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Antianginal drugs

Calcium channel blockers are used to treat angina and hypertension by blocking L-type calcium channels. This prevents calcium entry into cardiac and smooth muscle cells, causing vasodilation, decreased heart rate and blood pressure. Nitrates are commonly used to treat angina via conversion to nitric oxide which causes smooth muscle relaxation and vasodilation, reducing workload on the heart. Verapamil and diltiazem have more prominent cardiac effects while dihydropyridines like nifedipine are potent vasodilators. Calcium channel blockers are effective for various types of angina, hypertension, arrhythmias and other uses.

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Dr. Binu Babu Ph.D., M.Sc. (N), MBA Mrs. Jincy Ealias M.Sc. (N)
 Anti - anginal drugs are the drugs that prevent or terminate attacks of angina pectoris.
• Eg: Nitroglycerin (GTN), isosorbide dinitrate, isosorbide mononitrate, pentaerythritol tetranitrate. Nitrates • Eg:Verapamil, diltiazem, amlodipine, nifedipine. Calcium channel blockers • Eg: Propranolol, atenolol β- adrenergic blockers • Eg: Nicorandil, pinacidil. Potassium channel openers • Dipyridamole, aspirin, trimetazidine, ranolazine, ivabradine. Miscellaneous
 Nitrates are vasodilators.  Nitrates act directly on smooth muscles and produce relaxation.  Commonly used nitrate is nitroglycerine (GTN).
Short acting nitrates Used to terminate acute attack of angina Eg: Nitroglycerin (GTN) Long acting nitrates Used to prevent an attack of angina Eg: isosorbide dinitrate, isosorbide mononitrate, pentaerythritol tetranitrate
 In the smooth muscles nitrates are converted to nitric oxide.  This nitric oxide activates vascular guanylyl cyclase (GC) which in turn increases the synthesis of cGMP (Cyclic guanosine monophosphate).  This cGMP causes sequestration of Ca2+ , which is responsible for relaxation of the smooth muscles.  Results in vasodilation.
Vasodilation Relax vascular smooth muscle Relaxation of smooth muscles cGMP causes sequestration of Ca2+ Increases the synthesis of cGMP Activates vascular guanylyl cyclase Nitrates converted to nitric oxide
1. Reduction of preload 2. Reduction of afterload 3. Coronary dilation 4. Other actions 1. Dilation of other vasculature 2. Relaxation of other smooth muscles 3. Effects on platelets.
Nitrates are vasodilators. 1. Reduction of preload Venodilation reduces venous return to the heart thereby reduce preload. 2. Reduction of afterload Arteriolar dilation reduces vascular resistance thus decrease afterload 3. Coronary dilation Nitrates cause coronary vasodilation, thus relieves vasospasm and increases coronary blood flow. As both preload and afterload are reduced, workload of the heart is decreased, thereby reducing oxygen requirement of the heart.
4. Other actions Dilation of other vasculature • Dilation of blood vessels in skin results in flushing. • Dilation of meningeal vessels results in headache. Relaxation of other smooth muscles Nitrates relax the bronchial, gastrointestinal and genitourinary smooth muscles for a short period. Effects on platelets Nitric oxide from nitrates inhibits platelet aggregation.
 Nitrates are available for oral, Sublingual, spray parenteral, ointment and transdermal patch.  Nitrates are well-absorbed orally, but they undergo extensive first pass metabolism.  So the oral bioavailability of nitrate is poor.  Sublingual route is preferred in case of emergency for rapid absorption and better bioavailability.  Sublingual tablets acts within 1-2 minutes whereas Sublingual spray acts faster than tablets.
Sublingual Spray Transdermal patch
Drug Dose Route Nitroglycerin (GTN) 0.5 mg Sublingual 5 mg Oral 2% Ointment 0.4-0.8 mg Sublingual spray 5-20 μg/min IV 14-16 hrs/day Transdermal patch Isosorbide dinitrate (Sorbitrate) 5-10 mg Sublingual 10-20 mg Oral Isosorbide mononitrate (Ismo) 10-20 mg Oral pentaerythritol tetranitrate 10-40 mg Oral
 Headache (common)  Flushing of face  Nausea and vomiting  Sweating  Tachycardia  Palpitation  Weakness  Postural hypotension  Rashes  Contact dermatitis  Local hypersensitivity reaction for topical use
 Exertional angina  Acute anginal attacks : ▪ Sublingual nitroglycerin ▪ Drug of choice for acute anginal attacks. ▪ Relieves pain in 2 to 5 minutes. ▪ If the pain is not relieved, the dose is repeated-upto 3 tablets in 15 minutes.  Prophylaxis of angina ▪ NTG can be used for chronic prophylaxis. ▪ Longer acting nitrates are preferred. ▪ Nitroglycerin ointment orTransdermal patch may be used.
