To evaluate the time course of reversed remodeling after pulmonary endarterectomy (PEA) in patients with chronic thromboembolic pulmonary hypertension(CTPEH), we studied 22 patients (age: 60 +/- 13 years) with MRI immediately before, 1 month, 3 months, and 6 months after PEA. MRI included assessment of biventricular function, aortic and pulmonary artery(PA) flow, and right ventricular (RV) overload using the ratio of RV-to-biventricular diameter. Except in one patient, who died 2 months post-surgery, clinical improvement occurred early after PEA (NYHA class: 3.3 +/- 0.6 to 1.5 +/- 0.8, p < 0.0001) with a decrease of systolic pulmonary artery pressures (79 +/- 14 to 44 +/- 14 mmHg, p < 0.0001). At 1 month post PEA, RV end-diastolic volumes decreased (198 +/- 72 to 137 +/- 59 ml, p < 0.0001), and the RV ejection fraction (EF) improved (31 +/- 9 to 47 +/- 10%, p < 0.0001). No further significant improvement in pulmonary pressures or RV function occurred at 3 months or 6 months. Although no significant change was found in LV volumes or function, aortic flow increased early after surgery. PEA had only a beneficial effect on right PA flow. RV overload decreased early after PEA (ratio RV-to-biventricular diameter: before: 0.67 +/- 0.04, after: 0.54 +/- 0.06, p < 0.0001), showing a good correlation with the improvement in RVEF (r = 0.7, P < 0.0001). In conclusion, reversed cardiac remodeling occurs early after PEA, to slow down after 1 month. At 6 months, cardiac remodeling is incomplete as witnessed by low-normal RV function and residually elevated PA pressures.
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http://dx.doi.org/10.1007/s00330-007-0829-1 | DOI Listing |
Front Cardiovasc Med
January 2025
Department of Cardiovascular Medicine, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
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December 2024
State/National Key Laboratory of Biotherapy, Sichuan University, Chengdu, Sichuan, 610000, P. R. China.
In this study, we integrated transcriptomic and metabolomic analyses to achieve a comprehensive understanding of the underlying mechanisms of diabetic cardiomyopathy (DCM) in a diabetic rat model. Functional and molecular characterizations revealed significant cardiac injury, dysfunction, and ventricular remodeling in DCM. A thorough analysis of global changes in genes and metabolites showed that amino acid metabolism, especially the breakdown of branched-chain amino acids (BCAAs) such as valine, leucine, and isoleucine, is highly dysregulated.
View Article and Find Full Text PDFESC Heart Fail
January 2025
School of Clinical Medicine, Fujian Medical University, Department of Cardiology, Affiliated Hospital of Putian University, Putian, China.
Purpose: Vericiguat, a soluble guanylate cyclase (sGC) stimulator, has been demonstrated effective in improving prognosis of patients with heart failure with reduced ejection fraction. However, there are limited data concerning the effect of vericiguat in patients with doxorubicin (DOX)-induced cardiomyopathy (DIC). In this study, we investigated the effects of vericiguat on cardiac structure and function in rats with DIC as well as their potential mechanisms of action.
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January 2025
Department of Pharmacology (SKLFZCD, State Key Laboratory-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin, 150081, China.
Diabetic cardiomyopathy (DCM) is a medical condition characterized by cardiac remodeling and dysfunction in individuals with diabetes mellitus. Sarcoplasmic reticulum (SR) and mitochondrial Ca overload in cardiomyocytes have been recognized as biological hallmarks in DCM; however, the specific factors underlying these abnormalities remain largely unknown. In this study, we aimed to investigate the role of a cardiac-specific long noncoding RNA, D830005E20Rik (Trdn-as), in DCM.
View Article and Find Full Text PDFEuropace
January 2025
Department of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Ibrutinib, a widely used anti-cancer drug, is known to significantly increase the susceptibility to atrial fibrillation (AF). While it is recognized that drugs can reshape the gut microbiota, influencing both therapeutic effectiveness and adverse events, the role of gut microbiota in ibrutinib-induced AF remains largely unexplored. Utilizing 16S rRNA gene sequencing, fecal microbiota transplantation, metabonomics, electrophysiological examination, and molecular biology methodologies, we sought to validate the hypothesis that gut microbiota dysbiosis promotes ibrutinib-associated AF and to elucidate the underlying mechanisms.
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