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Reduce mortality in patients with systolic HF
- ACEI/ARB, beta blockers, aldosterone antagonists (ARA)
- ACEI and ARAs - class effect
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BiDil
- Hydralazine/isosorbide DInitrate
- Adjunct with ACEI/ARB in self-ID African American with NYHA Class III-IV -- to reduce mortality
- Patients NYHA II-III who cannot tolerate ACEI/ARB for mortality reduction
- SE: HA with any nitrate (can pretreat with APAP)
- CI: PDE-5 inhibitors (sildenafil)
- SE: Lupus-like syndrome from hydralazine (fever, joint/muscle aches, fatigue)
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HF beta blockers
- Carvedilol (IR and ER) (Coreg): nonselective beta blocker + alpha-1 blocking in arterial walls
- - Target dose of Coreg <85 kg is 25mg BID
- Metoprolol succinate (Toprol XL): beta-1 selective, split tab on scored line
- Bisoprolol (Zebeta)
- For all HF patients to reduce mortality
- BBW: do not withdrawn abruptly, TAPER use
- Warning: Do not use in severe bradycardia (HR <55), mask hypoglycemia (sweating, hunger not masked), HYPERglycemia with non-selective BB
- Titrate every 2 weeks
- MOA: binds to beta-adrenergic receptors and blocks Epi and NE
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ACEI/ARB/ARNI
- For all patients to reduce mortality
- Sacubitril/valsartan (Entresto): stop ACEI 36 hours before starting Entresto, do not use with other ACEI/ARB
- BBW: pregnancy
- CI: bilateral renal artery stenosis, h/o angioedema
- SE: dry cough (accumulation of bradykinin 2/2 inhibition of ACE)
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Drugs that worsen HF
- Thiazolidinediones (TZD): pioglitazone (Actos)-- BBW in patients with NYHA III-IV, d/t increase risk of edema
- Class 1 antiarrhythmics: mexiletine, propafenone, procainamide, quinidine
- - Amiodarone and dofetilide -- less risk of worsening HF
- Oncology agents: anthracyclines (doxorubicin, daunorubicin have lifetime max dose)
- Nondihydropyridine CCBs: diltiazem, verapamil (works heart harder, negative inotropic effects)
- NSAIDs: increases NA and water retention
- Immunosuppressants: TNF inhibitors, interferons (certolizumab, infliximab, etanercept, rituximab), MTX is okay
- Itraconazole
- Prednisone
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Loop diuretic drugs
- Ethacrynic acid (Edecrin)
- Torsemide (Demadex)
- Bumetanide (Bumex)
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Monitor K+
- When starting or up-titrating an ACEI, ARB, aldosterone antagonist, diuretic
- When patient's renal function changes
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ACEI/ARB drugs
- ACEI MOA: blocks conversion of angiotensin I to angiotensin II
- ARB MOA: blocks AT II directly at a receptor site on the smooth muscle wall of vessel
- Irbesartan (Avapro)
- Captopril (Capoten): shortest t1/2, dosed TID
- Enalapril (Vasotec)
- Quinapril (Accupril)
- Ramipril (Altace)
- Valsartan (Diovan)
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Aldosterone receptor antagonists (ARA)
- MOA: blocks aldosterone (causes Na and water retention, increases BP), cause increase in serum K+
- Eplerenone (Inspra): selective ARA
- - CI: strong 3A4 inhibitors (voriconazole), should not exceed 25mg daily with moderate 3A4 inhibitors (diltiazem)
- Spironolactone (Aldactone): non-selective ARA; also blocks androgen (gynecomastia, breast tenderness, impotence)
- Do not start if K >5 mEq/L
- If already on it, stop when K reaches 5.5 mEq/L, hold until K <5
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Coreg IR to CR conversion
- Carvedilol 3.125 mg BID = Coreg CR 10 mg daily
- Carvedilol 6.25 mg BID = Coreg CR 20 mg daily
- Carvedilol 12.5 mg BID = Coreg CR 40 mg daily
- Carvedilol 25 mg BID = Coreg CR 80 mg daily
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Loop diuretic conversion
Furosemide 40 mg= bumetanide 1 mg
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Digoxin
- MOA: inhibits Na/K/ATPase pump, digoxin and K+ compete for binding. When K+ is low, less competition at receptor --> more digoxin toxicity
- Maintain K+ between 4-5 mEq/L
- TI: 0.5-0.9 ng/mL (for HF)
- + inotrope, - chronotrope (increase force of heart's contraction, decrease HR)
- Reduces HF hospitalizations only
- Antidote: DigiFab (Digoxin Immune Fab)
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Loop diuretics
- Only for sx control
- MOA: inhibit Na reabsorption in thick ascending limb of Loop of Henle
- Ethacrynic acid: highest risk for ototoxicity, no sulfa moiety
- Other ototoxic drugs: vancomycin, aminoglycosides
- Least to most potent: ethacrynic acid, furosemide, torsemide, bumetanide
- Reduces: Na, K, Mg, Cl, Ca
- Increases: uric acid, TG, total cholesterol
- SE: hyperglycemia, photosensitivity, hyperuricemia
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Causes of HF
- Common: MI, long-standing HTN
- Less common: chronic alcohol, illicit drugs, valvular disease
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K+ formulations
- Klor-Con M: can be cut and/or dissolved in water
- Micro-K: can be opened and sprinkled on food
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Ivabradine
- Ivabradine (Corlanor)
- Indication: EF <35%, normal sinus rhythm (NSR), HR >= 70 BPM
- SE: phosphenes (brightness/flashes of light)
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Natural products for HF
- Fish oils (proven by most studies)
- Hawthorn, coenzyme Q10 (proven by some studies)
- Avoid: Ma huang (ephedra)
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ARNI (angiotensin receptor blocker neprilysin inhibitor)
- Entresto
- MOA: inhibits neprilysin and blocks the AT 1 receptor (hence actions of AG II)
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Digoxin amiodarone DDI
- Due to inhibition of P-glycoprotein and 3A4
- Digoxin = P-gp substrate
- Amiodarone = P-gp inhibitor
- Reduce digoxin dose by 50% when starting amiodarone
- Other drugs that interact with digoxin: dronedarone, verapamil, macrolides, itraconazole
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Lifestyle mod- fluid restriction
Fluid restriction only beneficial in NYHA Class IV
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HFrEF- normal EF versus reduced EF
- Systolic dysfunction
- Normal EF: 55-70%
- Reduced EF: <40%
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