1. Drugs for Ischemic Heart Disease (IHD) Other names Coronary Artery Disease (CAD) Coronary Heart Disease (CHD)

4. Angina Definition: A clinical syndrome characterized by a deep, poorly localized chest or arm discomfort associated with physical exertion or emotional stress & relieved promptly by rest or SL nitroglycerin. it is caused by inadequate blood flow to heart due to coronary arteries narrowing/ plaque in arteries/or vessel spasm. O 2 lack causes pain. it is caused by inadequate blood flow to heart due to coronary arteries narrowing/ plaque in arteries/or vessel spasm. O 2 lack causes pain. Anginal attacks may lead to myocardial infarction (heart attack) & sudden death. Anginal attacks may lead to myocardial infarction (heart attack) & sudden death.

5. Angina-Types Classic (stable, effort ) angina – occur with physical activity/stress/exertion. Need chronic &/or prophylactic drugs to prevent pain Unstable (preinfarction) angina - occurs throughout the day with  sing severity. Mostly due to a ruptured coronary plaque. Urgent & aggressive Tt needed Variant (vasospastic, Prinzmetal's) angina - Occurs at rest. Patients young with few/no cardiac risk factors. Pain often cyclical & unpredictable

6. O 2 Supply & Demand Supply Supply Blood oxygenation Coronary perfusion Demand Demand Wall tension HRContractility Preload & afterload

7.  sed O 2 Supply Diastolic perfusion pressure Coronary vascular resistance Blood PO 2 O 2 carrying capacity of blood  sed O 2 demand o  Ventricular wall tension o  Heart rate o  Ventricular Contractility o  filling pressure- Preload o  resistance to ejection - afterload

8. CAD Atheromatous plaque SpasmThrombosis

9. Etiology..  oxygen reqiurement aortic valve stenosis / insufficiency aortic valve stenosis / insufficiency Systemic hypertension (HTN) Systemic hypertension (HTN) Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy Pulmonary hypertension Pulmonary hypertension

10. Etiology  perfusion of myocardium Atherosclerosis Angiospasm Systemic disease - diabetic microangiopathy Other diseases of coronary arteries - A -V anastomosis - traumatic changes - embolism

11. Nitrovasodilators Organic nitrates-(C-O-NO2) low mol. mass:- Nitroglycerine Organic nitrates-(C-O-NO2) low mol. mass:- Nitroglycerine High Mol. mass : Erythrityl tetra nitrate Penta erythrityl tetra nitrate Isosorbide di nitrate Organic nitrites (C-O-NO) esters of nitrous acid Organic nitrites (C-O-NO) esters of nitrous acid Amyl nitrite-(volatile liquid) Nitro compounds(C-NO2) Nitro compounds(C-NO2)

12. Mechanism of action Organic nitrates and nitrites Organic nitrates and nitrites Denitration Denitration NO (nitric oxide) Activates guanylyl cyclase Increased cyclic AMP Vasodilation

13. Nitro vasodilators Amyl Nitrite.3ml inhalation in glass pearls Amyl Nitrite.3ml inhalation in glass pearls NitroglycerinT. 0.3 to 0.6mg SOS NitroglycerinT. 0.3 to 0.6mg SOS spray. 0.4 SOS spray. 0.4 SOS Oint. 2.5 to 5cm, 2% 4-8hrly Buccal. 1mg-3-5hrly Trans dermal disc. 2.5 to 15mg for 12 to 24hrs i/v.2µgm/min Isosorbide di nitrate:T. 2.5 to 10mg,2-3hrly Isosorbide di nitrate:T. 2.5 to 10mg,2-3hrly Isosorbide 5-mononitrate:T. 10-40mg BD Isosorbide 5-mononitrate:T. 10-40mg BD CR. 60-120mg OD CR. 60-120mg OD Erythrityl tetranitrate: T. 5-10mg SOS Erythrityl tetranitrate: T. 5-10mg SOS T(O).10mg tds

14. Risk Factors Age Age Gender Gender Family history Family history Hypertension Hypertension Smoking Smoking Hyperlipidemia Hyperlipidemia HDL < 35 mg/dL HDL < 35 mg/dL Diabetes Obesity Sedentary lifestyle Cerebrovascular dz Peripheral vas dz

15. Therapy - Principles improve quality of life (  pain episodes) improve quality of life (  pain episodes) improve prognosis improve prognosis Design: Therapy of atherosclerosis Therapy of atherosclerosis  perfusion of impaired area  perfusion of impaired area Prevent thrombotic occlusion Prevent thrombotic occlusion Therapy of risk factors Therapy of risk factors

