Abstract
BackgroundChronic heart failure (CHF) is a global health problem. Increased sympathetic outflow, cardiac arrhythmogenesis and irregular breathing patterns have all been associated with poor outcomes in CHF. Several studies showed that activation of the renin-angiotensin system (RAS) play a key role in CHF pathophysiology. Interestingly, potassium (K+) supplemented diets showed promising results in normalizing RAS axis and autonomic dysfunction in vascular diseases, lowering cardiovascular risk. Whether subtle increases in dietary K+ consumption may exert similar effects in CHF has not been previously tested. Accordingly, we aimed to evaluate the effects of dietary K+ supplementation on cardiorespiratory alterations in rats with CHF.MethodsAdult male Sprague–Dawley rats underwent volume overload to induce non-ischemic CHF. Animals were randomly allocated to normal chow diet (CHF group) or supplemented K+ diet (CHF+K+ group) for 6 weeks. Cardiac arrhythmogenesis, sympathetic outflow, baroreflex sensitivity, breathing disorders, chemoreflex function, respiratory–cardiovascular coupling and cardiac function were evaluated.ResultsCompared to normal chow diet, K+ supplemented diet in CHF significantly reduced arrhythmia incidence (67.8 ± 15.1 vs. 31.0 ± 3.7 events/hour, CHF vs. CHF+K+), decreased cardiac sympathetic tone (ΔHR to propranolol: − 97.4 ± 9.4 vs. − 60.8 ± 8.3 bpm, CHF vs. CHF+K+), restored baroreflex function and attenuated irregular breathing patterns. Additionally, supplementation of the diet with K+ restores normal central respiratory chemoreflex drive and abrogates pathological cardio-respiratory coupling in CHF rats being the outcome an improved cardiac function.ConclusionOur findings support that dietary K+ supplementation in non-ischemic CHF alleviate cardiorespiratory dysfunction.
Highlights
Chronic heart failure (CHF) is a global health problem
CHF rats that received diet supplemented with K+ showed a significant reduction in the number of arrhythmias compared to CHF rats (31.0 ± 3.7 vs. 67.8 ± 15.1 events/hour, CHF+K+ vs. CHF, respectively; p < 0.05) (Fig. 1A, B)
Inspiratory phase (Ins) agreement with previous investigations, CHF rats displayed a heightened cardiac sympathetic drive compared to Sham healthy rats (ΔHR to propranolol: − 97.4 ± 9.4 vs. − 24.5 ± 3.6 bpm, CHF vs. Sham, respectively; p < 0.05) and this was normalized by the enriched-K+ diet in CHF
Summary
Cardiac arrhythmogenesis and irregular breathing patterns have all been associated with poor outcomes in CHF. The prevalence of non-ischemic CHF is increasing in the worldwide population and mortality remains high. Pathophysiological hallmarks of CHF patients include autonomic dysfunction characterized by cardiac sympathetic overactivity and parasympathetic withdrawal [5, 6], alterations in heart rate variability, and reduction of cardiac baroreflex sensitivity [7]. Enhanced cardiac sympathetic drive is a potent trigger for cardiac arrhythmogenesis which may lead to increase the risk of decompensation and mortality in CHF [8]. Almost ~ 50% of CHF patients display alterations in resting breathing patterns (i.e. apneas, hypopneas, periodic breathing) [9] that add more stress to the heart through chemoreflex activation of the sympathetic nervous system. Increased chemoreflex activation promotes the development of altered breathing patterns creating a vicious cycle that compromises further deterioration in cardiac function [10]
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