Arrhythmogenic mechanisms of obstructive sleep apnea in heart failure patients

Abstract

Heart failure (HF) affects 23 million people worldwide and results in 300000 annual deaths. It is associated with many comorbidities, such as obstructive sleep apnea (OSA), and risk factors for both conditions overlap. Eleven percent of HF patients have OSA and 7.7% of OSA patients have left ventricular ejection fraction <50% with arrhythmias being a significant comorbidity in HF and OSA patients. Forty percent of HF patients develop atrial fibrillation (AF) and 30%-50% of deaths from cardiac causes in HF patients are from sudden cardiac death. OSA is prevalent in 32%-49% of patients with AF and there is a dose-dependent relationship between OSA severity and resistance to anti-arrhythmic therapies. HF and OSA lead to various downstream arrhythmogenic mechanisms, including metabolic derangement, remodeling, inflammation, and autonomic imbalance. (1) Metabolic derangement and production of reactive oxidative species increase late Na+ currents, decrease outward K+ currents and downregulate connexin-43 and cell-cell coupling. (2) remodeling also features downregulated K+ currents in addition to decreased Na+/K+ ATPase currents, altered Ca2+ homeostasis, and increased density of If current. (3) Chronic inflammation leads to downregulation of both Nav1.5 channels and K+ channels, altered Ca2+ homeostasis and reduced cellular coupling from alterations of connexin expression. (4) Autonomic imbalance causes arrhythmias by evoking triggered activity through increased Ca2+ transients and reduction of excitation wavefront wavelength. Thus, consideration of these multiple pathophysiological pathways (1-4) will enable the development of novel therapeutic strategies that can be targeted against arrhythmias in the context of complex disease, such as the comorbidities of HF and OSA.

Bisphosphonates and atrial fibrillation: revisiting the controversy

“…49 A recent prospective study showed a significant association between BP use and the prevalence of nocturnal AF, the odds ratio of which was even higher in the subset of men with moderate-to-severe sleep disordered breathing (SDB). 50 As SDBs are known to be associated with arrhythmias, 51 this finding may highlight that sufferers of SDB should be prescribed BPs with caution.…”

“…Oxidative stress is in turn associated with proarrhythmic changes both at the anatomical level in terms of remodeling 64 and at the level of ion channel and gap junction functional alteration. 51 The latter includes increased late Na + currents, decreased rectifier K + currents, and reduced intercellular connectivity through gap junction connexins. 51 Ultimately, these changes facilitate the development of both arrhythmic triggers and substrates.…”

Kalium Nitrat (KNO3): Karakteristik Senyawa dan Transpor Ion

“…KNO3(1-3) merupakan suatu senyawa garam yang disusun oleh kation K + dan anion NO3 -. Senyawa (4,5) ini bersifat elektrolit kuat dan merupakan suatu sumber nitrogen paling penting dialam, biasanya kalium nitrar sering disebut sebagai sendawa chili. Karena bersifat elektrolit kuat yang mudah terionisasi menjadi ion-ion, kalium nitrat memiliki kelarutan yang tinggi di dalam air, dengan keadaan 0 0 C dalam 1L air kalim nitrat yang larut dapat mencapai 133g, namun kelarutannya tidak sebesar NaNO3 dengan kondisi yang sama (89,(91)(92).…”

Circular RNA Expression Profiles in Plasma from Patients with Heart Failure Related to Platelet Activity

“…Heart failure (HF), often known as congestive HF, occurs when the heart fails to properly pump sufficient blood to the whole body. HF is a major public health concern and is a leading cause of morbidity and mortality worldwide, affecting over 23 million worldwide and resulting in 300,000 annual deaths [1,2]. Accurate and timely diagnosis of HF is essential to ensure appropriate treatment for patients.…”