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Published on : Jul 18, 2021 | Views : 1889 | Downloads : 10

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Assoc. Prof. Iv. Lambev www.medpharm-sofia.eu DRUGS USED IN THE TREATMENT OF CARDIAC FAILURE (Summary)
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Cardiac failure develops as a result of decreased cardiac output, when the heart becomes unable to provide adequate amount of blood to the organs according to their needs.
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Echocardiography – ejection fraction (EF) < 45%
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The treatment of CHF aims to reduce preload and afterload and to increase myocardial contractility mainly by administration of: ACE inhibitors, diuretics, beta-blockers, alpha-blockers, cardiac glycosides, organic nitrates, cardioprotecors, etc. I. CONGESTIVE HEART FAILURE (CHF)
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1. АСЕ inhibitors
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ACE inhibitors reduce pre- and afterload. They are administered in lower doses alone or together with diuretics, cardiac glycoside, antiischemic agents, etc. in all stages of CHF, due to systolic dysfunction. In preparations with t1/2 ≥ 24 h (Perindopril, Ramipril, Trandolapril) the risk of lowering blood pressure after the first dose is avoided.
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2. SACUBITRIL & VALSARTAN – film-coated tablets: A combination of sacubitril (whose active metabolite – sacubitrilat, blocks the enzyme neprilysin that breaks atrial and brain natriuretic peptide and reduced blood volume) and valsartan (inhitors of (angiotensin II1-receptors). Indicated for the oral treatment of adult patients with CHF with reduced ejection fraction (FI). Brand names: Entresto® and Neparvis® in three fixed and graded doses
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3. Thiazides and loop diuretics They increase salt and water loss, reduce blood volume and lower excessive venous filling pressure, reduce circulating blood volume and preload. The congestive features of oedema, in the lungs and periphery, are alleviated, cardiac output is also increased. Diuretics are administered together with ACE inhibitors and other drugs.
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4. Cardiac glycosides (CGs)
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Digitalis lanata Digoxin The first experiments were carried out by Professor P. Nikolov (1894–1990), (who was the first head of our Dept.)
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Herba Adonidis vernalis (Pheasant’s eye) Convallaria majalis (Lily of the valley) Convallotoxin
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(Aglycon) (Glycon)
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Na+/K+ ATP-ase Na+/Ca2+ exchange Ca2+ 3Na+ 3Na+ 2K+ DIGOXIN Ex In (–)
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SR – Sarcoplasmic reticulum, TnC – Troponin C
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Digoxin: Positive inotropic effect without increasing of oxygen consumption Positive batmotropic effect Negative chronotropic effect Negative dromotropic effect ARs: bradycardia, AV block, Extrasystoles arrhythmias, accumulation and intoxication.
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Potassium and calcium have antagonistic action. Hypokalemia and hypercalcemia potentiate the action of CGs. Specific antidote for digitalis intoxication are Digoxin-specific Fab-antibody (Digoxin Immune Fab – Digibind®, DigFab®) in the form of intravenous infusion. Antibodies interact also with Digitoxin. One vial of Digibind® (38 mg) or DigFab® (40 mg) associated approximately 0,5 mg Digoxin or Digitoxin.
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Preparations of Digitalis (foxglove) Digitoxin (t1/2 168 h) Digoxin (t1/2 40 h): p.o. or i.v. Semisynthetic derivatives of Digoxin – Acetyldigoxin (Lanatilin®): p.o. – Methyldigoxin (Lanitop®): p.o. Preparations of Strophanthus gratus – Strophanthin G (Ouabain®) – i.v. CGs are effective in CHF, occuring with normal or accelerated heart rhythm, especially in cases of atrial fibrillation.
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In cases of severe heart failure low doses of Spironolactone are added to the therapy while regularly checking creatinine and electrolyte levels. Spironolactone is a weak diuretic. It blocks aldosterone receptors in the distal renal tubules and reduces increased aldosterone levels in CHF. 5. Aldosterone antagonists
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In low doses (25 mg/24 h) Spironolactone potentiates the effects of ACE inhibitors. It also saves K+ and Mg2+ and has anti- arrhythmic activity. Spironolactone prevents myocardial fibrosis, caused by aldosterone, and in this way increases myocardial contractility. Similar to spironolactone is another aldosterone antagonist – Eplerenone.
