Background: We investigated a correlation between electromechanical properties of the myocardium and response to CD34+ cell therapy in patients with chronic heart failure.
Methods And Results: We enrolled 40 patients with ischemic cardiomyopathy (ICM) and 40 with nonischemic dilated cardiomyopathy (DCM). All patients were in New York Heart Association functional class III and had a left ventricular ejection fraction (LVEF) <40%. CD34+ cells were mobilized by granulocyte colony-stimulating factor and collected via apheresis. Electroanatomic mapping was performed to define areas of myocardial scar and hibernation, and CD34+ cells were injected transendocardially in the hibernating areas. Patient were followed for 6 months; responders were defined as patients with LVEF increase of >5%. At baseline, the groups did not differ in sex, LVEF, creatinine, N-terminal pro-B-type natriuretic peptide or electroanatomic parameters (scar area: 53 ± 18% in ICM vs 55 ± 23% in DCM [P = .83]; hibernating area: 23 ± 13% vs 22 ± 12% [P = .56]). At 6 months we found similar rates of responders in both groups (60% in ICM vs 65% in DCM [P = .95]). When compared with nonresponders, responders had less myocardial scar (47 ± 17% vs 58 ± 15% [P = .003]).
Conclusions: In patients with chronic heart failure due to ICM and DCM we observed similar electroanatomic properties of the myocardium. In both groups, lower myocardial scar burden was associated with better clinical response to CD34+ cell therapy.
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http://dx.doi.org/10.1016/j.cardfail.2016.08.002 | DOI Listing |
Macromol Rapid Commun
January 2025
Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University, Chengdu, Sichuan, 610031, China.
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Hannover Medical School, Institute of Functional and Applied Anatomy, 30625 Hanover, Germany.
Small mammals have a higher heart rate and, relative to body mass (Mb), a higher metabolic rate than large mammals. In contrast, heart weight and stroke volume scale linearly with Mb. With mitochondria filling approximately 50% of a shrew cardiomyocyte - space unavailable for myofibrils - it is unclear how small mammals generate enough contractile force to pump blood into circulation.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biomedical Sciences, Dubai Medical College for Girls, Muhaisanah-1, Dubai, UAE.
Hypervitaminosis D leads to toxic effects, including hypercalcemia, which can cause severe damage to various organs. Fetuin-A, a glycoprotein with anti-inflammatory properties, may protect tissues from such damage. This study explores the role of Fetuin-A in mitigating hypervitaminosis D-induced damage in renal, hepatic, and cardiac tissues.
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Bioinspired Engineering and Biomechanics Center, Xi'an Jiaotong University, Xi'an 710049, China.
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View Article and Find Full Text PDFBioengineering (Basel)
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Translational Cardiothoracic Surgery Research Lab, Department of Cardiothoracic Surgery, Erasmus Medical Center, 3015 GD Rotterdam, The Netherlands.
Heart failure is characterized by intricate myocardial remodeling that impairs the heart's pumping and/or relaxation capacity, ultimately reducing cardiac output. It represents a major public health burden, given its high prevalence and associated morbidity and mortality rates, which continue to challenge healthcare systems worldwide. Despite advancements in medical science, there are no treatments that address the disease at its core.
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