Pharmacotherapy of Heart Failure
Four-Pillar GDMT, Symptomatic Agents & the New Preserved-EF Frontier
Past RGUHS + DNB + MPMSU + MUHS + VNSGU · 39
RGUHSMay '25
MPMSUMay '25
MPMSUOct '25
MPMSUMay '25
MPMSUJan '25
MPMSUMay '25
DNBJun '25
VNSGUSep '25
MUHSWinter '24
MPMSUJun '23
MUHSWinter '23
DNBDec '22
VNSGUApr '22
DNBJun '21
MPMSUJul '20
DNBJun '20
RGUHSNov '19
RGUHSMay '19
MUHSSummer '19
MPMSU2018
MPMSU2018
MPMSU2018
MUHSSummer '18
MUHSWinter '18
RGUHSNov '16
RGUHSJun '16
MUHSSummer '16
MUHSSummer '16
DNBDec '14
MPMSU2013
MPMSU2013
DNBDec '13
DNBDec '12
RGUHSMay '11
MPMSU2011
DNBDec '11
RGUHSMay '10
MPMSU2010
RGUHSOct '08
Introduction
- Definition — Heart failure (HF) is a clinical syndrome — the heart cannot pump blood to meet tissue metabolic demand, or only at elevated filling pressure; modern definitions anchor it to raised natriuretic peptides + objective congestion.
- Final common pathway — of ischaemic heart disease (commonest cause of HFrEF, ~75%), chronic hypertension, valvular disease, cardiomyopathies, myocarditis and cardiotoxins (alcohol, doxorubicin, trastuzumab, checkpoint inhibitors).
- Two haemodynamic syndromes — forward (low-output) failure → fatigue, exertional dyspnoea; backward (congestive) failure → pulmonary/peripheral oedema, hepatic congestion.
- Grim prognosis — ~50% 5-year mortality (~42% survival), ~40% of deaths sudden; survival has improved tracking the rising use of ACEI/ARB, β blockers & MRAs — drug therapy drives survival.
- Therapeutic split — symptomatic / no mortality benefit (diuretics, digoxin, inotropes) vs disease-modifying / prolongs survival (ACEI/ARB, β blocker, MRA, ARNI, SGLT2i) — the four-pillar GDMT lives in the latter.
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Heart Failure Pharmacotherapy
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