ANTIANGINAL DRUG

1. -: PRESENTED BY :-
Prof. Zeeshan Nathani
M.Pharm
Dept. pharmacology
PROF. RAVINDRA NIKAM COLLEGE OF B. PHARMACY
GONDHUR, DHULE 424001

2. CONTENTS
1. Angina pectoris
2. Types of angina
3. Etiology
4. Symptoms
5. Pathogenesis of angina
6. Classification of antianginal drug

3. Angina refers to severe pain in middle of the chest during exercise or
effort due to decreased supply of oxygenated blood to the heart.
The pain may further spread to other parts of the body such as neck,
left arm, back, throat etc.
1) Atherosclerosis of large coronary arteries
2) Cigarette smoking
3) Hypertension
4) Heart valve disease
ANGINA PECTORIS
Etiology

4. 1. Chest pain
2. Difficulty in breathing
3. Sweating
4. Weakness
5. Nausea
6. Vomiting
SYMPTOMS

5. Types of Angina
Stable Angina
Variant Angina
Unstable Angina
Microvascular Angina

6. Increased
oxygen Demand
Increased ventricular
pressure and Size
Increased Heart rate
Increased myocardial
contractlity
Myocardial Ischaemia
Angina Pain
Fig. Pathogenesis of Angina pectoris
PATHOGENESIS OF ANGINA PECTORIS

7. CLASSIFICATION OF ANTIANGINAL DRUG

8. Nitrate compounds:
The nitrate compounds are potent vasodilators and are most commonly
used in the treatment of angina.
Example:
 Tri nitroglycerin (nitroglycerine)
 Amyl nitrate

9. The organic nitrates such as tri nitroglycerine produce reactive free radical
nitric oxide (NO)through enzymatic denization.
 This nitric oxide activates the cytosolic guanyl cyclase enzyme that
causes an increase in the production of Cyclic GMP.
 This cyclic GMP causes dephosphorylation of myosin light chain kinase
(MLCK)enzyme which is essential for the activation of myosin pigment.
 Deficiency of this enzyme results in lack of interaction the actin and
myosin which leads to decrease interaction.
 This ultimately results in relaxation of smooth muscles.
MODE OF ACTION

10. Dephosphoryl-ated MLCK
organic Nitrates
Generates
Nitric Oxide
Inactive Guanylyl Cyclase Active GC
Increased Production of cGMP
cGmp dependent Protein kinase MLCK
Phosphorylated MLCK

11. 1.Facial Flushing
2.Weakness most common
3.Dizziness
4.Skin rashes
5.Marked fall in BP when combination with
other potent vasodilators
6.Drug tolerance
ADVERSE EFFECTS

12. 1.Treatment Angina pectoris
2.Treatment of CHF
3.Treatment of left ventricular Fibrillation
4.Treatment of Myocardial infraction
USES

13. Uses
Treatment of Angina pectoris etc.
1) SHORT ACTING COMPOUNDS
Example
 Tri nitroglycerine
Adverse Effects
1. Dizziness
2. headache
3. Anxiety
4. dysrhythmias
5. postural
hypotension
6.nausea
7.diarrhea
 Isosorbide Mononitrate
 Isosorbide Dinitrate
 Erythrityl Tetranitrate
 Pentaerythrityl Tetranitrate.
2) LONG ACTING COMPOUNDS
Example

14.  Propranolol decrease the requirement oxygen by the heart even at any
given level of stimulation.
 It blocks the B-adrenergic receptors Stimulated by the catecholamine
such as adrenaline , Ach etc., which increases the activity of heart.
 It results in systemic decrease in myocardial contractions and a fall in
blood pressure.
 The ultimate effect of B-blockers is advantageous during exercise due to
delayed onset pain and increased work capacity
B- Blocker
Example
 Propranolol
 Atenolol
 Nadolol
PROPRANOLOL MODE OF ACTION

15. 1. Slow or uneven heart beat
2. Swelling of ankles or feet
3. Nausea
4. Stomach pain
5. Jaundice etc..
Uses
used for treatment of moderate to severe angina
It is used to relieve hypertension.
2. ATENOLOL
Specific B, receptor Antagonist.
MODE OF ACTION ATENOLOL
It is similar to that of propranolol
ADVERSE EFFECTS

