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SATENDRA PRADHAN, Assistant Professor, Collage of Pharmacy, SVITS, profile picture
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Comprehensive Overview of Angina and Antianginal Pharmacotherapy

This presentation provides a comprehensive, study-oriented overview of Angina Pectoris and its pharmacological management. Developed specifically for pharmacology learning, it explains the pathophysiology of myocardial ischemia, classification of angina, and the mechanisms of action, therapeutic uses, adverse effects, and clinical applications of major antianginal drug classes. The content is presented in a structured, evidence-based format with clear flowcharts and simplified explanations, making it an ideal resource for B.Pharm, D.Pharm, Pharm.D, MBBS, Nursing, and Allied Health Science students, as well as aspirants preparing for GPAT, NIPER other competitive examinations.

Health & Medicine◦
Related topics:
angina-pectoris• Coronary Artery Disease•
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Mr. SATENDRA PRADHAN Assistant Professor Department of Pharmacology COP, SVITS, Bilaspur Ms. MANISHA SAHU Assistant Professor Department of Pharmacology SCCP, Rajnandgaon
INTRODUCTIO N What is Angina Pectoris? A clinical syndrome of transient myocardial ischemia Definition Angina is chest pain or discomfort caused by an imbalance between myocardial oxygen demand and oxygen supply, most often due to coronary artery narrowing. Angina is a clinical syndrome characterized by chest pain or discomfort caused by temporary myocardial ischemia (reduced blood supply to the heart muscle) without causing permanent damage (myocardial infarction). O2 Supply Determined by coronary blood flow & O2 content; reduced by coronary stenosis, spasm, or thrombus. O2 Demand Determined by heart rate, contractility, and wall tension; rises with exertion, tachycardia, or hypertension. Angina occurs when demand outstrips supply
INTRODUCTIO N Types of Angina Stable (Classic) Angina Predictable, exertional pain due to fixed atherosclerotic narrowing. Relieved by rest or nitrates within minutes. Fixed obstruction Unstable Angina New-onset, worsening, or rest pain from plaque rupture and thrombus; a medical emergency (ACS spectrum). Plaque rupture Variant (Prinzmetal) Angina Occurs at rest, often at night, due to focal coronary artery spasm; ST elevation during attack. Coronary spasm
INTRODUCTIO N Pathophysiology: Supply-Demand Imbalance Determinants that drive myocardial ischemia CoronaryArtery Disease / Spasm Reduced Coronary O2 Supply vs. Increased Myocardial O2 Demand Myocardial Ischemia Angina (Chest Pain) ↑ DEMAND FACTORS Heart rate Contractility Wall tension (preload/afterload) ↓ SUPPLY FACTORS Coronary artery diameter Diastolic filling time Coronary perfusion pressure Goal of therapy: reduce O2 demand and/or increase O2 supply to relieve or prevent ischemia.
CLASSIFICATIO N Classification of Antianginal Drugs
CLASSIFICATIO N Classification of Antianginal Drugs Four major pharmacological classes 1. Organic Nitrates Glyceryl trinitrate, Isosorbide dinitrate/mononitrate 2. Beta-Adrenergic Blockers Atenolol, Metoprolol, Propranolol, Bisoprolol 3. Calcium Channel Blockers Dihydropyridines (Amlodipine) & Non-DHP (Verapamil, Diltiazem) 4. Newer / Miscellaneous Agents Ranolazine, Ivabradine, Nicorandil, Trimetazidine
CLASS 1 — ORGANIC NITRATES Nitrates: Mechanism of Action Nitric oxide-mediated smooth muscle relaxation Organic nitrate enters vascular smooth muscle cell Denitrated → releases Nitric Oxide (NO) NO activates guanylate cyclase ↑ cGMP → dephosphorylation of myosin light chain Vascular smooth muscle relaxation (vasodilation) PREDOMINANT EFFECT Venodilation (predominant) → ↓ Venous return → ↓ Preload Mild arteriolar dilation → ↓ Afterload Coronary vasodilation → improves collateral/subendocardial flow Net result: ↓ Myocardial O2 demand, relief of ischemic pain
CLASS 1 — ORGANIC NITRATES Nitrates: Uses & Side Effects Glyceryl trinitrate · Isosorbide dinitrate · Isosorbide mononitrate Clinical Uses • Acute relief of angina (sublingual GTN) • Prophylaxis of exertional/stable angina • Unstable angina & acute coronary syndrome (IV) • Acute left ventricular failure / cardiogenic pulmonary edema • Controlled hypotension during surgery Side Effects • Throbbing headache (from meningeal vasodilation) • Postural (orthostatic) hypotension & dizziness • Reflex tachycardia • Facial flushing • Tolerance with continuous use (needs nitrate-free interval) • Methemoglobinemia (rare, high dose) Caution: Avoid co-administration with PDE-5 inhibitors (e.g., sildenafil) — risk of severe hypotension.
