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CLINICAL PHARMACOLOGY OF ANTIANGINAL DRUGS. CLINICAL PHARMACOLOGY OF ANTIARRHYTHMIC DRUGS

CLINICAL PHARMACOLOGY OF ANTIANGINAL DRUGS. CLINICAL PHARMACOLOGY OF ANTIARRHYTHMIC DRUGS. ISCHEMIC HEART DISEASE. There are 35 risk factors for development of IHD 3 most important ones are – “ big triple ” hypercholesterolaemia arterial hypertension smoking

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CLINICAL PHARMACOLOGY OF ANTIANGINAL DRUGS. CLINICAL PHARMACOLOGY OF ANTIARRHYTHMIC DRUGS

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  1. CLINICAL PHARMACOLOGY OF ANTIANGINAL DRUGS. CLINICAL PHARMACOLOGY OF ANTIARRHYTHMIC DRUGS

  2. ISCHEMIC HEART DISEASE There are 35 risk factors for development of IHD 3 most important ones are – “big triple” hypercholesterolaemia arterial hypertension smoking 95 % of patients with IHD are observed to have aterosclerotic changes in coronary arteries

  3. Antianginal(coronary active)drugs a group of drugs which using different mechanisms even out irregularities between myocardium need in oxygen and it’s blood supply by coronary arteries clinically it is manifested by removalor prevention of stenocardia attacks (improvement of disease current) and increasing of patients’ tolerance to physical load

  4. ANTIANGINAL (CORONARY ACTIVE) DRUGS І. Nitrates and sidnonims which are close to the first ones ІІ. Bets-adrenoblockers ІІІ. Antagonists of calcium ions ІУ. Activators of potassium channels • Inhibitors of ATE • Antiaggregants and anticoagulants • Drugs with metabolic influence on miocardium

  5. NITRATES nitroglycerin isosorbiddinitrate isosorbid-5-mononitrate

  6. MECHANISM OF ACTION OF NITRATES • Interaction with sulfhydryl (SH-) groups (nitrate receptors) insidecells of vascular smooth muscles • Stimulation of formation of endothelial factor of relaxation of vessels (ЕRF)– nitrogen oxide (NO) • Decreasing of ionized Са2+ contents • Relaxation, dilation of vessels, including coronary vessels

  7. MECHANISM OF ACTION OF NITRATES • Decreasing of tone of venules – decreasing of preloading (income of blood into heart during diastole) – decreasing of work of left ventricle and heart output • Decreasing of tone of arterioles– decreasing of afterloading (decreasing of arterial pressure, end diastolic pressure in left ventricle and it’s volume, decreasing of tension of myocardium wall • decreasing of heart need in oxygen • improvement of blood float in ischemic zone of myocardium – redistribution of coronary blood circulation with increasing of perfusion of subendocardial areas • dilation of large coronary vessels if they are in spasm or narrowed with aterosclerotic mass • development of anastomoses between arteries in myocardium (in case of prolonged administration)

  8. NITROGLYCERINE • Tablets (under the tongue) • 1 % alcohol or oil solution(under the tongue) • aerosol Latent period - 2-3 min Duration of action - 20-30 min • ampoules1 % solution – intravenously dropply 0,01%solution • prolongedforms of nitroglycerine: trinitrolong, sustak, nitrong, ointment, plaster

  9. NitroglycerineUnique transdermal system in a form of plaster

  10. SIDE EFFECTS OF NITROGLYCERINE bursting, pulsating headache decreasing of arterial pressure (heartbeat, dizziness, collapse) skin redness, feeling of fever

  11. Contraindications for nitroglycerine use • Close-angled form of glaucoma • increasing of intracranial pressure, insult • acute myocardium infarction(in case of presence of hypotonia and collapse)

  12. PROLONGED FORMS OF NITROGLYCERINE • Trinitrolong– polymer films (0,001 gor 0,002 gof nitroglycerine)action develops immediately, lasts for 3-5 hours • Sustac Sustaс-mite (contains 0,0026 g of nitroglycerine) and Sustac-forte (0,0064 g of nitroglycerine) beginning of action – after 10 min, maximal action – after 1 hour, duration of action – 4-5 hours • Nitrong – microcapsule form of nitroglycerine of prolonged action latent period – 30-60 min, maximal effect- after 3-4 hours, action duration - 6-8 hours