16. Non-Pharmacologic management Coronary intervention Coronary intervention Aggressive Lifestyle modification Aggressive Lifestyle modification Diet Diet Weight reduction Weight reduction Exercise Exercise Smoking cessation Smoking cessation

17. Pharmacologic management Nitrates, Beta-blockers, CCBs Nitrates, Beta-blockers, CCBs Antiplatelet agents Antiplatelet agents ASA, ADP inhibitors, GP IIb/IIIa inhibitors ASA, ADP inhibitors, GP IIb/IIIa inhibitors Anticoagulants Anticoagulants Heparin, coumarin Heparin, coumarin ACE inhibitors ACE inhibitors HMG-CoA reductase inhibitors HMG-CoA reductase inhibitors Thrombolytic agents Thrombolytic agents

18. ANTIANGINAL DRUGS Organic nitrates Glyceryl trinitrate or nitroglycerin Glyceryl trinitrate or nitroglycerin Isosorbide dinitrate Isosorbide dinitrate Isosorbide mononitrate Isosorbide mononitrate Calcium channel blockers (CCBs) Nifedipine, Nicardipine, Diltiazem Nifedipine, Nicardipine, Diltiazem Beta blockers Propranolol, Metoprolol, Atenolol Propranolol, Metoprolol, Atenolol Antiplatelet agents Aspirin, ticlopidine Aspirin, ticlopidine

19. Types of Antianginal Drugs 3 main types: – Nitrates (  se demand &  supply) – Beta - adrenergic blockers ((  se demand) – Calcium channel blockers (CCBs) - (  se demand &  supply) These drugs  se blood flow by  sing O 2 supply or by  sing O 2 demand by the heart muscle

20. Nitrates Dilates veins which  preload &  O 2 demand Dilates veins which  preload &  O 2 demand Relax coronary arteries which  vasospasm &  O 2 supply Relax coronary arteries which  vasospasm &  O 2 supply Effective in treating vasospastic angina & stable angina Effective in treating vasospastic angina & stable angina NITRATES CAN CAUSE HYPOTENSION

21. Mechanism Nitrate - metabolized by glutathione S- transferase in vessel  nitric oxide (NO) formed Nitrate - metabolized by glutathione S- transferase in vessel  nitric oxide (NO) formed NO is “EDRF“  cause vasodilation NO is “EDRF“  cause vasodilation NO + heme group in guanylyl cyclase -  cGMP - sequestration of free ca ++ in sarcoplasmic reticulum  relax smooth muscle NO + heme group in guanylyl cyclase -  cGMP - sequestration of free ca ++ in sarcoplasmic reticulum  relax smooth muscle NO also inhibits platelet function NO also inhibits platelet function

22. Nitric oxide pathway

23. Nitrate tolerance NO release from GTN needs SH groups NO release from GTN needs SH groups SH exhaustion readily occurs & causes loss of GTN efficacy – tolerance SH exhaustion readily occurs & causes loss of GTN efficacy – tolerance Tolerance - avoided by intermittent usage– i.e ~10 hrs of nitrate free interval Tolerance - avoided by intermittent usage– i.e ~10 hrs of nitrate free interval Tolerance can develop with all forms of nitrates Tolerance can develop with all forms of nitrates Tolerance can develop after only a few doses Tolerance can develop after only a few doses

24. Hemodynamic effects Nitrates - more selective venodilatation -  preload  ventricular filling, chamber diameter, wall tension - all  [tension proportional to diameter -Laplace]-  cardiac work & o 2 demand. Nitrates - more selective venodilatation -  preload  ventricular filling, chamber diameter, wall tension - all  [tension proportional to diameter -Laplace]-  cardiac work & o 2 demand. arterial tone mild  -  ses afterload -  o 2 demand arterial tone mild  -  ses afterload -  o 2 demand improved coronary flow due to NO- coronary relaxation-  o 2 NO- coronary relaxation-  o 2 supply  LVEDP (this improves forward flow in coronaries)  LVEDP (this improves forward flow in coronaries)

