Liver cirrhosis is characterized by a long course that lasts between 15 and 20 years. The natural history of this disease depends mainly on the occurrence and progression of single complications which are today more fully understood and therefore more treatable. More specifically, those complications involving hemodynamic mechanisms have been extensively studied in recent years. Indeed, the mechanisms involved in the occurrence of sodium positive balance and ascites, with or without renal dysfunction, have been clarified. It is now possible to distinguish between two different stages in the presence of hemodynamic modifications. In the first stage, an increasing accumulation of water and sodium may occur, leading to an increase in total plasma flow. Subsequently, there is a period of vascular instability and finally, the progressive appearance of typical signs of hyperdynamic circulation. During the second stage, cardiac function may be modified and consequently profoundly altered. The early administration of diuretics (antialdosteronics) seems to be capable of modifying cardiac dysfunction, leading to a return towards a physiological status through a rapid increase in diuresis and natriuresis and a decrease in plasma volume.
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J Mol Med (Berl)
January 2025
Cardiovascular Surgery Department of The First Affiliated Hospital of Harbin Medical University, and Pharmacology Department of Pharmacy College of Harbin Medical University, Harbin, 150081, China.
Myocardial ischemia/reperfusion (IR) injury is a common adverse event in the clinical treatment of myocardial ischemic disease. Autosis is a form of cell death that occurs when autophagy is excessive in cells, and it has been associated with cardiac IR damage. This study aimed to investigate the regulatory mechanism of circRNA CDR1AS on autosis in cardiomyocytes under IR.
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January 2025
Division of Cardiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Myocyte disarray and fibrosis are underlying pathologies of hypertrophic cardiomyopathy (HCM) caused by genetic mutations. However, the extent of their contributions has not been extensively evaluated. In this study, we investigated the effects of genetic mutations on myofiber function and fibrosis patterns in HCM.
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January 2025
Cardiovascular Research Center, Rajaie Cardiovascular, Medical, and Research Center, University of Medical Sciences, Tehran, Iran.
Assessing myocardial viability is crucial for managing ischemic heart disease. While late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) is the gold standard for viability evaluation, it has limitations, including contraindications in patients with renal dysfunction and lengthy scan times. This study investigates the potential of non-contrast CMR techniques-feature tracking strain analysis and T1/T2 mapping-combined with machine learning (ML) models, as an alternative to LGE-CMR for myocardial viability assessment.
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January 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Road, Nanchang, 330006, Jiangxi, China.
The study aimed to elucidate the underlying pharmacological mechanism of the traditional Chinese medicine Pue in ameliorating myocardial ischemia-reperfusion injury (MIRI), a critical clinical challenge exacerbated by reperfusion therapy. In vivo MIRI and in vitro anoxia/reoxygenation (A/R) models were constructed. The results demonstrated that Pue pretreatment effectively alleviated MIRI, as manifested by diminishing the levels of serum CK-MB and LDH, mitigating the extent of myocardial infarction and enhancing cardiac functionality.
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January 2025
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Doxorubicin, a representative drug of the anthracycline class, is widely used in cancer treatment. However, Doxorubicin-induced cardiotoxicity (DIC) presents a significant challenge in its clinical application. Mitochondrial dysfunction plays a central role in DIC, primarily through disrupting mitochondrial dynamics.
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