 Vasospastic angina  Unstable angina  Acute coronary syndrome  Cardiac failure  Myocardial infarction  Cyanide poisoning  Nitrates are life saving in cyanide poisoning.  Amylnitrite is given by inhalation and sodium nitrite by IV injection (10 ml of 3% solution). Then Sodium thiosulphate is given IV (50 ml of 25% solution).
 Role of nitrates in cyanide poisoning.  Nitrates (Amylnitrite and sodium nitrite) convert hemoglobin into methemoglobin, which has high affinity for cyanide and forms cyano- methemoglobin.  Cyano-methemoglobin reacts with Sodium thiosulphate to form thiocyanate which is easily excreted by the kidneys.
 Relieve esophageal spasm  Sublingual NTG is taken just before meals to counter the spasm.  Relieve biliary colic  Sublingual NTG is also useful as a spasmolytic.
 Monitor BP before and after administration.  Nitroglycerine is sensitive to light, heat and moisture, so stored in tightly closed amber colored glass bottles.  Give sublingual preparations under the tongue or in the buccal pouch.  Nitroglycerine IV preparation is mixed in 5% Dextrose Injection or 0.9% Sodium Chloride.  Instruct the patient that a sublingual dose may be repeated in 5 minutes if pain is not relieved, for a total of 3 doses.
 Calcium channel blockers (CCBs) are the drugs that disrupt calcium movement by blocking voltage-dependent Ca2+ channels used to treat angina and supraventricular tachydysrhythmias as well as hypertension.  Also known as calcium antagonists.
Calcium channel blockers Dihydropyridines 1st generation Eg: Nifedipine 2nd generation Eg: Isradipine, Nicardipine, Felodipine 3rd generation Eg: Amlodipine Phenilalkylamines Eg:Verapamil Benzothiazepines Eg: Diltiazem
Decrease myocardial contraction, Decrease heart rate and AV conduction velocity, also cause Vascular smooth muscle relaxation Decrease calcium entry into cardiac and smooth muscle cells Block L-type calcium channels Calcium channel blockers
 Cardiac and smooth muscle cell contraction depends upon the activation of calcium channels in the cardiac myocytes. For depolarization of cardiac and other smooth muscles cells, entry of calcium into the cells occurs through these calcium channels. This calcium triggers the release of intracellular calcium from sarcoplasmic reticulum.
 On vascular smooth muscles and Coronary circulation  On other smooth muscles  On heart
 On vascular smooth muscles and Coronary circulation Vascular smooth muscle relaxation peripheral Coronary artery vascular dilation dilation Decrease peripheral Increase coronary vascular resistance blood flow Decrease Decrease Increase myocardial BP afterload O2 supply Decrease myocardial O2 consumption HTN treatment Angina treatment
 Dihydropyridine CCBs have prominent effect on blood vessels.  Nimodipine crosses the blood brain barrier and relaxes the cerebral blood vessels. On other smooth muscles  Relax GI and bronchial smooth muscles  Relax uterus, so used in premature labor.
 On heart Decrease myocardial DecreaseAV Contraction conduction velocity Decrease heart Rate Bradycardia Reduce myocardial workload Decrease myocardial O2 Consumption Angina treatment Arrhythmia treatment
 Verapamil, bepridil and diltiazem have promi- nent cardiac effects.
 CCBs are well-absorbed orally but undergo extensive first pass metabolism.  They are metabolized in the liver.  Excreted through kidneys.  Onset of action is in 30-60 minutes after oral administration while on IV use the action is quick.
1. Verapamil  Decrease heart rate (negative chronotropic effect)  Decrease force of myocardial contraction (negative ionotropic effect)  DecreaseAV conduction  Vasodilator effect of verapamil is less potent.  Used in arrhythmia and angina.  Dose: 40-160 mgTDS orally and 5 mg by slow IV inj.  Adverse effects  Nausea  Constipation  Bradycardia  Heart block  Hypotension  Skin rashes
2. Diltiazem  Decrease heart rate (negative chronotropic effect)  Decrease force of myocardial contraction (negative ionotropic effect)  Vasodilator effect is less potent.  Dose: 30-60 mgTDS orally.  Adverse effects –same as verapamil.