25. Nitroglycerin Common antianginal drug Common antianginal drug Also called as GTN (glyceryl trinitrate) Also called as GTN (glyceryl trinitrate) sublingually (SL) to terminate acute attack sublingually (SL) to terminate acute attack SL because it undergoes first pass hepatic metabolism if swallowed SL because it undergoes first pass hepatic metabolism if swallowed Average dose: 0.4mg q 5min X 3 as needed Average dose: 0.4mg q 5min X 3 as needed If pain persists seek medical assistance - it may be myocardial infarction (MI) If pain persists seek medical assistance - it may be myocardial infarction (MI)

26. Nitrates-administration GTN also available as: - Sublingual (SL) - oral (extended release tab/cap) - aerosol spray - transdermal (ointment/patch) - IV Indications - Acute – sublingual, chewable, spray, IV - Chronic – oral, transdermal Pharmacologic Issues - Variable bioavailability - short t½ - tolerance

27. Pharmacokinetics Absorption: SL-rapid, ointment & patch - slow absorption Absorption: SL-rapid, ointment & patch - slow absorption onset:1-3 min, peak:4 min, duration:20-30 min onset:1-3 min, peak:4 min, duration:20-30 min Liver metabolism: t½ 1-4 min Liver metabolism: t½ 1-4 min Excretion: urine Excretion: urine Patch: onset: ½ -1h, duration:~24 hrs Patch: onset: ½ -1h, duration:~24 hrs Remove patch at night to allow a 10h nitrate free interval to avoid tolerance Remove patch at night to allow a 10h nitrate free interval to avoid tolerance

28. Long-Acting Nitrates Isosorbide dinitrate & mononitrate Oral Pros vs. sublingual nitro Less frequent dosing —> better compliance Cons Tolerance w/ long-term use  action of SL nitro in acute angina Unsuitable for acute attack (slow onset) Importance of drug-free intervals to reduce tolerance

29. ADR headache (  ses with continued use & by decreasing dose) headache (  ses with continued use & by decreasing dose) flushing flushing Postural hypotension Postural hypotension dizziness, weakness, faintness, syncope- treatment by positioning to facilitate venous return) dizziness, weakness, faintness, syncope- treatment by positioning to facilitate venous return) When discontinuing-taper dose over several weeks to prevent rebound or severe pain When discontinuing-taper dose over several weeks to prevent rebound or severe pain tachyphylaxis (acute tolerance) occur with continuous than intermittent therapy tachyphylaxis (acute tolerance) occur with continuous than intermittent therapy

30. Drug Interactions Beta-blockers, calcium channel blockers, vasodilators, & alcohol can increase the hypotensive effect of nitrates Beta-blockers, calcium channel blockers, vasodilators, & alcohol can increase the hypotensive effect of nitrates Patients on nitrates should not take sildenafil (Viagra) – it may prove fatal Patients on nitrates should not take sildenafil (Viagra) – it may prove fatal IV nitroglycerin may antagonize the effect of heparin IV nitroglycerin may antagonize the effect of heparin

31. Indications: CAD CAD pulmonary edema due to LV failure pulmonary edema due to LV failure hypertensive emergency hypertensive emergency Nitrates also relax non-vascular smooth muscles so may relieve pain of esophageal spasm so may relieve pain of esophageal spasm & biliary/renal colic (cause diagnostic confusion) & biliary/renal colic (cause diagnostic confusion)Contraindications:  hypotension  increased intracranial pressure  aortic stenosis

32. Treatment of Angina Pectoris Treatment of ppting factors: HT, anemia thyrotoxicosis, obesity, heart failure, cardiac arrhythmias, Ac. Anxiety Treatment of ppting factors: HT, anemia thyrotoxicosis, obesity, heart failure, cardiac arrhythmias, Ac. Anxiety Stop smoking Stop smoking Stop overeating Stop overeating Correction of HT & hyperlipidemia Correction of HT & hyperlipidemia Daily Aspirin or thienopyridine eg. Clopidrogel/Ticlopidine Daily Aspirin or thienopyridine eg. Clopidrogel/Ticlopidine Avoid exposure to nasal decongestants Avoid exposure to nasal decongestants Nitroglycerin; most useful drug Nitroglycerin; most useful drug