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Carvedilol is a blocker of β- and α- receptors. It also has antioxidant, vasodilating and cardioprotective effects. It decreases cardiac output, peripheral vascular resistance and afterload. Carvedilol lowers mortality with 25–67%, but it is contraindicated in CHF, occuring with cor pulmonale. The treatment begins with low doses (3.125 mg/12 h). 6. Beta- and alpha-blocking agents
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7. Beta-blocking agents Cardioselective beta-blockers Bisoprolol and Metoprolol decrease with 31% mortality in patients with CHF, if used in combination with diuretics, ACE inhibitors and Digoxin.
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8. Оrganic nitrates Organic nitrates dilate capacity vessels, reduce preload and myocardium oxygen needs. They connect with thiol groups (-SH) and release nitric oxide (NO). NO combines with new thiol groups in vascular endothelium to form nitrosothiol (R-SNO). Nitrosothiols activates guanylate cyclase which raises the concentration of cyclic GMP. This reduces the bioavailability of intracellular calcium and produces vasodilation.
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Ca2+ Organic nitrate (R-ONO2) Endothelium Smooth muscle Celullar action of nitrates SR - sarcoplasmatic reticulum GTP - guanosine triphosphate GMP - guanosine monophosphate
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In congestive left-ventricular heart failure Isosorbide dinitrate and Isosorbide-5-mononitrate are prescribed. To prevent tolerance development are necessary 8–12 hours intervals without nitrates.
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9.Prazosin is a postsynaptic alpha-1-blocker which reduces afterload. It is used for treatment of resistant CHF in low doses together with diuretics and cardiac glycosides.
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10. Metabolic cardioprotective agents Trimetazidine has prolonged concentration plateau lasting up to 11 h. It increases ATP synthesis and decreases acidosis in ischemic tissues. It supplies energy for Na+/K+ transmembrane pump, but can cause parkinsonism. (+ >>fish!)
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Levocarnitine is a N-containing amino acid in muscle, which has antioxidant activity. It is indicated in cardiomyopathy and muscle dystrophy caused by carnitine deficiency. Preparations containing Coenzyme Q10 (a part of the mitochondrial redox system), stimulate ATP synthesis and improve myocardial contractility in CHF.
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11. Calcium sensitizers Levosimendan (Simdax®) increases sensitivity of troponin in the heart to calcium. This results in increased myocardial contractility. It is infused i.v. for short treatment of severe heart failure.
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II. Acute heart failure (AHF) 1. Phosphodiesterase III inhibitors (PDE): Amrinone, Enoximone, Milrinone These agents are indicated in severe congestive AHF, resistant to other drugs; usually for short i.v. treatment. They have positive inotropic effect, but they increase oxygen consumption. ARs: ventricular and SV arrhythmias, angina, hypotension, headache, hypokalemia.
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ATP 3’,5’-AMP AC PDE III Amrinone Enoximone Milrinone (–) cAMP
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2. Cardioselective beta-1- adrenomimetic agents In AHF with cardiogenic shock Dobutamine (β1-agonist) and Dopamine are administered by i.v. infusion. In high doses dopamine may increase peripheral vascular resistance, while dobutamine does not influence it.
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Dopamine in low doses activates D2-receptors in renal and mesenterial vessels and in coro- naries. It causes arterial vasodilation, acti- vates D5-receptors in myocardium and increases myocardial contractility. Used in low doses (2 to 5 mcg/kg/min i.v.) dopamine does not increase blood pressure. In high doses (> 5 mcg/kg/min i.v.) its α- and β-effects dominate.
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3. Organic nitrates They dilate capacity vessels (vein, venules) which normally can take up to 80% of the total blood volume. They decrease intraventricular pressure and reduce myocardial wall distention. Organic nitrates reduce myocardial oxygen needs too. Glyceryl trinitrate is prescribed sublingually at 18–20 min intervals in acute left-ventricular heart failure, but it is more effective when infused i.v. in doses from 10 to 100 mcg/min.
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4. Non-organic nitrates Sodium nitroprusside is indicated in resistant to other pharmacotherapy congestive heart failure (often in combination with dopamine) and also in acute left-ventricular heart failure.
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3. Alternative methods for treatment of severe CHF Cardiac transplantaion
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“The heart never stops. When it stops, it stops forever”. Leonardo da Vinci Modern medicine often disproves this saying.