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 patient’s 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.

Beta–Blockers

 

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 catecholamine’s irritates the  heart causing an
imbalance in supply and demand, which can lead to life–threatening dysrhythmias. Beta–blockers block the  harmful effects of catecholamine’s improving survival
after an MI.

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

 

Indications

 

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.

Indications

 

First–line treatment for:

 

1. Angina

 

2. Hypertension