Angina Pectoris Medication

Updated: Jul 19, 2018
  • Author: Jamshid Alaeddini, MD, FACC, FHRS; Chief Editor: Eric H Yang, MD  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Antiplatelet agents

Class Summary

Prevent thrombus formation by inhibiting platelet aggregation. Aspirin is proven beneficial in primary and secondary prevention of coronary artery disease. In patients with aspirin intolerance, use clopidogrel. Clopidogrel is also used in combination with aspirin after coronary stent placement. Recently, clopidogrel use in addition to aspirin has been shown to be significantly superior to aspirin alone in patients with acute coronary syndrome without ST-segment elevation MI.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Prevents platelet aggregation by irreversible cyclooxygenase inhibition with subsequent suppression of thromboxane A2. Antiplatelet effect can last as long as 7 d.

Clopidogrel (Plavix)

Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of GPIIb/IIIa complex, thereby inhibiting platelet aggregation. Consider in patients with contraindication to aspirin.

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Beta-adrenergic blocking agents

Class Summary

Work by competing with endogenous catecholamines for beta-adrenergic receptors. Reduce myocardial oxygen consumption via several effects, including decrease in resting and exercise heart rates and reductions in myocardial contractility and afterload. Classified as nonselective, beta-1 selective, and having intrinsic sympathomimetic effects.

Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. Is lipophilic and penetrates CNS.

Atenolol (Tenormin)

Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors. Is hydrophilic and does not penetrate CNS.

Propranolol (Inderal)

Nonselective beta-blocker that is lipophilic (penetrates CNS). Although generally short-acting agent, long-acting preparations also available.

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Calcium channel blockers

Class Summary

Reduce transmembrane flux of calcium via calcium channels. Cause smooth muscle relaxation, resulting in peripheral arterial vasodilation and afterload reduction. Indicated when symptoms persist despite treatment with beta-blockers or when beta-blockers are contraindicated. Also indicated in patients with Prinzmetal angina with or without nitrates.

Amlodipine (Norvasc)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Diltiazem (Cardizem CD, Dilacor)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Verapamil (Calan, Covera)

During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.

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Short-acting nitroglycerins

Class Summary

Suitable for immediate relief of exertional or rest angina. Can also be used for prophylaxis several minutes before planned exercise to avoid angina. Reduce myocardial oxygen demand by reduction of LV and arterial pressure, primarily by reducing preload.

Nitroglycerin IV (Nitrostat, Nitro-bid, Nitrol)

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic GMP production. Result is decrease in BP.

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Long-acting nitroglycerins

Class Summary

Reduce LV preload and afterload by venous and arterial dilation, which subsequently reduces myocardial oxygen consumption and relieves angina. Also cause dilation of epicardial coronary arteries, which is beneficial in patients with coronary spasm. In addition, nitroglycerin has antithrombotic and antiplatelet effects in patients with angina pectoris. No evidence suggests that nitrates improve survival or slow progression of coronary artery disease.

Isosorbide (Isordil, ISMO)

Relaxes vascular smooth muscle by stimulating intracellular cyclic GMP. Decreases LV pressure (ie, preload) and arterial resistance (ie, afterload). Reduces cardiac oxygen demand by decreasing LV pressure and dilating arteries.

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Angiotensin-converting enzyme inhibitors

Class Summary

Angiotensin-converting enzyme (ACE) Inhibitors have been shown to reduce rates of death, MI, stroke, and need for revascularization procedures in patients with coronary artery disease or diabetes mellitus and at least one other cardiovascular risk factor, [61]  irrespective of the presence of hypertension or heart failure. The 2009 Canadian Hypertension Education Program recommends beta-blockers and ACE inhibitors as first-line therapy in patients with angina, recent myocardial infarction or heart failure. [62]

Ramipril (Altace)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

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Anti-ischemic agents, miscellaneous

Class Summary

Ranolazine elicits action unlike beta-blockers, calcium antagonists, or nitrates. It does not affect hemodynamics or contractile and conduction parameters.

Ranolazine (Ranexa)

Cardioselective anti-ischemic agent (piperazine derivative) that partially inhibits fatty acid oxidation. Also inhibits late sodium current into myocardial cells and prolongs QTc interval. Indicated for chronic angina unresponsive to other antianginal treatments. Used in combination with amlodipine, beta-blockers, or nitrates. Unlike beta-blockers, calcium channel blockers, and nitrates, does not reduce blood pressure or heart rate. Effect on angina rate or exercise tolerance appears to be smaller in women than in men. Absorption is highly variable but unaffected by food.

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