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Drug Therapy of Heart Failure

Drug Therapy of Heart Failure. Dr. Munir Gharaibeh November 2009. Drug Therapy of Heart Failure. Definition of Heart Failure Causes Classifications. Compensatory Mechanisms in Heart Failure. Frank Starling Mechanism Increased Activity of SNS: a- Tachycardia and increased CO.

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Drug Therapy of Heart Failure

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  1. Drug Therapy of Heart Failure Dr. Munir Gharaibeh November 2009

  2. Drug Therapy of Heart Failure Definition of Heart Failure Causes Classifications

  3. Compensatory MechanismsinHeart Failure • Frank Starling Mechanism • Increased Activity of SNS: • a- Tachycardia and increased CO. • b- Increased myocardial contractility • c- Vasoconstriction leading to redistribution of blood to important viscera • d- Renin release leading to increased plasma volume • Myocardial Hypertrophy leading to increased wall tension.

  4. Objectives of Long Term Management of Chronic Cardiac Failure: • Improve cardiac performance at rest and during exercise. • Improve myocardial efficiency. • Improve quality of life (particularly symptom-free and effort tolerance). • Improve patient survival.

  5. Angiotensin Converting Enzyme Inhibitors"ACEI" • Pharmacological Actions: • Reduce angiotensin II levels. • Increase bradykinin. • Inhibit SNS, leading to decreased NE release and upregulation of 1 receptors. • Balanced vasodilators. • Reduce myocyte & fibroblast growth factors • Reduce salt and water retention. • Reduce K+ loss. • Reduce ventricular arrhythmias.

  6. Angiotensin Converting Enzyme Inhibitors"ACEI" Therapeutic Value: • Nowadays drugs of choice. • No tolerance. • Retard progression of HF. • Decrease arrhythmias. • Decrease mortality only with the highest tolerated doses.

  7. Angiotensin Converting Enzyme Inhibitors"ACEI" • Captopril • Enalapril • Lisinopril • Quinapril • Fosinopril All are similarly effective Might differ in toxicity

  8. Angiotensin Converting Enzyme Inhibitors"ACEI" Toxicity: • Hypotension • Renal Impairment ............ proteinurea • K+ retention • Cough

  9. Angiotensin (AT1) Receptor BlockersARBs • Losartan. • Candesartan. • Valsartan. • Irbesartan. • Telmisartan. Not superior to ACEIs, but may be useful for patients who can not tolerate ACEIs because of cough.

  10. Positive Inotropic Agents • Cyclic AMP Independent Agents: • Cyclic AMP Dependant Agents: -adrenergic Agonists Phosphodiesterase Inhibitors

  11. Positive Inotropic Agents Cyclic AMP Independent Agents: • Digitalis: inhibits Na/KATPase. • Pimobendan: sensitizes myocytes to Ca++, also inhibits PDE.

  12. Digitalis Glycosides History: • Egyptians ------- Squill • Chinese -------- Toad skin • William Withering ----- Foxglove 1785 • Digitalis purpura • Digitalis lanata • Strophanthus

  13. Digitalis Glycosides Mechanism: • Inhibition of Na+/K+ ATPase

  14. Digitalis Glycosides Actions: • Positive Inotropic • Vascular Muscle • Vagal Stimulation • Electrical Stimulation

  15. Digitalis Glycosides Toxicity: • G.I.T. • Visual. • Neurologic. • Cardiac. • Interactions. Treatment of Toxicity: Reduce the dose. Cardiac pacemeker. Digitalis antibodies( Digoxin Immune Fab)

  16. Digitalis Glycosides Therapeutic Benefits: • CCHF with supraventricular arrhythmia • Morbidity • ? Withdrawal • ? Mortality

  17. Positive Inotropic Agents Cyclic AMP Dependent Agents: -adrenergic Agonists: NE Dopamine Dobutamine Phosphodiesterase Inhibitors: Amrinone Inamrinone Milrinone Vesanirone Sildenafil

  18. Positive Inotropic Agents Cyclic AMP Dependent Agents: -adrenergic Agonists: All increase myocardial oxygen consumption, so not helpful for chronic use. May be used (IV) for short term or in acute heart failure. NE: Was used in cardiogenic shock, but caused severe vasospasm and gangrene . Ep: Still used in cardiac arrest, by intracardiac injection.

  19. Positive Inotropic Agents Dopamine: Widely used in cardiogenic shock. Low doses: stimulates DA1 receptors leading to renal vasodilation and improved renal function. Intermediate doses: works on β1 receptors leading to positive inotropic actions. High doses: stimulates α receptors leading to vasoconstriction and elevation of blood pressure. Can cause arrhythmias and ischemic changes. Dobutamine: Selective β1 agonist, used intermittently (IV) in CCHF. Has more inotropic than chronotropic actions.

  20. Positive Inotropic Agents Phosphodiesterase Inhibitors: PDE inhibition leads to accumulation of cAMP and cGMP leading to positive inotropic activity and peripheral vasodilation. Toxic: arrhythmias, and thrombocytopenia. Short acting, so reserved for parenteral therapy of acute heart failure. Inamrinone (PDE-3) Milrinone (PDE-3) Vesanirone (PDE-3) Sildenafil (PDE-5)

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