Finally, a growing body of evidence suggests that hyperkalemia might negatively impact outcomes in the long term in patients with chronic heart failure or kidney failure through underdosing or withholding of cardiovascular medication (e.g. renin-angiotensin-aldosterone system inhibitors).
The underlying mechanism for clinical and biochemical manifestations of chronic heart failure (HF) may be due in part to neurohumoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems in the periphery and the brain.
Effect of neprilysin inhibition on renal function in patients with type 2 diabetes and chronic heart failure who are receiving target doses of inhibitors of the renin-angiotensin system: a secondary analysis of the PARADIGM-HF trial.
Impact of Hyperkalemia and Worsening Renal Function on the Use of Renin Angiotensin Aldosterone System Inhibitors in Chronic Heart Failure With Reduced Ejection Fraction.
In the present review article, alongside with a brief re-evaluation of general aspects of HF physiopathology, we summarize recent advances in the cross talk between renin-angiotensin-aldosterone system (RAAS) with natriuretic peptides (NPs) which have been shown to play a relevant role in the development of severe HF.
The use of renin-angiotensin-aldosterone system (RAAS) inhibitors in the treatment of chronic heart failure (HF) and arterial hypertension is recommended by the European Society of Cardiology Guidelines on the basis of consolidated evidence supporting their efficacy in the development of such a disease.
The beta-AR blockers and the inhibitors of the renin-angiotensin-aldosterone axis form the mainstay of current medical management of chronic heart failure.
Although the aldosterone escape mechanism is well known, aldosterone has often been neglected in the pathophysiologic consequences of the activated renin-angiotensin-aldosterone system in arterial hypertension and chronic heart failure.