This document discusses different types of drugs used to treat angina pectoris. It describes 5 main classes of antianginal drugs: 1) Nitrates like glyceryl trinitrate that work by releasing nitric oxide to cause vasodilation. 2) Beta blockers like propranolol that reduce cardiac workload and oxygen demand. 3) Calcium channel blockers like verapamil and nifedipine that relax arteries by decreasing intracellular calcium. 4) Potassium channel openers like nicorandil that activate potassium channels to cause vasodilation. 5) Other drugs like trimetazidine that reduce angina frequency through non-hemodynamic mechanisms. The document provides details on the mechanisms and uses

1. Antianginal Drugs
Suresh Kumar Ghritlahare
Assist. Professor
SRU, Raipur, (C.G.)

2. Antianginal drugs
Antianginal drugs: Antianginal drugs are those
that prevent, abort or terminate attacks of angina
pectoris.
Angina pectoris: It is a pain syndrome due to
induction of an adverse oxygen supply/demand
situation in a portion of the myocardium.
Two principal forms are recognized:
(a)Classical angina: (common form)
(b)Variant/Prinzmeta/Vasospastic angina:
(uncommon form)

3. Types of Angina
(a) Classical angina: (common form) Attacks are
predictably provoked (stable angina) by exercise,
emotion, eating or coitus and subside when the
increased energy demand is withdrawn.
(b)Variant/Prinzmetal/Vasospastic angina:
(uncommon form) Attacks occur at rest or during
sleep and are unpredictable. They are due to
recurrent localized (occasionally diffuse)
coronary vasospasm (Fig.) which may be
superimposed on arteriosclerotic coronary artery
disease.

4. Fig.: Diagrammatic representation of coronary artery
calibre changes in classical and variant angina

5. CLASSIFICATION
1. Nitrates:
(a) Short acting: Glyceryl trinitrate (GTN, Nitroglycerine)
(b) Long acting: Isosorbide dinitrate (short acting by sublingual
route), Isosorbide mononitrate, Erythrityl tetranitrate,
Pentaerythritol tetranitrate
2. β Blockers: Propranolol, Metoprolol, Atenolol and others.
3. Calcium channel blockers:
(a) Phenyl alkylamine: Verapamil
(b) Benzothiazepine: Diltiazem
(c) Dihydropyridines: Nifedipine, Felodipine,Amlodipine,
Nitrendipine,Nimodipine, Lacidipine Lercanidipine,Benidipine
4. Potassium channel opener : Nicorandil
5. Others: Dipyridamole, Trimetazidine, Ranolazine, Ivabradine,
Oxyphedrine

6. Mechanism of action
1. Nitrates:
Organic nitrates are rapidly denitrated enzymatically in the smooth
muscle cell to release the reactive free radical nitric oxide (NO)
which activates cytosolic guanylyl
Increased cGMP
causes dephosphorylation of myosin light chain kinase (MLCK)
through a cGMP dependent protein kinase . Reduced availability of
phosphorylated (active) MLCK interferes with activation of myosin
it fails to interact with actin to cause contraction. Consequently
relaxation occurs. Raised intracellular cGMP may also reduce Ca2+
entry
contributing to relaxation.

8. Adverse effects :These are mostly due to
vasodilatation.
1. Fullness in head, throbbing headache; some
degree of tolerance develops on continued use.
2. Flushing, weakness, sweating, palpitation,
dizziness and fainting; these are mitigated by
lying down. Erect posture and alcohol accentuate
these symptoms.
3. Methemoglobinemia: is not significant with
clinically used doses. However, in severe
anaemia, this can further reduce O2 carrying
capacity of blood.
4. Rashes are rare, though relatively more common
with pentaerythritol tetranitrate.

9. Uses:
1. Angina pectoris
2. Acute coronary syndromes (ACS)
3. Myocardial infarction (MI)
4. CHF
5. Cyanide poisoning

10. 2. β BLOCKERS:
β- blocker reduce cardiac work load and oxygen conjumption
This drug do not dilate coronaries blood vessel, total coronary flow is reduced due
to blockage of β2 receptor
Βeta-blocker increase exercize tolerance in classical angina
Decrease frequency and severity of attack

11. 3. CALCIUM CHANNEL BLOCKERS:
Three important classes of calcium channel blockers are examplified by:
• Verapamil—a phenyl alkylamine, hydrophilic
• papaverine congener.
• Nifedipine—a dihydropyridine (lipophilic).
• Diltiazem—a hydrophilic benzothiazepine.
Calcium channels:
Three types of Ca2+ channels have been described in smooth muscles (other
excitable cells as well):
(a) Voltage sensitive channel: Activated when membrane potential drops to
around –40 mV or lower.
(b) Receptor operated channel: Activated by Adr and other agonists—
independent of membrane depolarization (NA contracts even depolarized
aortic smooth muscle by promoting influx of Ca2+ through this channel
and releasing Ca2+ from sarcoplasmic reticulum).
(c) Leak channel: Small amounts of Ca2+ leak into the resting cell and are
pumped out by Ca2+ATPase. Mechanical stretch promotes inward
movement of Ca2+, through the leak channel or through separate stretch
sensitive channel.

12. MOA: Smooth muscle Smooth muscles depolarize
primarily by inward Ca2+ movement through
voltage sensitive channel. These Ca2+ ions trigger
release of more Ca2+ from intracellular stores and
together bring about excitation-contraction
coupling through phosphorylation of myosin light
chain as depicted in Fig. The CCBs cause
relaxation by decreasing intracellular availability
of Ca2+. They markedly relax arterioles but have
mild effect on veins. Extravascular smooth
muscle (bronchial, biliary, intestinal, vesical,
uterine) is also relaxed.

13. Use:
 Hypertension
 Angina pectoris
 Cardiac arrhythmias
 Hypertropic cardiopathy
 Other use: Nifedipine- premature labour

14. 4. POTASSIUM CHANNEL OPENERS: Nicorandil
This dual mechanism antianginal drug activates ATP
sensitive K+ channels (KATP) thereby hyperpolarizing
vascular smooth muscle. The vasodilator action is partly
antagonized by K+ channel blocker glibenclamide. Like
nitrates it also acts as a NO donor—relaxes blood vessels
by increasing cGMP. Thus, arterial dilatation is coupled
with venodilatation.
5. OTHER ANTIANGINAL DRUGS: Trimetazidine
This antianginal drug acts by nonhaemodynamic
mechanisms. There is no effect on determinants of
myocardial O2 consumption, such as HR and BP, both at
rest as well as during exercise, but angina frequency is
reduced and exercise capacity is increased.

15. References
• Tripathi KD, “Essentials of Medical
Pharmacology” published by Jaypee Brothers
Medical Publishers (P) Ltd, Seventh Edition:
2013, New Delhi, p.p. no-539-555.