CLASS 2 — BETA-BLOCKER S Beta-Blockers: Mechanism of Action Reducing myocardial oxygen demand via β1-blockade Competitive blockade of cardiac β1-adrenergic receptors ↓ Sympathetic (catecholamine) drive to the heart ↓ Heart Rate (negative chronotropy) ↓ Contractility (negative inotropy) ↓ AV conduction velocity ↓ Myocardial oxygen demand & consumption Longer diastole also improves coronary perfusion → Relief of Angina
CLASS 2 — BETA-BLOCKER S Beta-Blockers: Uses & Side Effects Atenolol · Metoprolol · Propranolol · Bisoprolol Clinical Uses • First-line prophylaxis for chronic stable angina • Reduces frequency & severity of anginal episodes • Post-myocardial infarction — improves survival • Concurrent hypertension or arrhythmia • Improves exercise tolerance in stable angina Side Effects • Bradycardia & AV block • Bronchospasm (avoid/caution in asthma, COPD) • Fatigue, cold extremities, exercise intolerance • Masking of hypoglycemia symptoms in diabetics • Erectile dysfunction; vivid dreams/depression • Abrupt withdrawal → rebound angina/MI Contraindicated in variant (Prinzmetal) angina — unopposed alpha-mediated coronary spasm may worsen ischemia.
CLASS 3 — CALCIUM CHANNEL BLOCKERS Calcium Channel Blockers: Mechanism of Action Blockade of L-type calcium channels Block L-type voltage-gated Ca²⁺ channels ↓ Ca²⁺ influx into vascular smooth muscle & cardiac myocytes Vascular smooth muscle: Arteriolar/coronary vasodilation → ↓ Afterload, ↑ coronary flow (esp. DHPs) Cardiac myocytes (non-DHPs): ↓ Heart rate & contractility (negative chrono-/inotropy) ↓ Myocardial O2 demand + ↑ Myocardial O2 supply Relief / Prevention of Anginal attacks
CLASS 3 — CALCIUM CHANNEL BLOCKERS Calcium Channel Blockers: Uses & Side Effects Dihydropyridines (Amlodipine, Nifedipine) & Non-DHP (Verapamil, Diltiazem) Clinical Uses • Variant (Prinzmetal) angina — drug of choice • Stable angina, especially with hypertension • Alternative when beta-blockers are contraindicated (e.g., asthma) • Non-DHPs also used for rate control in atrial fibrillation • Often combined with nitrates or beta-blockers Side Effects • DHPs: flushing, headache, ankle edema, reflex tachycardia • Non-DHPs: bradycardia, AV block, constipation (verapamil) • Negative inotropy → caution in heart failure • Gingival hyperplasia (long-term use) • Hypotension and dizziness Avoid combining non-DHP CCBs with beta-blockers — additive risk of severe bradycardia and AV block.
CLASS 4 — NEWER AGENTS Newer Antianginal Agents Alternative mechanisms for refractory or intolerant patients Ranolazine Inhibits late inward Na⁺ current → reduces intracellular Ca²⁺ overload → ↓ diastolic wall tension, without changing HR/BP Ivabradine Selectively inhibits the If ("funny") current in the SA node → pure heart-rate reduction, no effect on contractility/BP Nicorandil K⁺ATP channel opener + nitrate-like moiety → arterial & venous dilation plus coronary vasodilation Trimetazidine Metabolic modulator — shifts myocardial energy metabolism from fatty acid to glucose oxidation, improving efficiency
CLASS 4 — NEWER AGENTS Newer Agents: Uses & Side Effects Drug Primary Use Key Side Effects Ranolazine Chronic stable angina refractory to first-line agents QT prolongation, dizziness, constipation, nausea Ivabradine Stable angina with contraindication/intolerance to beta- blockers; HR reduction Visual disturbances (phosphenes), bradycardia, headache Nicorandil Prophylaxis & treatment of stable angina Headache, flushing, oral/GI ulceration, hypotension Trimetazidine Add-on prophylactic therapy for stable angina GI disturbances, dizziness, rarely parkinsonism/movement disorders Note: These agents are typically used as add-on therapy alongside, or as alternatives to, first-line classes.
SUM M ARY Comparative Summary of Antianginal Drug Classes Hemodynamic effects at a glance Class Heart Rate Contractility Preload Afterload Nitrates ↑ (reflex) No direct change ↓↓ ↓ Beta-Blockers ↓↓ ↓↓ No change / ↑ No change CCBs (DHP) No change / ↑ (reflex) No change No change ↓↓ CCBs (Non-DHP) ↓↓ ↓ No change ↓ Ivabradine ↓↓ (selective) No change No change No change Nitrates: venodilation-dominant → preload reduction Beta-blockers: best for reducing cardiac workload CCBs: preferred for coronary vasospasm
K E Y T A K E A W A Y S Angina & Antianginal Drugs — Summary 1 Angina reflects a mismatch between myocardial O2 supply and demand — stable, unstable, and variant forms have distinct mechanisms. 2 Nitrates relieve ischemia primarily by venodilation, lowering preload; effective for acute and prophylactic use. 3 Beta-blockers reduce heart rate, contractility, and O2 demand — first-line for chronic stable angina, but avoided in variant angina. 4 Calcium channel blockers dilate coronary vessels and are the treatment of choice for vasospastic (Prinzmetal) angina. 5 Newer agents (ranolazine, ivabradine, nicorandil, trimetazidine) offer alternative mechanisms for refractory or intolerant patients.
Comprehensive Overview of Angina and Antianginal Pharmacotherapy