Antianginal Drugs


Antianginal Drugs


Angina medications are used for angina pectoris or chest pain. 

The types of chest pain are chronic stable angina (which is associated with atherosclerosis), unstable angina (early stage of progressive coronary artery disease), and vasospastic angina (which results from spasms in the layer of smooth muscle that surrounds atherosclerotic coronary arteries). 

The three main classes of drugs used to treat angina pectoris are nitrates and nitrites, beta-blockers, and calcium channel blockers.

The goal of the treatment is:


1. Minimize the frequency of attacks and decrease the duration and intensity of angina pain

2. Improve the patients functional capacity with as few adverse effects as possible


3. Increase blood flow to ischemic heart muscle and decrease myocardial oxygen demand

4. Prevent or delay the worst possible outcome, which is a myocardial infarction


Nitrates and Nitrites


Nitrates are available on many forms including sublingual, chewable tablets, oral capsules/tablets,  IV  solutions,  transdermal patches,  ointments  and  translingual sprays. 

They are broken down into rapid-acting forms and long-acting forms. 

The rapid-acting forms include sublingual and IV solutions. 

These are used to treat acute angina attacks. 

The long-acting forms are used to prevent angina episodes

Mechanism of Action

Nitrates dilate all blood vessels; however, they predominately affect venous vascular beds and have a dose-dependent arterial vasodilator effect. This vasodilation happens because of relaxation of smooth muscle cells.

1. Vasodilation results in reduced myocardial oxygen demand and therefore more oxygen to ischemic myocardial tissue and reduction of angina symptoms.

2. By causing venous dilation, the nitrates reduce venous return and in turn reduce the leftventricular end-diastolic volume (preload) and results in a lower left ventricular pressure.

Adverse Effects

Headache is the most common undesirable effect. If nitrate-induced vasodilation


occurs too rapidly, reflex tachycardia occurs which is characterized by an increase in heart rate. This is because the cardiovascular system tries to overcompensate. Other adverse effects include postural hypotension and tolerance may develop.



The  beta-blockers  that  are  classified  as  antianginal  are  atenolol,  metoprolol

(Lopressor), propranolol (Inderal) and nadolol (Corgard).


Mechanism of Action


Beta blockers block beta1-receptors on the heart. This allows:


1.  Decrease  in  heart  rate  which  decreases  myocardial  oxygen  demand  and increases oxygen delivery to the heart.

2.  Decreases  myocardial contractility helping  to  conserve  energy  or  decrease demand.

3. After an MI, a high level of catecholamines irritates the  heart causing an imbalance in supply and demand, which can lead to life-threatening dysrhythmias. Beta-blockers block the  harmful effects of catecholamines improving survival after an MI.

4. The heart spends more time in diastole than in systole.




1. Most effective in the treatment of exertional angina


2. Antihypertensive treatment

3. Cardiac dysrhythmias


4. Cardio-protective effects following an MI


5. Approved for migraine headaches, essential tremors and tachycardia caused by stage fright.

Adverse Effects


Adverse effects include decreased in heart rate, cardiac output and cardiac contractility. 

Therefore, bradycardia, hypotension and AV block. In the CNS, it can cause dizziness, fatigue, depression, and lethargy. 

In diabetic patients, beta- blockers can cause hyperglycemia and/or hypoglycemia as well as masks the signs and symptoms of hypoglycemia and the patients might not be able to tell when exactly the sugar is too low.

Calcium Channel Blockers


CCBs that are used for the treatment of chronic stable angina include amlodipine (Norvasc), diltiazem (Cardizem),  nicardipine (Cardene), nifedipine (Procardia), and verapamil.

Mechanism of Action


Prevents calcium from entering the muscle of the heart to prevent muscle contraction and promote muscle relaxation. 

When the muscle relaxes, it causes the blood vessels to dilate and therefore increases the blood flow to the ischemic heart, which in turn increases the oxygen supply and helps shift the supply/demand ratio back to normal. 

CCBs cause peripheral arterial vasodilation decreasing systemic vascular  resistance and  decreasing the  workload  of  the  heart,  which  leads  to decrease in myocardial oxygen demand.



First-line treatment for:


1. Angina


2. Hypertension

3. Supraventricular tachycardia


Also, used to treat coronary artery spasms (prinzmetal angina) as well as the short - term  management of  atrial  fibrillation,  atrial  flutter,  migraine  headaches,  and Raynauds disease.

Adverse Effects


Limited adverse effects and those are related to overexpression of therapeutic effects including hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea.

Post a Comment