This document discusses antianginal drugs, which are used to treat or prevent angina pectoris, a type of chest pain caused by reduced blood flow to the heart. It classifies antianginal drugs into several categories, including nitrates, beta blockers, calcium channel blockers, and others. Nitrates like glyceryl trinitrate work by dilating blood vessels, reducing cardiac workload and oxygen demand. This decreases blood pressure and relieves angina by increasing oxygen supply to the heart. Nitrates are used to both abort acute angina attacks and prevent chronic episodes. Common side effects include headaches and low blood pressure.

2.  Antianginal drugs are those that prevent,
abort or terminate attacks of angina
pectoris.
 Angina pectoris is a pain syndrome due to
induction of an adverse oxygen
supply/demand situation in a portion of the
myocardium. Metabolites that accumulate
due to myocardial ischaemia elicit the pain.

4. Classification of antianginal
drugs:
A) Nitrates:
a) short-acting:
1) Glyceryl trinitrate
2) Isosorbide dinitrate (by
sublingual route)

5. b) long-acting:
1) Isosorbide dinitrate (by oral
route)
2) Isosorbide mononitrate
3) Erythrityl tetranitrate
4) Pentaerythritol tetranitrate

6. B) Beta (β) – blockers
1) Metoprolol
2) Atenolol
3) Propranolol
4) Others

7. C) Calcium channel blockers
a) Phenyl alkalamines: Verapamil
b) Benzothiazepine: Diltiazem
c) Dihydropyridines: Amlodipine,
Nifedipine, Felodipine,
Nitrendipine, Nimodipine,
Lacidipine, Lercanidipine,
Benidipine.

8. D) Potassium channel opener:
Nicorandil
E) Other antianginal drugs:
1) Trimetazidine
2) Ranolazine
3) Ivabradine
4) Dipyridamole

9. Clinical classification of antianginal drugs:
a) Used to abort or terminate attack:
GTN, Isosorbide dinitrate
(sublingually)
b) Used for chronic prophylaxis: All
other antianginal drugs.

10. Nitrates
 GTN is the prototype antianginal nitrate.
Mechanism of action:
Organic nitrates are rapidly denitrated
enzymatically in the smooth muscle cell
to release the reactive free radical Nitric
Oxide (NO) which activates cytosolic
soluble guanylyl cyclase leading to
increased cGMP.

11. cGMP causes dephosphorylation of MLCK
(myosin light chain kinase) through a
cGMP-dependent protein kinase (PKG).
Reduced availability of phosphorylated
(active) MLCK interferes with actication of
myosin. Myosin fails to interact with actin
so that contraction doesn’t occur.
Consequently, relaxation of the smooth
muscle occurs.
Raised intracellular cGMP may laso reduce
Calcium ion entry into the smooth muscle
cell, thus contributing to relaxation.

13. Relaxation of smooth muscle cells forming
the walls of blood vessels cause
vasodilatation.
Effects of vasodilation:
i)Nitrates dilate veins more prominently than
arteriloes. Hence, peripheral pooling of
blood leading to decreased venous return
and hence preload reduction occurs. This
causes decreased cardiac output, which
means there is a reduced oxygen
consumption by the cardiac muscles.

14. ii) Some Arterial vasodilation also occurs, which
leads to decreased total peripheral resistance
(tpr) leading to decreased afterload on heart.
This contributes to decreased cardiac work,
which means the total oxygen demand by
heart muscle is reduced.
iii) Coronary arteries vasodilation causes
increased blood flow to the heart muscle.
All these 3 processes contribute to relief in
angina pectoris.

15. Uses/Indications of Nitrates
1) In Angina pectoris
2) Acute coronary syndrome (ACS)
3) Myocardial infarction (MI)
4) Congestive heart failure and acute left
ventricular failure.

16. 5) Biliary colic
6) Esophageal spasm
7) Cyanide poisoning

17. Adverse effcts
1) Fullness in head, throbbing headache : may
decrease with continuous use.
2) Flushing, weakness, sweating, palpitation,
dizziness and fainting : Due to postural
hypotension.
3) Methemoglobinaemia leading to reduced
oxygen carrying capacity in severe anaemia.
4) Rashes (more common with pentaerythritol
tetranitrate).

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