The Four Pillars of GDMT in HFrEF
ARNI, beta-blocker, MRA, SGLT2i — start all four, titrate simultaneously.
Neurohormonal Activation in HFrEF
In HFrEF, reduced cardiac output triggers compensatory activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, which initially preserve perfusion but drive pathologic remodeling, fibrosis, and myocyte loss over time. Angiotensin II and aldosterone promote vasoconstriction, sodium retention, and hypertrophy, while chronic sympathetic activation increases myocardial oxygen demand and predisposes to arrhythmia. The natriuretic peptide system counter-regulates these effects but is relatively overwhelmed as disease progresses. GDMT pillars each interrupt a distinct point in this cascade, which is why combining them produces additive rather than redundant benefit.