ANTIANGINAL

DRUGS
By Maryam Shoukat, Mahnoor Fatima & Rahymin Sheikh 
ANGINA
Angina pectoris is a
syndrome which produces
a sensation of
strangulation, squeezing,
and pressure in the chest
region. It is caused by
inadequate coronary blood
flow that fails to meet
oxygen demands of the
heart tissue and is
associated with acute
myocardial ischemia.
Characteristics of 
Angina Pectoris
TYPES OF Angina pectoris has

ANGINA
three overlapping
patterns
TYPES OF ANGINA:

1) effort-induced, stable, classical, or typical

angina

2) unstable angina; and

3) Prinzmetal, variant, vasospastic, or rest

angina.
  Classic angina is the most common form of
angina and, therefore, is also called typical
angina pectoris. 
 It is characterized by a short lasting burning,
effort- heavy, or squeezing feeling in the chest. 
induced,
 Chest pain lasting less than 20 minutes. 
stable,
classical, or  Secondary to atherosclerosis ( >70% stenosis).

typical angina  Pain radiates to left arm or jaw, diaphoresis

(sweating) and shortness of breath occur.
 Typical angina pectoris is promptly relieved by
rest or nitroglycerin, which decreases
myocardial oxygen demand. 
UNSTABLE ANGINA
Unstable angina is classified between stable angina and myocardial infarction.

In unstable angina, chest pains occur with increased frequency, duration, and
intensity and are precipitated by progressively less effort.
Any episode of rest angina longer than 20 minutes

The symptoms are not relieved by rest or nitroglycerin.

Unstable angina requires hospital admission and more aggressive therapy to

prevent death and progression to myocardial infarction
Prinzmetal, variant,
vasospastic, or rest angina
 Prinzmetal angina is an uncommon pattern of
episodic angina that occurs at rest and is due to
coronary artery spasm. 
 Symptoms are caused by decreased blood flow to
the heart muscle from the spasm of the coronary
artery. Although individuals with this form of
angina may have significant coronary
atherosclerosis, the angina attacks are unrelated to
physical activity, heart rate, or blood pressure. 
 Prinzmetal angina generally responds promptly to
coronary vasodilators, such as nitroglycerin and
calcium-channel blockers
ANTIANGINAL DRUGS 
ORGANIC
NITRATE
ORGANIC
NITRATE
 Organic nitrates (and nitrites) used in
the treatment of angina pectoris are
simple nitric and nitrous acid esters
of glycerol. 
 These compounds cause a rapid
reduction in myocardial oxygen
demand, followed by rapid relief of
symptoms. They are effective in
stable and unstable angina as well as
in variant angina pectoris. 
ORGANIC NITRATE
Mechanism of action
 Nitrates inhibit coronary
vasoconstriction or spasm, increasing
perfusion of the myocardium and,
thus, relieving VASOSPASTIC ANGINA.
In addition, nitrates relax the veins
(venodilation), decreasing preload
and myocardial oxygen consumption.
Because of this action, nitrates are
effective in treating effort-induced
angina (classic angina)
Effects on the
cardiovascular system
 All of these agents are effective, but they differ in their
onset of action and rate of elimination.
 For prompt relief of an ongoing attack of angina precipitated
by exercise or emotional stress, sublingual (or spray
form) nitroglycerin is the drug of choice. 
 At therapeutic doses, nitroglycerin has two major effects. 

 First, it causes dilation of the large veins, resulting in

pooling of blood in the veins. This diminishes preload
(venous return to the heart) and reduces the work of the
heart. 
 Second, nitroglycerin dilates the coronary vasculature,
providing an increased blood supply to the heart
muscle. Nitroglycerin decreases myocardial
oxygen consumption because of decreased cardiac work
β-ADRENERGIC BLOCKERS
 The β-adrenergic–blocking agents  decrease the oxygen
demands of the myocardium by lowering both the rate
and the force of contraction of the heart. 
 They suppress the activation of the heart by  blocking β1
receptors, 
 ⬇ Heart rate                    
 ⬇ Force of contraction
 ⬇ Blood pressure
 ⬇ Cardiac output 
 With β-blockers, the demand for oxygen by the
myocardium is reduced both during exertion and at rest. 
 Because of these effects, β-blockers are the drugs of
choice to treat effort-induced angina. 
β-ADRENERGIC BLOCKERS
 The β-blockers reduce the frequency and severity of
angina attacks. 
 β-Blockers are ineffective against and should not be used
in vasospastic angina. Propranolol is the prototype for
this class of compounds, but it is not cardioselective.
Thus, other β-blockers, such as metoprolol and atenolol,
are preferred. 
 [Note: All β-blockers are nonselective at high doses and
can inhibit β2 receptors. This is particularly important to
remember in the case of asthmatic patients.] 
β-ADRENERGIC BLOCKERS
 Note: It is important not
to discontinue β-blocker
therapy abruptly. The
dose should be
gradually tapered off
over 2 to 3 weeks to
avoid rebound angina,
myocardial infarction,
and hypertension.
 The calcium-channel blockers protect the
tissue by inhibiting the entrance of calcium
into cardiac and smooth muscle cells of the CALCIUM-
coronary and systemic arterial beds. All
calcium-channel blockers are, therefore, CHANNEL
arteriolar vasodilators that cause a decrease BLOCKER
in smooth muscle tone and vascular
resistance. 
 NIFEDIPINE VERAPAMIL DILTIAZEM

CALCIUM •CHANNEL
• Arteriolar vasodilator. BLOCKER
Slows the cardiac atrio ventricular • Diltiazem has CVS effects similar to
conduction directly and decreases Verapamil.
• Nifedipine administered orally
the heart rate, contractility, blood
• Both drugs slow AV conduction and
• Its vasodilation effects is useful in pressure and oxygen demand.
decrease the heart rate ,lesser
treatment of variant angina.
• Care must be taken to adjust the extent than Verapamil, and also
• Nifedipine can cause flushing, dose in patient with liver decreases blood pressure.
headache, hypotension and dysfunction.
• Diltiazem can relieve coronary
peripheral edema.
• Verapamil is contraindicated  in artery spasm and particularly useful
• As with all calcium channel patients with preexisting in patients with Variant angina.
blockers CONSTIPATION is a depressed cardiac function or AV
• The incidence of side effects are
problem. conduction abnormalities.
low.
• It also causes constipation.
• Contraindications are same as
Verapamil.
CALCIUM-
CHANNEL BLOCKER
Note: Verapamil mainly affects the myocardium, whereas nifedipine exerts a
greater effect on smooth muscle in the peripheral vasculature. Diltiazem is
intermediate in its actions.

All calcium-channel blockers lower blood pressure. They may worsen heart

failure due to their negative inotropic effect. 

Note: Variant angina caused by spontaneous coronary spasm, either at work or

at rest , rather than by increased myocardial oxygen requirement, is controlled
by organic nitrates or calcium-channel blockers. β-Blockers are contraindicated.
SODIUM-CHANNEL BLOCKER

 Ranolazine is indicated for the

treatment of chronic angina and may be
used alone or in combination with other
traditional therapies, but is most often used
as an option in angina patients who have
failed all other antianginal therapies. 
 It is not to be used to treat an acute attack
of angina.