DRUGS USED IN HEART FAILURE

A N Mahendra

Department of Pharmacology & Therapy,

Faculty of Medicine, Udayana University
Heart Failure (HF)
 Definition
 Classification:
 Low-output
 High-output
 Acute
 Chronic
 Right HF
 Left HF
 CHF
 HF triggers counter-regulatory responses 
worsening of HF per se
Therapy of HF

 Therapeutic goals: reduce/relieves sx.,

prolongation of survival, halt disease
progression
 Modulation of cardiac performance
determinants
 Preload: salt restriction, diuretics, venodilators
 Afterload: drugs acting on SANS & RAAS, arteriolar
dilator
 Contractility: cardiac glycosides, beta-blockers
 Heart Rate: beta -blockers
HF Therapies
DIURETICS
Furosemide: inhibits Na-K-Cl symporter in loop of
Henle; high-ceiling diuretic
 Clinical uses: acute & chronic HF, severe HT,
edematous states
 Toxicity: hypovolemia, hypokalemia, orthostatic
hypotension, ototoxicity, sulfonamide allergy
HCT: inhibits Na-Cl symporter in DCT
 Clinical uses: mild chronic HF, mild-moderate HT
ALDOSTERONE ANTAGONISTS

Spironolactone: blocks aldosterone receptors in

collecting tubules
 Clinical uses: chronic HF, aldosteronism
(cirrhosis, adrenal tumors), HT
 Toxicity: hyperkalemia, antiandrogenic effect
Eplerenone: more selective antialdosterone
effect without significant antiandrogenic
effect
ACEIs

 ACEIs: reduces aldosterone secretion,

reduces cardiac remodelling
 Use: Chronic HF, HT, DKD
 Toxicity: cough, angioneurotic edema
 ARBs: pharmacological antagonism on AT1-R
 Use: patient intolerant to ACEIs
 Toxicity: Hyperkalemia, angioneurotic edema
BETA-BLOCKERS

Bisoprolol, Metoprolol, & Carvedilol

 Negative inotropes & chronotropes
 May modulate RAAS (unknown precise
mechanism)
 Use: Chronic HF, to reduce mortality in
moderate-severe HF
 Toxicity: bronchospasm, bradycardia, AV
block
CARDIAC GLYCOSIDE

 Digoxin: Inhibits Na-K-ATPase in excitable

tissues
 Use: Chronic symptomatic HF
 Toxicity: N/V, diarrhea, arrhythmias
 Toxicity tx: digoxin antibodies
Digoxin PD
VASODILATORS

 Venodilators: ISDN
 Arteriolar dilators: Hydralazine
 Combined: Nitroprusside
BETA AGONIST

Dobutamine: increases cardiac contractility,

increases cAMP synthesis
 Use: acute decompensated HF
 Toxicity: Arrhythmias
Dopamine: increases renal blood flow
 Use: acute decompensated HF
 Toxicity: Arrhythmias
BIPYRIDINES

 Inamrinone & Milrinone: inhibit PDE3, and

decrease cAMP breakdown
 Use: Acute decompensated HF
 Toxicity: Arrhythmia
NATRIURETIC PEPTIDE

 Nesiritide: activates BNP receptor; increases

cGMP
 Use: Acute decompensated HF
 Toxicity: renal damage, hypotension
Chronic HF Classification & Therapies
Systolic vs. Diastolic HF
Acute HF Management
Rule: Use IV therapy
 Furosemide
 Dopamine or Dobutamine
 Levosimendan (noninferiority vs dobutamine)
 Nitroprusside
 Nitroglycerine
 Nesiritide
 Conivaptan (V1a & V2 receptor antagonist)
 Tolvaptan (V2 receptor antagonist)
 Omecamtiv mecarbil: investigational
Related experimental studies
in Indonesia…
 PSP Anthocyanin increases eNOS expression
in thoracic aortae of rodent model of HT (Jawi
et al., 2012) (Available at: Univers J Med
Dentistry)
 Telmisartan ameliorates cardiac remodelling
via PPAR-γ/TGF-β in NaCl-induced HF model
(Hidayat, 2014)  thesis
Thank You