scholarly journals Use of Renin–Angiotensin–Aldosterone System Inhibitors in Older Patients with Heart Failure and Reduced Ejection Fraction

2019 ◽  
Vol 5 (2) ◽  
pp. 70-73 ◽  
Author(s):  
Davide Stolfo ◽  
Gianluigi Savarese

Patients enrolled in randomised clinical trials may not be representative of the real-world population of people with heart failure (HF). Older patients are frequently excluded and this limits the strength of evidence which supports the use of specific HF treatments in this patient group. Lack of evidence together with fear of adverse effects, drug interactions and lower tolerance may lead to the undertreatment of older patients and a less favourable outcome. Renin–angiotensin–aldosterone system (RAAS) inhibitors are the cornerstone of treatment for patients with HF with reduced ejection fraction (HFrEF), but despite the class I recommendation for all patients regardless of age in the guidelines, there are signs that RAAS inhibitors are underused among older patients. Large registry- based studies suggest that RAAS inhibitors may be at least as effective in older patients as younger ones, but these findings need to be confirmed by randomised clinical trials.

2020 ◽  
Vol 15 (9) ◽  
pp. 1-9
Author(s):  
Kate O'Donovan

Heart failure with reduced ejection fraction is associated with decreased functional capacity, poor quality of life and increased mortality risk. The neurohormonal compensatory response to a reduced cardiac output is mainly comprised of the sympathetic nervous system, natriuretic peptides and the renin–angiotensin–aldosterone system, which attempt to maintain peripheral perfusion. The renin–angiotensin–aldosterone system is an integral mechanism in increasing afterload by promoting angiotensin II-mediated vasoconstriction and increasing preload via the secretion of aldosterone which causes sodium and water retention. Albeit compensatory mechanisms attempt to increase cardiac output and perfusion, their effects are maladaptive as left ventricular function deteriorates in response to an increased afterload, preload and ventricular remodelling. In an attempt to interrupt this vicious circle, first-line pharmacological therapy in the treatment of heart failure is beta blockade and inhibition of the renin–angiotensin–aldosterone system. Integral to this treatment strategy are mineralocorticoid receptor antagonists, also known as aldosterone antagonists. This class of drug inhibits the action of aldosterone, decreases preload and reduces left ventricular workload, thus preserving ventricular function. This translates into reduced mortality incidence, decreased episodes of hospitalisations for cardiac causes and improvement in clinical signs and symptoms. Although patient benefits are explicit, adverse effects such as hyperkalaemia and renal impairment are associated with this therapy. Regular patient follow up and monitoring for potential adverse effects and drug interactions are essential to the success of the therapy.


2018 ◽  
Vol 20 (5) ◽  
pp. 923-930 ◽  
Author(s):  
Joost C. Beusekamp ◽  
Jasper Tromp ◽  
Haye H. van der Wal ◽  
Stefan D. Anker ◽  
John G. Cleland ◽  
...  

2020 ◽  
Vol 4 (4) ◽  
pp. 1-4 ◽  
Author(s):  
Santiago Jiménez-Marrero ◽  
Cristina Enjuanes ◽  
Sergi Yun ◽  
Josep Comín-Colet

Abstract Background Chronic heart failure (CHF) is a growing epidemic. The cornerstone of pharmacological therapy in CHF patients with reduced ejection fraction (HFrEF) is the inhibition of the renin–angiotensin–aldosterone system (RAAS). One of the adverse effects of RAAS blockade is the development of hyperkalaemia, which often limits the optimization of recommended, Class I treatments. In this context, potassium binders patiromer or sodium zirconium cyclosilicate (ZS-9) provide an opportunity to optimize the pharmacological management of these patients. Case summary We present a case report illustrating our real-life experience using the potassium-binder patiromer in a patient with HFrEF, in whom recurrent hyperkalaemia (up to 6.3 mmol/L with low doses of enalapril) was preventing titration of RAAS inhibition therapies. Use of patiromer allowed re-introducing ramipril (subsequently switched to sacubitril/valsartan) and eplerenone. Serum potassium levels remained normal with patiromer 16.8 g/24 h, and the patient’s tolerance to patiromer was excellent. Discussion In patients with HFrEF and recurrent hyperkalaemia, optimal RAAS inhibition is often discontinued. In this context, novel potassium binders such as patiromer or ZS-9 have been shown to be effective in lowering potassium and maintaining normokalaemia, with a good safety profile and patient tolerance, all of which make them promising alternative options. Our preliminary experience suggests that patiromer may be a helpful and well-tolerated treatment option, which may aid in achieving optimal RAAS inhibition in HFrEF patients with recurrent hyperkalaemia. Registries of HFrEF patients will help better understand whether therapies such as patiromer have prognostic benefits through facilitating optimal RAAS blockade.


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