33. Nitroglycerin-Angina Rapid action, long established efficacy, low cost Rapid action, long established efficacy, low cost Treatment: Initial dose; 0.3mg-relieve pain within 3min. Active tab produces burning sensatio under the tongue. Treatment: Initial dose; 0.3mg-relieve pain within 3min. Active tab produces burning sensatio under the tongue. Prophylaxis: prevents anginal pain if taken prior to exercise or stress. Prophylaxis: prevents anginal pain if taken prior to exercise or stress. Advise: to seek medical attention immediately when three tabs taken over a 15min period do not relieve a sustained attack as may be indicative of MI/another cause of pain Advise: to seek medical attention immediately when three tabs taken over a 15min period do not relieve a sustained attack as may be indicative of MI/another cause of pain For long term prophylaxis: TDP For long term prophylaxis: TDP For short term prophylaxis: transmucosal/Buccal nitroglycerin. Exercise tolerance increased for 5 hrs. For short term prophylaxis: transmucosal/Buccal nitroglycerin. Exercise tolerance increased for 5 hrs. Nocturnal angina: Ointment Nocturnal angina: Ointment

34. Nitroglycerin-CHF To relieve pulmonary congestion, increase Cardiac output To relieve pulmonary congestion, increase Cardiac output

35. Nitroglycerin-Unstable angina ECG will show either elevation or depression of ST segment, T wave abnormalities ECG will show either elevation or depression of ST segment, T wave abnormalities Treatment: Treatment: Aspirin-improves survival, heparin-to reduce angina and prevent infarction, Aspirin-improves survival, heparin-to reduce angina and prevent infarction, Nitrates- decrease vasospasm and control angina i/v + Nitrates- decrease vasospasm and control angina i/v + Calcium channel blockers added for complete control Calcium channel blockers added for complete control

36. Nitroglycerin -MI To reduce size of infarct, preserve viable tissue by decreasing O2 demand of myocardium (Cause is intra coronary thrombosis) To reduce size of infarct, preserve viable tissue by decreasing O2 demand of myocardium (Cause is intra coronary thrombosis) Treatment-reperfusion therapy, thrombolytic agents, Antiplatelet agents, percutaneous coronary angioplasty, atherectomy, stent deployment, revascularization procedures Treatment-reperfusion therapy, thrombolytic agents, Antiplatelet agents, percutaneous coronary angioplasty, atherectomy, stent deployment, revascularization procedures

37. Variants angina-Nitrates Long acting nitrates-sometimes effective, aspirin,beta blockers, CCBs Long acting nitrates-sometimes effective, aspirin,beta blockers, CCBs

38.  -adrenoceptors are linked via G-proteins to adenylyl cyclase, so endogenous  -agonists (NA or adrenaline)  se cAMP are linked via G-proteins to adenylyl cyclase, so endogenous  -agonists (NA or adrenaline)  se cAMP In heart cAMP: -  force of contraction & rate - is arrhythmogenic in arterioles - vasodilatation in kidney - renin release in airways - bronchorelaxation So  sed symp. activity (exercise, emotion, cold exposure) precipitates angina by  sing myocardial O 2 consumption So  sed symp. activity (exercise, emotion, cold exposure) precipitates angina by  sing myocardial O 2 consumption

39. Beta-blockers-Pharmacological effects They  cardiac work by -tive inotrope,-ive chronotrope & hypotensive effects They  cardiac work by -tive inotrope,-ive chronotrope & hypotensive effects so  myocardial o 2 consumption so  myocardial o 2 consumption Improves myocardial perfusion due to  heart rate Improves myocardial perfusion due to  heart rate so  anginal pain & attack frequency. so  anginal pain & attack frequency. They paradoxically worsen coronary spasm, because of unopposed  -mediated vasoconstriction, hence C/I in variant angina They paradoxically worsen coronary spasm, because of unopposed  -mediated vasoconstriction, hence C/I in variant angina most  -blockers are similarly effective despite pharmacological differences. most  -blockers are similarly effective despite pharmacological differences. Used for prophylaxis of classic (stable) angina Used for prophylaxis of classic (stable) angina

40. Pharmacokinetics Well absorbed orally Well absorbed orally Can be given as tab/SR caps Can be given as tab/SR caps metabolized & excreted by liver metabolized & excreted by liver Nonselective Beta-blockers duration: 4-12 hrs duration: 4-12 hrs Cardioselective Beta-blockers duration: 24 hrs duration: 24 hrsIndications Chronic & acute management Chronic & acute management

41.  -blockers Non-selective Non-selective propranolol, nadolol, timolol, pindolol, carteolol Cardio-selective Cardio-selective atenolol, metoprolol, esmolol, betaxolol, bisoprolol, acebutolol With  blockade With  blockade labetalol, carvedilol

