-methyl iodophenyl-pentadecanoic acid) might be associated with cardiac-derived death in hemodialysis patients.
Study Design: Prospective observational study.
Setting & Participants: Asymptomatic hemodialysis patients with one or more cardiovascular risk factors, but without known coronary artery disease, were followed up for 3 years at 48 Japanese hospitals (406 men, 271 women; mean age, 64 years).
Predictor: Baseline BMIPP summed scores semiquantified using a 17-segment 5-point system (normal, 0; absent, 4).
Outcomes: Cardiac-derived death, including cardiac and sudden death.
Measurements: HRs were estimated using a Cox model for associations between BMIPP summed scores and cardiac-derived death, adjusting for potential confounders of age, sex, body mass index, dialysis duration, and cardiovascular risk factors.
Results: Rates of all-cause mortality and cardiac-derived death were 18.5% and 6.8%, respectively. Cardiac-derived death (acute myocardial infarction [n = 10], congestive heart failure [n = 13], arrhythmia [n = 2], valvular heart disease [n = 1], and sudden death [n = 20]) accounted for 36.8% of all-cause deaths. Cardiac-derived death (n = 46) was associated with age, history of heart failure, and BMIPP summed scores of 4 or higher (HR, 2.9; P < 0.001). Three-year cardiac-derived death-free survival rates were 95.7%, 90.6%, and 78.8% when BMIPP summed scores were 3 or lower, 4-8, and 9 or higher, respectively. BMIPP summed score also was a predictor of all-cause death (HR, 1.6; P = 0.009).
Limitations: Sudden death of unknown cause was considered to have been cardiac derived, although a coronary origin was not confirmed.
Conclusions: Abnormal myocardial fatty acid metabolism is associated with cardiac-derived death in hemodialysis patients. BMIPP single-proton emission computed tomography appears clinically useful for predicting cardiac-derived death in this population.
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http://dx.doi.org/10.1053/j.ajkd.2012.09.017 | DOI Listing |
J Nanobiotechnology
July 2024
Research Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, 150 Jimo Rd, Pudong, Shanghai, 200092, China.
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February 2022
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, U.K.
Myocardial infarction is a leading cause of death globally due to the inability of the adult human heart to regenerate after injury. Cell therapy using cardiac-derived progenitor populations emerged about two decades ago with the aim of replacing cells lost after ischaemic injury. Despite early promise from rodent studies, administration of these populations has not translated to the clinic.
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Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan 430060, China. Electronic address:
Meteorin-like (METRNL) protein is a newly identified myokine that functions to modulate energy expenditure and inflammation in adipose tissue. Herein, we aim to investigate the potential role and molecular basis of METRNL in doxorubicin (DOX)-induced cardiotoxicity. METRNL was found to be abundantly expressed in cardiac muscle under physiological conditions that was decreased upon DOX exposure.
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San Diego Heart Research Institute, San Diego State University, 5500 Campanile Drive, San Diego, CA, 92182, USA.
Cellular therapy to treat heart failure is an ongoing focus of intense research, but progress toward structural and functional recovery remains modest. Engineered augmentation of established cellular effectors overcomes impediments to enhance reparative activity. Such 'next generation' implementation includes delivery of combinatorial cell populations exerting synergistic effects.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!