  13. Iso MakRetard 20mgIso Mak Retard 40mg IsomakRetard 60mg(isosorbid dinitrate)

  14. IsoketIsosorbid dinitrate

  15. SIDE EFFECTS OF NITRATES • bursting, pulsating headache • decreasing of arterial pressure (heartbeat, dizziness, collapse) • skin redness, feeling of fever • development of tolerance • nitrate dependence • syndrome of cancellation

  16. Other nitrates Nitrosorbid – isosorbid dinitrate latent period 30-50 min, duration of action – 4-6 hours and more With sublingual administration of the drug latent period grows short to 3-5 min • buccal form (Dinitrolslrbilong) • tablets of prolonged action (Isoket-retard) • ointment • aerosol • drugs for intravenous introduction Isosorbid-5-mononitrate - pharmacologically active metabolite of isosorbid dinitrate duration of action- from 6 till 24 hours

  17. SYDNONIMS Molsydomin –corvaton -sydnopharm • is metabolized in liver forming a substance – SIN-1awhich contains freeNОgroup (doesn’t need previous interaction withSH-groups) • nitrogen oxide stimulates guanilatecyclase that activates synthesis ofcGMP • cGMP causes dilation of vessels 2 mg of molsydomin=0,5 mg of nitroglycerine

  18. Molsydomin • latent period - 20 min (5-10 min – if administered sublingually),action duration - 6 hours. • can be used for prophylaxis and releasing stenocardia attacks in patients with glaucoma (doesn’t increase intraoccular pressure) • indicated for patients who make breaks in using nitrates to decrease tolerance towards them • doesn’t lead to development of tolerance (doesn’t need previous combining with sulfhydryl groups) • absence of cancellation syndrome

  19. BETA-ADRENOBLOCKERS Mechanism of action during stenocardia • blockade of b1-adrenoreceptors of heart:decreasing of power and frequency of heart contractions and as follows cardiac need in oxygen • decreasing of thrombocyte aggregation and prevention of thrombus formation • increasing of diastole duration – improvement of coronary vessels saturation with blood– improvement of perfusion of ischemic areas of myocardium • Decreasing of calcium ions accumulation – releasing of cardiac muscle tension, improvement of metabolic processes, increasing of ATP synthesis • in case of acute myocardium infarction– increasing of blood supply of ischemic areas of heart, decreasing of size of infarction seat, prevention of development of cardiac arrhythmias

  20. Anaprilinβ1- β 2adrenoblocker

  21. Vasocardin 100 mgMethoprolol tartrate

  22. Nadolol(β1, β 2- adrenoblocker)

  23. CALCIUM IONS ANTAGONISTS 1.Derivatives of difenilalkilamin (verapamil) 2. Derivatives of benzothiazepine (dylthiazem) 3. Derivatives of dyhydropyridine (nifedipin, amlodipin, nimodipin) Drugs of 1 and 2 groups dominantly influence on heart (depress automatism of sinus node, conductivity through conductive heart system), show antiarrhythmic, antiangina and hypotensive action. Derivatives of dyhydropyridine (group of nifedipin) – decrease blood pressure and cause dilation of coronary vessels,cause reflective tachycardia

  24. Nifedipin -corinfar - fenigidin -adalate Doesn’t depress conductivity in myocardium, has a weak antiarrhythmic action Maximal concentration of the drug in blood occurs after45-60 minafter administrationorallyand after2-3 min – if administered sublingually Effect lasts for 4-6 hours

  25. Antagonists of calcium ions – derivatives of dyhydropyridine ofІІ generation (amlodipin, isradipin, nicardipin) • almost don’t cause tachycardia • areindicated for prolonged treatment of patients with stabile stenocardia • aren’t indicatedin case of non stabile stenocardia(long lasting latent period)

  26. Usage of calcium ions antagonists Illness Drugs -recommended drug --should be used carefully

  27. Nifedipin(Са2+ions antagonist of dyhydropyrydine series)

  28. Nifedipin (Са2+ions antagonist of dyhydropyrydine series)

  29. Nifedipin (Са2+ions antagonist of dyhydropyrydine series)

  30. ACTIVATORS OF POTASSIUM CANALS NICORANDIL • activates Са2+-depending potassium canals • causesrelaxation of smooth muscles of vessels – coronary, arteriolar and venous vasodilation • improvement of blood supply of myocardium, decreasing of pre- and afterloads of heart,decreasing of myocardial need in oxygen, separation of ischemic damage zone