3. Nifedipine  Potent vasodilator and causes a significant fall in BP and evokes reflex tachycardia.  Myocardiac depressant effect is weak  It can be given orally or sublingually. Patches also  Dose: 5-20 mg BD  Adverse effects  Headache  Flushing  Palpitation  Dizziness  Fatigue  Hypotension  Leg cramps  Ankle edema  Long-term use : gum hypertrophy
3. Nimodipine  Crosses the blood brain barrier and relaxes the cerebral blood vessels.  Used in haemorrhagic stroke and subarachnoid haemorrhage.  Dose: 30-60 mg QID.
4. Amlodipine, felodipine, nitrendipine, nicardipine  High vascular effects.  Long acting CCBs.  Can be given once daily.  Useful HTN.
 Angina pectoris  As prophylaxis for exertional angina ▪ Verapamil and diltiazem for prophylaxis  Variant angina  Vasospastic angina ▪ Verapamil and amlodipine are preferred  Unstable angina ▪ Verapamil is used  Dihydropyridine CCBs like amlodipine with beta blockers for long term management.
 Hypertension  Chronic hypertension : ▪ Long acting CCBs. ▪ Amlodipine is preferred  Hypertensive crisis: nifedipine used sublingually  Arrhythmias  Supraventricular Arrhythmias : premature atrial contraction, atrial tachycardia, atrial fluttr, atrial fibrillation  Verapamil, diltiazem and bepridil
 Peripheral vascular disease  Nifedipine, felodipine and diltiazem can be used in Raynaud's disease.  Migraine  Prophylaxis- verapamil is useful  Hypertrophic cardiomyopathy  Verapamil is useful  Subarachnoid hemorrhage and haemorrhagic stroke  Nimodipine is useful.  Preterm labor  Nifedipine is useful.
 Verapamil and diltiazem should be avoided in patients receiving beta-adrenergic blockers because the myocardiac depressant effects get added up.  Verapamil can precipitate digoxin toxicity by increasing digoxin levels (verapamil reduces digoxin excretion).
 Beta blockers are the drugs that block beta receptors thereby inhibiting the actions of sympathetic stimulations (catecholamines).  Beta antagonist.
• Eg: Propranolol, nadolol, timolol, sotalol Nonselective • Eg: Metoprolol, atenolol, acebutolol, esmolol Cardioselective (β1) • Eg:- Pindolol, oxprenolol, carteolol, bopindolol, penbutotol Partial agonists • Eg: Labetalol, carvedilol With additional alpha blocking property • Eg: Celiprolol β1 blocker β2 agonist
1. Nonselective  Blocks both β1 and β2 receptors. 2. Cardioselective (β1)  Blocks cardiac specific β1 receptors. β2 receptor blockade is weak. 3. Partial agonists  Have some sympathomimetic action due to partial β agonist property. 4. With additional alpha blocking property  Blocks both α and β (β1 and β2) receptors. 5. β1 blocker β2 agonist  Blocks only cardiac specific β1 receptors.
1st generation (Non selective) Eg: Propranolol, timolol, sotalol, 2nd generation (Cardioselective) Eg: Metoprolol, atenolol, acebutolol, esmolol 3rd generation (With additional α blocking property & vasodilator property) Eg: Labetalol, carvedilol, Celiprolol
Reduce cardiac workload Reduce myocardial O2 demand Decrease heart rate, Decrease force of contraction, Decrease cardiac output, Decrease BP, Delay AV conduction Inhibit sympathetic (catecholamines) stimulations Blocks beta receptors
 CVS  Act as cardiac depressant  Decrease heart rate (negative chronotropic effect)  Decrease force of contraction (negative ionotropic effect)  Decrease cardiac output  Decrease BP  Delay AV conduction (negative dromotropic effect)  Reduce myocardial O2 demand  Reduce cardiac workload.  Improve exercise tolerance in angina patients.
 Respiratory tract  Blockade of B2 receptors in the bronchial smooth muscle causes increase in airway resistance.  May precipitate acute attack in asthmatics.  Eye  Reduce intraocular pressure by decreased secretion of aqueous humor.  Metabolism  β-antagonists block lipolysis & glycogenolysis – cause rise in plasma free fatty acid and triglyceride.Also interfere with recovery from hypoglycemia in diabetics
 Well absorbed orally.  Given intravenously in emergencies.  Low oral bioavailability due to extensive first pass metabolism.  Highly lipid soluble, so crosses blood brain barrier.  Metabolized in the liver.  Excreted through kidneys.
