This presentation discusses angina pectoris and its treatment. It is caused by an imbalance between myocardial oxygen supply and demand. There are three main types of angina - stable, variant, and unstable - depending on the triggers and severity. The main classes of drugs used to treat angina are organic nitrates, beta-blockers, and calcium channel blockers. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers decrease heart rate and contractility to lower oxygen demand. Calcium channel blockers dilate coronary arteries and reduce afterload. The presentation discusses the mechanisms and effects of representative drugs from each class.

1. Presentation by-
ANURAG CHANDA
B.Pharm 6th semester
Roll no- 14
Gurunanak institute of pharmaceutical
science and technology.

2. Angina pectoris-
The primary cause of angina is an
imbalance between myocardial oxygen
demand and oxygen supplied by
coronary vessels
This imbalance may be due to:
•a decrease in myocardial oxygen
delivery
•an increase in myocardial oxygen
demand
•or both
The discomfort abates when supply
becomes adequate for demand.
Typically angina lasts for seconds to
minutes, up to 15 minutes
Classically angina is not
associated with ischemic cell
death

4. Types of Angina Pectoris
Stable Angina Variant Angina Unstable Angina
Effort , Typical.
Atherosclerosis
Exercise,
Emotion,
Heavy meal.
↓
Pain
Prinzmetal.
↓
α- receptor
mediated
Vasoconstriction
With or without
atherosclerosis.
↓
Pain even at rest
Accelrated
Severe type
Due to rupture of
an atheromatous
plaque attracting
platelet deposition
and progressive
occlusion of the
coronary artery

5. Antianginal Agents
Three major classes of agents are used individually
or in combination to treat angina:
1. Organic nitrates:
 Vasodilate coronary arteries
 Reduce preload and aferload
2. Beta-adrenergic blockers:
 Decrease heart rate and contractility - decrease in
cardiac work and O2 consumption
 Improve myocardial perfusion due to decrease in heart
rate – decreased in ventricular wall tension
 Exercise tolerance
3. Calcium channel blockers:
 Vasodilate coronary arteries
 Reduce afterload
 The non-dihydropyridines (verapamil and diltiazem)
also decrease heart rate and contractility

6. Mechanism of Action of Nitrovasodilators
Nitrates become denitrated by glutathione S-transferase
to release
Nitric Oxide
activates
converts
Guanylate Cyclase*
GTP
cGMP
activates
cGMP-dependent protein kinase
Activation of PKG results in phosphorylation
of several proteins that reduce intracellular calcium
causing smooth muscle relaxation

7. Actions of Nitrates - GTN
1. Preload reduction:
 Dilatation of veins more than arteries – peripheral pooling of Blood –
decrease venous return
 Will lead to reduction in preload – decreased end diastolic size – decrease in
fibre length
 Less wall tension to develop for ejection (Laplace`s law) – less oxygen
consumption and reduction in ventricular wall pressure (crunch abolished)
2. Afterload reduction:
 Some amount of arteriolar dilatation – Decrease in peripheral Resistance
(afterload reduction) – reduction in Cardiac work (also fall in BP)
 Standing posture – pooling of Blood in legs – reflex tachycardia (prevented
by lying down and foot end raising)
 However in large doses opposite happens – marked fall in BP – reflex
tachycardia – increased cardiac work – precipitation of angina

8. Actions of Nitrates - contd.
3.Mechanism of angina relief:
 Variant angina – coronary vasodilatation
 Classical angina – reduction in Cardiac load
 Increased exercise tolerance
4. Other actions: Cutaneous vasodilatation (flushing
occurs), meningeal vessels dilatation (headache) and
decreased renal blood flow

9. β-Adrenoceptor Blockers
β-Bs → Suppress the activation of the heart (β1).
Reduce the work of the heart by ↓ heart rate&
cardiac contractility → ↓ C.O.& slight ↓ B.P.
↓

10. Propranolol
.It is not a vasodilator , so it may worsen variant angina..
.It is used prophylactically to  severity& frequency of
typical anginal attacks.
.It  cardiac O2 demand through:
.-ve chronotropic & inotropic actions.
.Slight  of B.P.
Propranolol can be combined with Nitrates
for typical angina.
( to  side effects of both drugs).

11. Ca++ channel blockers
Nifedipine, Verapamil, Diltiazem
Mechanism of action on vascular tissue :
Blocking of Ca++ transmembrane
channels in vascular smooth muscle fibers.
→ interference with inward of
movement of Ca++
→ affects depolarization &
contraction processes
→with relaxant effects mainly
on arteriole smooth muscle.

12. Nifedipine: Prominent vasodilator actions, used in
all types
of angina with reflex tachycardia & leg oedema.
Verapamil: .Slows conduction & ↓ Heart rate.
.Greater –ve inotropic effect with
little Vasodialation effects.
Diltiazem: .CVS effects similar to verapamil.
.It is used in angina by ↓ coronary
spasm (variant angina).

13. Selection of antianginal drugs
For patients with concomitant diseases:
Concomitant disease Most preferred
drugs
Less preferred
drugs
Bronchial asthma.
Heart failure
Hypertension.
Diabetes Mellitus.
C.C.Bs, Nitrites& Nitrates.
Nitites & Nitrates.
β-Bs , C.C.Bs.
C.C,Bs ,Nitrites & Nitrates.
β-Bs.
β-Bs ,verapamil,
Diltiazem.
Nitrites & Nitrates.
β-Bs.

14. Reference-
1) Tripathi K.D,Essentials of medical pharmacology. Sixth edition.
2)Introduction to pharmacology by S.K kulkarni updated seventh edition.