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Mechanisms of physiological and pathological cardiac hypertrophy. Nakamura Michinari,Sadoshima Junichi Nature reviews. Cardiology Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. There are two types of hypertrophy: physiological and pathological. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure. Each form of hypertrophy is regulated by distinct cellular signalling pathways. In the past decade, a growing number of studies have suggested that previously unrecognized mechanisms, including cellular metabolism, proliferation, non-coding RNAs, immune responses, translational regulation, and epigenetic modifications, positively or negatively regulate cardiac hypertrophy. In this Review, we summarize the underlying molecular mechanisms of physiological and pathological hypertrophy, with a particular emphasis on the role of metabolic remodelling in both forms of cardiac hypertrophy, and we discuss how the current knowledge on cardiac hypertrophy can be applied to develop novel therapeutic strategies to prevent or reverse pathological hypertrophy. 10.1038/s41569-018-0007-y
The Microenvironment of the Pathogenesis of Cardiac Hypertrophy. Cells Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades' advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components. 10.3390/cells12131780
Perioperative considerations and anesthesia management in patients with obstructive sleep apnea undergoing ophthalmic surgery. Cok Oya Y,Seet Edwin,Kumar Chandra M,Joshi Girish P Journal of cataract and refractive surgery Obstructive sleep apnea (OSA) is a disorder characterized by breathing cessation caused by obstruction of the upper airway during sleep. It is associated with multiorgan comorbidities such as obesity, hypertension, heart failure, arrhythmias, diabetes mellitus, and stroke. Patients with OSA have an increased prevalence of ophthalmic disorders such as cataract, glaucoma, central serous retinopathy (detachment of retina, macular hole), eyelid laxity, keratoconus, and nonarteritic anterior ischemic optic neuropathy; and some might require surgery. Given that OSA is associated with a high incidence of perioperative complications and more than 80% of surgical patients with OSA are unrecognized, all surgical patients should be screened for OSA (eg, STOP-Bang questionnaire) with comorbidities identified. Patients suspected or diagnosed with OSA scheduled for ophthalmic surgery should have their comorbid conditions optimized. This article includes a review of the literature and highlights best perioperative anesthesia practices in the management of ophthalmic surgical patients with OSA. 10.1016/j.jcrs.2019.02.044
Case Report: Integrated echocardiographic assessment guided Liwen procedure for treating obstructive hypertrophic cardiomyopathy with ventricular aneurysm. Frontiers in cardiovascular medicine Hypertrophic cardiomyopathy (HCM) is a genetic myocardial disease, with an estimated incidence of 0.2%-6%, and is the main cause of sudden cardiac death (SCD) in young athletes. Left ventricular apical aneurysm (LVAA) is a rare subtype of HCM, accounting for about 5% of HCM patients, and has a higher incidence of cardiovascular adverse events. In cases of hypertrophic obstructive cardiomyopathy with LVAA (HOCM-LVAA) that do not respond adequately to optimized medical therapy, the echocardiography-guided percutaneous intra-myocardial septal radiofrequency ablation (PIMSRA, Liwen procedure) emerges as a promising and effective novel therapeutic approach. In this case report, we present for the first time a comprehensive application of echocardiographic techniques, including TTE, 2-D STE, and contrast enhancement, in the diagnosis, treatment, surgical guidance, and assessment of therapeutic outcomes in a case of HOCM-LVAA. 10.3389/fcvm.2023.1278457