 Bradycardia (common)  CCF  Acute pulmonary edema  Cold extremities (in patients with peripheral vascular disease)  Acute asthmatic attack (in asthmatics)  CNS  Insomnia  Depression  Halluçination (rare)  Fatigue, weakness  Decrease exercise capacity  Rebound hypertension and anginal attacks  Due to abrupt withdrawal of B-blockers after prolonged use.
 Hypertension  As first line drugs in mild to moderate hypertension  Used alone or with other antihypertensives.  Angina pectoris  Long term prophylaxis of exertional angina and classical angina.  Cardioselective drugs are preferred than non selective drugs.  Have to take on regular basis.  Cardiac arrnythmias  For both supraventricular & ventricular arrhythmias
 Myocardial infarction  Given IV infusion in acute MI to limit the size of infarct.  Long-term treatment prolongs survival.  Congestive cardiac failure  Obstructive cardiomyopathy  Pheochromocytoma  Propranolol is given before surgery to control hypertension.
 Thyrotoxicosis  Propranolol controls palpitation, tremors and affords symptomatic relief in thyrotoxicosis.  Used as adjuvant.  Also useful in thyrotoxic crisis.  Glaucoma  Timolol is used topically in open angle glaucoma.  Migraine  As prophylaxis.  Propranolol is used.  Anxiety  Propranolol prevents the acute panic symptoms
 Bradycardia  COPD  Asthma  Heart block
 Atenolol  Cardioselective  Longer acting-given once daily  Less lipid soluble-does not cross BBB-hence no CNS side effects  No side effects on lipid profile. Hence very commonly used  Dose: 25-100 mg daily.  IV (5-10 mg over 5 minutes) reduce short term mortality in MI and lowers incidence of arrhythmias.
 Esmolol  Cardioselective  Ultra short acting - t½ - 8 minutes.  Used IV.  Safer in critically ill patients and in emergencies.  Metoprolol  Cardioselective  Well-absorbed but undergoes first pass metabolism  Given twice daily  Dose: 50-200 mg  Used in hypertension and angina pectoris.
 Acebutolol  Cardioselective  Used in hypertension and arrhythmias.  Celiprolol  β1 blocker and β2 agonist  Safer in asthmatics  Used in hypertension.
 Propranolol  Nonselective  Dose: oral 10 mg BD to 160 mgTID.  First line drugs in mild to moderate hypertension  Used in HTN, angina, arrhythmias, migraine
 Potassium-channel openers are drugs that activate (open) ATP-sensitive K+ channels in vascular smooth muscle and results vascular smooth muscle relaxation.
Potassium channel openers Open ATP-sensitive K+ channels in vascular smooth muscle Enhance K+ efflux Membrane Hyperpolarization ↓ Ca 2+ entry Reduced intracellular calcium Smooth muscle relaxation
 Nicorandil is an arterial and venous dilator.  MOA Nicorandil Open ATP-sensitive Act as nitric oxide K+ channels donor Enhance K+ efflux Membrane Hyperpolarization ↓ Ca 2+ entry Reduced intracellular calcium Smooth muscle relaxation Decrease preload and afterload, increase coronary blood flow
 Use  Resistant angina  In combination with other drugs  Dose: 10-20 mg twice daily.  Adverse effects  Headache  Flushing  Palpitation  Dizziness  Hypotension
 Similar to nicorandil.  Uses  Angina  Hypertension
 Coronary vasodilator  But it is not used in angina as it diverts blood from ischemic zone to non ischemic zone.  It inhibits platelet aggregation for which it is used in post-MI and post-stroke patients tor prevention of coronary and cerebral thrombosis.  Dose 25-100 mgTID.
 Long-term administration of low dose aspirin is recommended to prevent myocardial infarction.  Inhibits platelet aggregation.  Dose: 75-100mg
 Anti-anginal action through inhibition of fatty acid metabolism, also known as fatty acid oxidation inhibitor.  Used in post MI patients.  Dose: 20 mgTID.
 Recently introduced trimetazidine congener.  MOA  Prevents calcium overload in the myocardium during ischemia and reduces myocardial O2 demand.  Uses  Prevention of angina as add on therapy.  Dose : 500 mg sustained release tablets twice daily.  Adverse effects  Weakness  Postural hypotension  Dizziness  Headache  Constipation
 Nitrates + β blockers  Nifedipine + β blockers  Nitrates + CCB  Nitrates + β blockers+ CCB  If not controlled by 2 drug combination.
Antianginal drugs