42. Pharmacokinetics Propranolol - prototype  -blocker, substantial presystemic metabolism (CYP2D6), so dose titration important. Propranolol - prototype  -blocker, substantial presystemic metabolism (CYP2D6), so dose titration important. Atenolol, metoprolol - largely replaced propranolol - "cardioselective" - need less frequent dosing, & useful dose range is less wide than propranolol -so easier to use. Atenolol, metoprolol - largely replaced propranolol - "cardioselective" - need less frequent dosing, & useful dose range is less wide than propranolol -so easier to use. Atenolol - largely excreted unchanged by kidneys Atenolol - largely excreted unchanged by kidneys metoprolol - inactivated by liver metabolism metoprolol - inactivated by liver metabolism

43. ADR & C/I Fatigue, depression, hypotension, bradycardia Fatigue, depression, hypotension, bradycardia all can precipitate cardiac failure, worsen heart block all can precipitate cardiac failure, worsen heart block worsen obstructive airways disease, so C/I in asthma, COPD worsen obstructive airways disease, so C/I in asthma, COPD avoid in peripheral vascular disease & Raynaud´s, diabetes (mask hypoglycemic symptoms) avoid in peripheral vascular disease & Raynaud´s, diabetes (mask hypoglycemic symptoms) abrupt stoppage - rebound  se in frequency & severity of IHD – due to upregulation of  -receptors- so taper dose when discontinuing abrupt stoppage - rebound  se in frequency & severity of IHD – due to upregulation of  -receptors- so taper dose when discontinuing

44. Calcium Channel Blockers (CCBs) Calcium  ses workload of the heart Calcium  ses workload of the heart So CCBs  se myocardial O 2 consumption via afterload reduction,  sed HR & contractility So CCBs  se myocardial O 2 consumption via afterload reduction,  sed HR & contractility Cause vasodilation of coronary arteries Cause vasodilation of coronary arteries Also inhibit platelets Also inhibit platelets Classes of drugs dihydropyridine – nifedipine dihydropyridine – nifedipine verapamil verapamil diltiazem diltiazem

45. Administration - for chronic therapy - orally Indications - CCBs are often given with nitrates to treat angina - CCBs are often given with nitrates to treat angina - when  -blockers or nitrates ineffective &/or - when  -blockers or nitrates ineffective &/or intolerable intolerable - main agents – verapamil, diltiazem - main agents – verapamil, diltiazem Pharmacologic issues - conduction abnormalities, -ive inotropic effect, - conduction abnormalities, -ive inotropic effect, drug interactions (including grape fruit juice) drug interactions (including grape fruit juice) - dihydropyridine (nifedipine – reflex tachycardia so - dihydropyridine (nifedipine – reflex tachycardia so not for effort angina but good for vasospastic) not for effort angina but good for vasospastic) CCBs

46. Drug combinations To maximise efficacy To maximise efficacy Minimise adverse effects Minimise adverse effects E.g. Nitrites + Beta blockers & or CCB

47. ADR Headache, dizziness Headache, dizziness hypotension, flushing hypotension, flushing edema of legs edema of legs constipation constipationContraindications Conduction abnormalities Conduction abnormalities Cardiac failure Cardiac failure

48. Antiplatelet agents Stable Angina Acetyl salicylic acid (ASA) 81 – 162 mg/day, indefinitely Acetyl salicylic acid (ASA) 81 – 162 mg/day, indefinitely clopidogrel 75mg/day po - alternative if ASA allergy clopidogrel 75mg/day po - alternative if ASA allergy Unstable Angina ASA 81 – 162 mg/day indefinitely ASA 81 – 162 mg/day indefinitely (clopidogrel 75mg qd, ticlopidine 250mg bid followed by warfarin if ASA allergy) (clopidogrel 75mg qd, ticlopidine 250mg bid followed by warfarin if ASA allergy) IV unfractionated heparin (UF) in addition to ASA & continued for 48 hrs or till revascularization done IV unfractionated heparin (UF) in addition to ASA & continued for 48 hrs or till revascularization done Alternative to UH- LMWH (enoxaparin or dalteparin) Alternative to UH- LMWH (enoxaparin or dalteparin) consider GPIIb/IIIa’s in unstable or high risk pts consider GPIIb/IIIa’s in unstable or high risk pts

