Angina pectoris, commonly referred to as angina, is a symptom of myocardial ischemia characterized by chest pain or discomfort due to insufficient blood flow to the heart muscle. Anti-anginal drugs are used to alleviate symptoms, improve exercise tolerance, and prevent acute coronary events.
Introduction
Anti-anginal drugs are medications designed to manage and treat angina pectoris. They work through various mechanisms to improve oxygen supply to the heart muscle or decrease its oxygen demand. The primary goals of anti-anginal therapy are to reduce the frequency and severity of angina attacks, improve quality of life, and prevent myocardial infarction and sudden cardiac death.
Classification of Anti-Anginal Drugs
Anti-anginal drugs can be classified into several categories based on their mechanism of action:
1. Nitrates
– Examples: Nitroglycerin, Isosorbide Mononitrate, Isosorbide Dinitrate
– Mechanism of Action:
– Nitrates are converted to nitric oxide (NO) in the vascular smooth muscle, leading to vasodilation.
– They primarily dilate veins, reducing venous return (preload) and decreasing myocardial oxygen demand.
– They also dilate coronary arteries, increasing blood flow to the ischemic areas of the heart.
– Uses: Acute angina attacks, prophylaxis of angina, heart failure.
– Side Effects: Headache, hypotension, reflex tachycardia, dizziness, flushing, nitrate tolerance.
2. Beta-Blockers
– Examples: Metoprolol, Atenolol, Propranolol
– Mechanism of Action:
– Beta-blockers inhibit beta-adrenergic receptors, decreasing heart rate and contractility, thus reducing myocardial oxygen demand.
– They also decrease blood pressure, further reducing the workload on the heart.
– Uses: Chronic stable angina, post-myocardial infarction, hypertension, heart failure.
– Side Effects: Bradycardia, fatigue, bronchoconstriction (in non-selective beta-blockers), depression, sexual dysfunction.
3. Calcium Channel Blockers (CCBs)
– Dihydropyridines
– Examples: Amlodipine, Nifedipine
– Mechanism of Action:
– Inhibit calcium influx into vascular smooth muscle, causing vasodilation, primarily in the arteries.
– Reduce afterload and improve oxygen supply to the heart.
– Uses: Chronic stable angina, Prinzmetal’s (variant) angina, hypertension.
– Side Effects: Peripheral edema, reflex tachycardia, headache, flushing.
– Non-Dihydropyridines
– Examples: Verapamil, Diltiazem
– Mechanism of Action:
– Inhibit calcium influx into both cardiac and vascular smooth muscle, reducing heart rate and contractility.
– Improve coronary blood flow and reduce myocardial oxygen demand.
– Uses: Chronic stable angina, Prinzmetal’s angina, hypertension, arrhythmias.
– Side Effects: Bradycardia, constipation (especially with verapamil), AV block, dizziness.
4. Ranolazine
– Example: Ranolazine
– Mechanism of Action:
– Ranolazine inhibits the late phase of the sodium current (late INa) in cardiac cells, reducing intracellular sodium and calcium overload.
– This improves myocardial relaxation and reduces oxygen consumption without significantly affecting heart rate or blood pressure.
– Uses: Chronic stable angina, especially in patients who are not adequately controlled with other anti-anginal medications.
– Side Effects: Dizziness, headache, constipation, nausea, QT interval prolongation.
5. Antiplatelet Agents
– Examples: Aspirin, Clopidogrel, Prasugrel
– Mechanism of Action:
– Inhibit platelet aggregation, reducing the risk of thrombus formation in the coronary arteries.
– Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1), preventing thromboxane A2 formation.
– Clopidogrel and Prasugrel inhibit the P2Y12 component of the ADP receptor on platelets.
– Uses: Secondary prevention of myocardial infarction, unstable angina, percutaneous coronary intervention (PCI).
– Side Effects: Bleeding, gastrointestinal ulcers (aspirin), bruising, allergic reactions.
6. Statins
– Examples: Atorvastatin, Rosuvastatin, Simvastatin
– Mechanism of Action:
– Inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, leading to reduced LDL cholesterol levels.
– Improve endothelial function, stabilize atherosclerotic plaques, and reduce inflammation.
– Uses: Primary and secondary prevention of cardiovascular events, hyperlipidemia.
– Side Effects: Myopathy, rhabdomyolysis, liver enzyme elevation, gastrointestinal symptoms.
 Mechanisms of Action of Anti-Anginal Drugs
– Improvement of Oxygen Supply:
– Nitrates and certain CCBs dilate coronary arteries, increasing blood flow to the heart.
– Nitrates also reduce coronary artery spasm in Prinzmetal’s angina.
– Reduction of Oxygen Demand:
– Beta-blockers and non-dihydropyridine CCBs decrease heart rate and contractility, reducing the workload on the heart.
– Nitrates and dihydropyridine CCBs reduce preload and afterload, decreasing myocardial oxygen demand.
– Ranolazine reduces intracellular calcium overload, improving myocardial efficiency.
– Prevention of Thrombus Formation:
– Antiplatelet agents prevent platelet aggregation and thrombus formation in coronary arteries.
– Stabilization of Atherosclerotic Plaques:
– Statins reduce LDL cholesterol levels and stabilize plaques, reducing the risk of plaque rupture and acute coronary events.
 Uses of Anti-Anginal Drugs
– Chronic Stable Angina: Most anti-anginal drugs are used to manage chronic stable angina, improving exercise tolerance and reducing angina frequency.
– Unstable Angina: Antiplatelet agents and nitrates are critical in the management of unstable angina to prevent myocardial infarction.
– Prinzmetal’s (Variant) Angina: Nitrates and CCBs, especially dihydropyridines, are effective in relieving coronary artery spasm.
– Post-Myocardial Infarction: Beta-blockers, antiplatelet agents, and statins are used to improve survival and prevent recurrent events.
– Hypertension: Beta-blockers and CCBs are also used in the treatment of hypertension, particularly in patients with coexisting angina.
– Heart Failure: Nitrates, beta-blockers, and certain CCBs (amlodipine) are used to manage heart failure in patients with angina.
 Side Effects of Anti-Anginal Drugs
– Nitrates: Headache, hypotension, reflex tachycardia, dizziness, flushing, nitrate tolerance.
– Beta-Blockers: Bradycardia, fatigue, bronchoconstriction (in non-selective beta-blockers), depression, sexual dysfunction.
– Calcium Channel Blockers:
– Dihydropyridines: Peripheral edema, reflex tachycardia, headache, flushing.
– Non-Dihydropyridines: Bradycardia, constipation (especially with verapamil), AV block, dizziness.
– Ranolazine: Dizziness, headache, constipation, nausea, QT interval prolongation.
– Antiplatelet Agents: Bleeding, gastrointestinal ulcers (aspirin), bruising, allergic reactions.
– Statins: Myopathy, rhabdomyolysis, liver enzyme elevation, gastrointestinal symptoms.