  31. Acetylsalicylic acid • 80-100 mg per day – as antiaggregative drug,decreases risk of development of acute myocardium infarction and decreases mortality of patients with IHD • In many world countries it is also used a basis treatment drug of IHD which can be used for years

  32. ACUTE MYOCARDIUM INFARCTION • one of the main reasons of disablement and mortality of people of employed age in many world countries, including Ukraine • mensuffer from MI almost 5 times more often than women • Mortality of patients with MI during first two hours starting from the beginning of the process makes around 50 % of all mortal cases connected with MI • themost often death causes –acute cardiac-vascular insufficiency (angina pectoris, lung edema, cardiogenic shock), heart rupture, heavy cardiac arrhythmia • othercomplications of MI – thrombosis and emboli, acute and chronic heart aneurisms, Dresler’s syndrome, chronic cardiac insufficiency

  33. TREATMENT OF MYOCARDIUM INFARCTION threestages • Immediate treatment – decreasing pain and treatment of stop of heart beats • Early treatment – separation of zone of infarction seat and prevention of early life threatening complications (cardiac arrhythmias, acute cardiac insufficiency) • Further treatment – prevention and therapy of late complications of MI, prophylaxis of recurrent MI and death of the patients

  34. TREATMENT OF ACUTE MYOCARDIUM INFARCTION Releasing of pain and prophylaxis of cardiogenic shock • nitroglycerin (1 tablet under the tongue every 7-10 min.) • Neuroleptanalgesia (fentanil with droperidol), morphine, omnopon, promedol (in combination with atropine, dimedrol, aminasine) • nitrous oxide in combination with neuroleptics • incase of remaining pain – non narcotic analgesics in combination with antihistamine and neuroleptic drugs • toincrease arterial pressure during cardiogenic shock – intravenously dropply dopamine(drugs of choice), noradrenalin, mesaton • sometimesglucocorticosteroids are used

  35. TREATMENT OF ACUTE MIOCARDIUM INFARCTION Size limitation of infarction seat • Intravenous dropply introduction of 0,01 % nitroglycerin solution • Administration of b-adrenoblockers

  36. TREATMENT OF ACUTE MYOCARDIUM INFARCTION Treatment and prophylaxis of heart arrhythmias Treatment of ventricular arrhythmias – i.v. slowly 0,2 % solution of xycain, novocainamidintramuscularly • Prophylaxis of ventricular extrasystolia and tachycardia –magnesium sulfate (intravenous dropping introduction of 4-5 % solution), -adrenoblockers • Arrhythmias of atrialorigin– heart glycosides, antagonists of calcium ions • Bradycardia- isadrin, atropine sulfate, alupent (i.v.)

  37. TREATMENT OF ACUTE MYOCARDIUM INFARCTION CORRECTION OF BLOOD CLOTTING • thrombolytic drugs streptokinase (1,5 mlnOD),urokinase (2 mlnOD), aktilise – recombinant tissue activator of plasminogen (100 mg) intravenous • after performing of thrombolytic therapy– intravenous introduction ofheparin, at first 10 000 OD, after 1000 ODper hour during 24-48 hours • anticoagulants of indirect action • acetylsalicylic acid (80-100-300 mg per day)

  38. TREATMENT OF ACUTE MYOCARDIUM INFARCTION Treatment of heart insufficiency • i.v.furosemid (40-120 mg); i.v.dropplynitroglycerine (12-20 hours),morphine • i.v.dropply dopamin and dobutamin • heart glycosides– in tachysystolic form of scintillatingarrhythmia or flutteringof atria with moderate left-ventricular insufficiency General measures • oxygen inhalation • correctionof acid-base balance

  39. ANTIARRHYTHMIC DRUGSCLASS Mechanism of Action Drug name IA Na+Channel blocker Disopyramide, procainamide, quinidine IB Na+Channel blocker Lidocaine, mexiletine, tocainide IC Na+Channel blocker Flecainide, propafenone II  Adrenoreceptor blocker Esmolol, metoprolol, pindolol, propranolol III K+Channel blocker Amiodarone, bretylium, sotalol IV Ca++ Channel blocker Diltiazem, verapamil Other antiarrhythmic drugs Adenosine, digoxin

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