49. Treatment Strategies Stable Angina - B-blockers, CCBs, nitrates Stable Angina - B-blockers, CCBs, nitrates HTN patients - B-blockers, CCBs, ACE-I HTN patients - B-blockers, CCBs, ACE-I Normotensive patients - Monotherapy with long-acting nitrates Normotensive patients - Monotherapy with long-acting nitrates HTN patients with sinus brady or AV node dysfunction - Long-acting dihydropyridines (amlodipine), ACE-I HTN patients with sinus brady or AV node dysfunction - Long-acting dihydropyridines (amlodipine), ACE-I Prinzmetal’s Angina - Nitrates & CCB Prinzmetal’s Angina - Nitrates & CCB

50. Treatment Strategies.. Unstable Angina Antithrombotic therapy Antithrombotic therapy Maximize  -blocker therapy, with additional long acting nitrate Maximize  -blocker therapy, with additional long acting nitrate Non-dihydropyridines if  -blocker ineffective Non-dihydropyridines if  -blocker ineffective iv management if persistent symptoms – including NTG, B-blocker, heparin, ± morphine iv management if persistent symptoms – including NTG, B-blocker, heparin, ± morphine

51. Angina treatment - summary A – aspirin, antianginals (& ACEI) A – aspirin, antianginals (& ACEI) B –  -blockers & BP B –  -blockers & BP C – cholesterol & cigarettes C – cholesterol & cigarettes D – diet & diabetes D – diet & diabetes E – education & exercise E – education & exercise

52. Drug therapy of MI - Principles Pain, anxiety - morphine 15 mg IV Pain, anxiety - morphine 15 mg IV Oxygen – inhalation Oxygen – inhalation Fluid volume & tissue perfusion - IV saline Fluid volume & tissue perfusion - IV saline Acidosis correction - Soda. bicarb IV Acidosis correction - Soda. bicarb IV Arrhythmias prevention & treatment - beta blocker/lidocaine Arrhythmias prevention & treatment - beta blocker/lidocaine Pump failure - Furosemide, Vasodilator- GTN, Inotropics- dopamine Pump failure - Furosemide, Vasodilator- GTN, Inotropics- dopamine Prevention of thrombus extension-heparin Prevention of thrombus extension-heparin Thrombolysis-streptokinase Thrombolysis-streptokinase Prevention of future attack Prevention of future attack antiplatelet drugs-aspirin antiplatelet drugs-aspirin control of hyperlipidemia control of hyperlipidemia

53. Self study Pharmacology (classification, MOA, kinetics, routes, uses & ADR) of drugs for IHD Pharmacology (classification, MOA, kinetics, routes, uses & ADR) of drugs for IHD Determinants of cardiac oxygen demand & their manipulation Determinants of cardiac oxygen demand & their manipulation Choice of a drug and the rationale Choice of a drug and the rationale Preparations of antianginal drugs Preparations of antianginal drugs Combination of drugs Combination of drugs Tolerance to drugs & how to overcome Tolerance to drugs & how to overcome Management of acute & chronic conditions including acute MI Management of acute & chronic conditions including acute MI Clinically important drug interactions Clinically important drug interactions Recent advances in drug therapy of IHD Recent advances in drug therapy of IHD Life style modification in IHD patients Life style modification in IHD patients Role of other drugs (e.g. aspirin) in IHD Role of other drugs (e.g. aspirin) in IHD

54. Drugs for Ischemic Heart Disease (IHD) Objectives:   To define, list the major types and the etiology of angina pectoris.   To explain the balance between myocardial oxygen supply and demand in relation to IHD.   To brief about the therapeutic principles underlying the management of IHD.   To classify antianginal drugs with suitable examples.   To discuss the pharmacology of prototype antianginal drugs (nitrates, beta adrenoceptor blockers and calcium channel blockers.

55. Learning outcomes The learner should be able to   Define, list the major types and the etiology of angina pectoris.   List the factors that balance myocardial oxygen supply and demand in relation to IHD.   Classify antianginal drugs with suitable examples

56.   Mention the role of antiplatelet agents in IHD.   To outline the treatment strategies towards prophylaxis and treatment of angina pectoris.   To outline the drug treatment of myocardial infarction.   To suggest topics related to drug treatment of IHD for self reading.

57.   Discuss the mechanism of action, pharmacological action, pharmacokinetics, indications, contraindications, clinically important drug interactions, combination therapy, routs of administration of   nitrate,   beta adrenoceptor blocker   calcium channel blocker   Briefly explain the role of antiplatelet agents in IHD.   Outline the treatment strategies towards management of angina pectoris.   Outline the drug treatment of myocardial infarction.