16. CALCIUM CHANNEL BLOCKERS (CCB)
 These drugs act by preventing the entry Cations into the cells.
 The Cations are require for the contraction of the muscle.
 These drugs act on the Cat2 channel receptors and cause block of the
calcium channels.
 The ultimate effect of these drugs would be relaxation of the muscular
system decrease in muscular activity and negative inotropic,
chronotropic and dromotropic elects on heart.
Uses
1. It is use in the treatment of Angina Pectoris
2. It is use in the treatment of Hypertension
3. It is use in the treatment of Cardiac Arrhythmias
4. It is use in the treatment of cardiac Hypertrophy

17. 1) The main mechanism is the blockade voltage gated calcium
channels. These channels are mainly located in the Sinoatrial (SA)
and antrioventricular (AV) nodes and promote the contraction of
heart.
2) The CCBs block the calcium channels and result in the suppression
SA and AV nodes that are Calcium dependent.
3) They cause dilation of the blood vessels by relaxing the tone of the
smooth muscles that line the blood vessels.
1.) Phenyl alkyl amine Derivatives
Example:- verapamil
Mechanism of action

18.  Nausea.
 Constipation.
 Bradycardia.
 Hypotension.
 Facial Flushing.
ADVERSE EFFECTS
Mostly used for the treatment of hypertension and in some cases to relieve
pain from angina

19. 2) Dihydropyridine Derivatives
Example:- Nifedipine
The vasodilation effect is due to its calcium channel blockade activity
leading to there relaxation of the smooth muscles of heart and blood
vessels.
Mechanism of action
1. It is a long acting calcium Chanel blocker.
2. The main mechanism of action action of the drug is arteriolar
Vasodilation by relaxation of the smooth muscles of the arteries.
3. This causes a decrease in total peripheral resistance and fall in BP.
3) Benzothiazepine Derivatives
Example:- Diltiazem
Mechanism of action

20. ADVERSE EFFECTS
1.Difficulty in breathing
2.Swelling of body parts
3.Dizziness

21. K+ CHANNEL ACTIVATORS
The opening of k+ channel results in rapid out flow of at ions from the
cell leading to an increase in the -ve value of the membrane potential.
This causes hyperpolarization of the cells.
This ultimately leads to relaxation of the smooth muscles.
Uses
1. Treatment of angina pectoris (Nicorandil)
2. Treatment of Hypertension
3. Used during CHF

22. 1. Facial Flushing
2. Palpitation
3. Headache
4. Nausea and vomiting
5. Diarrhea
6. Weakness etc.
ADVERSE EFFECTS (NICORANDIL)
Uses
1)Treatment of angina pectoris
2)Attain relief from hypertension
3)Treatment of Cardiac heart failure, MI

23.  The drug inhibits the uptake of adenosine back into cells such as
platelets , RBCs and endothelial cells and results in the accumulation
of adenosine extracellular.
 It further increases the levels of extracellular adenosine by inhibiting
the activity of the enzyme adenosine deaminase which breaks down
adenosine to inosine.
 The adenosine acts on the adenosine receptors and causes increase
in the cyclic AMP levels via the adenylate cyclase pathway.
 This cyclic AMP inhibits the aggregation of platelets and also cause
arteriolar smooth muscle relaxation.-
MISCELLANEOUS DRUGS
1. Antiplatelet Drugs
EXAMPLE :- Dipyridamole
Mechanism of action

24. 1. Dizziness
2. Stomachache
3. Headache
4. Vomiting
5. Diarrhea
ADVERSE EFFECTS
Uses
1. The drug is used to increase myocardial perfusion and left ventricular
function in patients with ischemic cardiomyopathy.
2. It is used along with aspirin in the secondary prevention of Stroke and
transient ischemic attack.

25. 1)Irritation of the gastrointestinal tract.
2)Restlessness.
3)Weakness and muscular cramps. in the treatment of along with other
antianginal drugs angina pectoris and post MI.
2) Cytoprotective Drugs
EXAMPLE :- TRIMETAZIDINE
It is a Cytoprotective drug that improves the tolerance of the cells to
ischemic conditions.
Mechanism of action
Adverse effects