10.11 : 심부전 약물: 레닌-안지오텐신 시스템 억제제

In heart failure, continuous RAAS activation intensifies cardiac workload, causing fatal tissue remodeling if untreated.

Heart failure pharmacotherapy helps reduce these harmful neurohumoral effects.

Angiotensin-converting enzyme or ACE inhibitors block the conversion of Angiotensin I to II, lowering its levels and enhancing bradykinin and substance P levels.

Next, angiotensin receptor blockers or ARBs selectively antagonize AT₁ receptors modulating Angiotensin II effects. They are therapeutic alternatives for ACE inhibitor-intolerant patients.

Further, mineralocorticoid receptor antagonists or MRAs block nuclear aldosterone receptors and act as K⁺  -sparing diuretics.

These strategies decrease peripheral resistance, cardiac afterload, and sympathetic activity while increasing natriuresis.

However, ACE inhibitors and ARBs have various adverse effects and are contraindicated in pregnancy. Additionally, ACE inhibitors can induce a dry cough, while MRAs may cause allergic reactions and gynecomastia in males.

Lastly, the pharmacotherapeutic arsenal includes β₁- blockers and combination therapies of ARBs with neprilysin inhibitors.