Objective: This prospective study aimed to investigate the myocardial energy metabolism in severe mitral regurgitation (MR) and explore its effect on postoperative differentiation of ejection fraction (EF).
Methods: A total of 85 patients with severe MR were prospectively enrolled from October 2018 to June 2019. During the study period, a total of 50 patients underwent mitral valve surgery and 49 patients were finally enrolled due to 1 missing data. Left ventricular function, circumferential end-systolic stress (cESS), and myocardial energy expenditure (MEE) were measured by transthoracic echocardiography preoperatively and 3 months after surgery. Patients were divided into 2 groups according to absolute difference of postoperative differentiation of EF.
Results: Nine patients underwent mitral valve repair and 40 underwent prosthetic valve replacement. Patients with reduced EF had higher MEE demonstrated with cESS and MEE. Negative correlation between preoperative EF and N-terminal pro-brain natriuretic peptide (NT-proBNP), cESS, MEEs, and MEEm and positive correlation between preoperative EF and effective regurgitant orifice area were found. Complications occurred in 12 patients during hospitalization. Basal NT-proBNP, left atrium (LA), and cESS were significantly higher in postoperatively decreased EF group. Taking into consideration the covariates of multiple logistic regression analysis, LA and cESS were found to be independent predictors of EF reduction postoperatively.
Conclusion: Higher LA and cESS are independent predictors of postoperative EF reduction. Preoperative high end-systolic stress could predict postoperative EF reduction and hence could be helpful for determining the timing of mitral valve surgery. Although MEE was higher in postoperatively decreased EF group, it did not reach statistical significance.
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http://dx.doi.org/10.14744/AnatolJCardiol.2020.03835 | DOI Listing |
J Cell Mol Med
December 2024
Institute of Cardiovascular Surgical Diseases, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Despite improvements in interventional techniques leading to faster myocardial reperfusion postmyocardial infarction, there has been a significant rise in the occurrence of myocardial ischaemia/reperfusion injury (MI/RI). A deeper understanding of the underlying mechanisms of MI/RI could offer a crucial approach to reducing myocardial damage and enhancing patient outcomes. This study examined the myocardial protective properties of puerarin (PUE) in the context of MI/RI using hypoxia/reoxygenation (H/R) or ischaemia/reperfusion (I/R) injury models were employed in H9c2 cells and C57BL/6 mice.
View Article and Find Full Text PDFMetabolites
November 2024
Division of Cardiology, Department of Internal Medicine, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul 05030, Republic of Korea.
Metabolic syndrome (MetS), a cluster of metabolic dysregulations, is recognized as a significant risk factor for the development of heart failure (HF). The pathophysiological mechanisms linking MetS to HF are complex and multifaceted, with the components of MetS contributing to cardiac deterioration through impaired myocardial energy metabolism, increased inflammation, and endothelial dysfunction. Numerous clinical studies have confirmed the relationship between MetS and HF.
View Article and Find Full Text PDFWound Repair Regen
December 2024
Department of Zoology, Trivenidevi Bhalotia College, Raniganj, West Bengal, India.
Hypoxia-mediated cardiac tissue injury and its repair or regeneration are one of the major health management challenges globally. Unlike mammals, lower vertebrate species such as zebrafish (Danio rerio) represent a natural model to study cardiac injury, repair and regeneration. Thyroxine (T3) has been hypothesised to be one of the endocrine factors responsible for the evolutionary trade-off for acquiring endothermy and regenerative capability in higher vertebrates.
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
Department of Cardiology, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Introduction: Patients with acute myocardial infarction (AMI) are at high risk of progressing to heart failure (HF). Recent research has shown that lipid droplet-related genes (LDRGs) play a crucial role in myocardial metabolism following MI, thereby influencing the progression to HF.
Methods: Weighted gene co-expression network analysis (WGCNA) and differential expression gene analysis were used to screen a transcriptome dataset of whole blood cells from AMI patients with (AMI HF, = 16) and without progression (AMI no-HF, = 16).
Small
December 2024
Cardiovascular Hospital, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, 430060, P. R. China.
The occurrence of myocardial infarction (MI)-induced malignant ventricular arrhythmias (VAs) is closely associated with the hyperactivation of left stellate ganglion (LSG). Proinflammatory M1 macrophage is reported to aggravate sympathetic overactivation and cause VAs. Therefore, the depletion of M1 macrophage is anticipated to inhibit LSG overactivation and alleviate MI-induced VAs.
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