Background: This study examined whether the serum PON1 activity is different in patients with ischaemic dilated cardiomyopathy (IDCM) and nonischaemic dilated cardiomyopathy (NDCM) and the relation between the serum PON1 activity and serum pro-BNP levels.
Methods And Results: In this study, we enrolled 60 patients with left ventricular systolic failure (New York Heart Association [NYHA] class III-IV) and a left ventricular ejection fraction (EF) < 40% as determined by echocardiography and 30 healthy subjects. The patients with systolic heart failure were divided into two groups: patients with IDCM and patients with NDCM. Blood samples were obtained to measure the serum PON1 activity and the serum pro-BNP levels. The median serum PON1 activities were lower among the patients with IDCM or with NDCM compared with the control subjects (p < .001, p = .043, respectively). Compared with the control subjects, the patients with IDCM or with NDCM had higher serum pro-BNP levels (p < .001, p < .001, respectively). The serum PON1 activity was negatively correlated with the serum pro-BNP levels in patients with IDCM (r = -0.548, p < .001). The area under the ROC curve of the serum PON1 activity was 0.798. Using a serum PON1 activity of 201.3 U/L as a cut-off value, the sensitivity was 86.84% and specificity was 66.67% for the diagnosis of IDCM.
Conclusions: In this study, the serum PON1 activity was significantly reduced in the patients with IDCM or with NDCM compared with the control subjects. The serum PON1 activity of the patients with IDCM was negatively correlated with the serum pro-BNP levels.
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http://dx.doi.org/10.1080/00015385.2017.1351237 | DOI Listing |
J Adv Res
January 2025
School of Basic Medical Sciences, Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China. Electronic address:
Background: The genetic variants of LMNA cause an array of diseases that often affect the heart. LMNA-related cardiomyopathy exhibits high-penetrance and early-onset phenotypes that lead to late-stage heart failure or lethal arrhythmia. As a subtype of dilated cardiomyopathy and arrhythmogenic cardiomyopathy, LMNA-related cardiac dysfunction is resistant to existing cardiac therapeutic strategies, leaving a major unmet clinical need in cardiomyopathy management.
View Article and Find Full Text PDFChin Med
January 2025
School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 102488, China.
Background: Dilated cardiomyopathy (DCM) stands as one of the most prevalent and severe causes of heart failure. Inflammation plays a pivotal role throughout the progression of DCM to heart failure, while age acts as a natural predisposing factor for all cardiovascular diseases. These two factors often interact, contributing to cardiac fibrosis, which is both a common manifestation and a pathogenic driver of adverse remodeling in DCM-induced heart failure.
View Article and Find Full Text PDFProg Mol Biol Transl Sci
January 2025
Department of Microbiology, Gargi College, University of Delhi, New Delhi, India. Electronic address:
The CRISPR-Cas system has emerged as a revolutionary tool in genetic research, enabling highly precise gene editing and significantly advancing the field of cardiovascular science. This chapter provides a comprehensive overview of the latest developments in utilizing CRISPR-Cas technologies to investigate and treat heart diseases. It delves into the application of CRISPR-Cas9 for creating accurate models of complex cardiac conditions, such as hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and various arrhythmias, which are essential for understanding disease mechanisms and testing potential therapies.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Department of Radiation Oncology, Mays Cancer Center at UT Health San Antonio MD Anderson, Joe R. and Teresa Lozano Long School of Medicine, TX, USA. Electronic address:
Manganese superoxide dismutase (MnSOD/SOD2) is an essential mitochondrial enzyme that detoxifies superoxide radicals generated during oxidative respiration. MnSOD/SOD2 lysine 68 acetylation (K68-Ac) is an important post-translational modification (PTM) that regulates enzymatic activity, responding to nutrient status or oxidative stress, and elevated levels have been associated with human illness. To determine the in vivo role of MnSOD-K68 in the heart, we used a whole-body non-acetylation mimic mutant (MnSOD) knock-in mouse.
View Article and Find Full Text PDFCirc Heart Fail
January 2025
Assistance Publique Hopitaux de Paris (APHP), Pitié-Salpêtrière Hospital, Institute of Cardiology and Institute for Cardiometabolism and Nutrition, Paris, France (A.H., M.L., P. Charron, E.G.).
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