This document discusses antianginal drugs used to treat angina pectoris. It defines angina and describes different types. Antianginal drugs work by increasing myocardial oxygen supply or decreasing demand. Nitrates and calcium channel blockers increase supply by dilating coronary arteries. Beta blockers decrease demand by lowering heart rate and contractility. Combination therapy using these classes is common. The document also discusses mechanisms, administration, effects, and side effects of these major antianginal drugs.

1. ANTI ANGINALS

2. • Antianginal drugs may relieve attacks of acute
myocardial ischemia by increasing myocardial
oxygen supply or by decreasing myocardial
oxygen demand

3. Definition of terms
Angina Pectoris – is the principal symptoms of
patient with ischemic heart disease.
Manifested by sudden, severe, pressing
substernal pain that often radiates to the
left shoulder and along the flexor surface of
the left arm.
Usually precipitated by exercise,
excitement or a heavy meal.

4. Types of Angina
Typical Angina ( Classical Angina )
 pain is commonly induced by exercise,
excitement or a heavy meal
 secondary to advanced atherosclerosis of
the coronary vessels
 associated with ST-segment depression
on ECG

6. Variant Angina ( Prinzmetal Angina)
pain is induced while at rest
associated with ST-segment elevation on
ECG
secondary to vasospasm of the coronary
vessels
Unstable angina
may involve coronary spasm and may also
have the component of atherosclerosis
the duration of manifestation is longer than
the first two and has the manifestation of
Myocardial infarction

8. Determinant of Myocardial Oxygen Supply
1.Coronary blood flow
Determined by: perfusion pressure
duration of diastole
coronary bed resistance
2.Arterio-venous oxygen difference

9. Determinant of Myocardial Oxygen demand
Major Determinants
1. Wall stress
intraventricular pressure
ventricular volume
wall thickness
2. Heart rate
3. Contractility

10. Treatment Plan:
A. decrease the risk factor
B. increase oxygen supply
C. decrease oxygen demand

11. ANTIANGINAL DRUGS
I. AGENTS WHICH ↓ O2 DEMAND & ↑ O2
SUPPLY
A. NITRATES
B. CALCIUM CHANNEL BLOCKERS
II. AGENTS WHICH ↓ O2 DEMAND
C. BETA BLOCKERS

13. NITRATES AND NITRITES
Classification of nitrates:
1. Rapidly acting nitrates
* used to terminate acute attack of angina
* e.g.- Nitroglycerin and Amyl nitrate
* usually administered sublingually
2. Long acting nitrates
* used to prevent an attack of angina
* e.g. -Erythrytyl tetranitrate, Isosorbide
dinitrate, Pentaerythrytol tetranitrate
* administered orally or topically

14. Nitrates
Coronary artery dilatation
Decrease coronary bed resistance
(Relieves coronary vasospasm)
Increase coronary blood flow
Increase oxygen supply

15. Nitrates
Reduction on peripheral resistance
(Secondary to dilatation of arterioles)
Decrease blood pressure
Decrease after load
Decrease workload
Decrease oxygen consumption

16. Nitrates
Reduced venous return
(Due to dilatation of the veins)
Decrease left ventricular volume
Decrease preload
Decrease workload
Decrease oxygen consumption

20. Effects
Coronary artery dilatation
Reduction of peripheral arterial
resistance – decrease after load
Reduce venous return – decrease
preload

21. Potential Beneficial Effects of Nitrates.
Beneficial effects Results
Decrease Ventricular vol. Decrease myocardial oxygen
requirement
Decrease arterial pressure
Decrease ejection time
Venodilatation of epicardial coronary
art.
Relief of coranary artery spasm
Increase collateral flow due to
venodilatation
Increase perfusion to ischemic
myocardium
Decrease left ventricular pressure
> decrease preload due to dilatation
of the vein
> decrease after load due to
dilatation of the arteries
Improved subendocardial perfusion

22. Deleterious Effects Results
Reflex tachycardia Increase myocardial
oxygen requirement
Reflex increase in
contractility
Decrease diastolic
perfusion
Decrease myocardial
perfusion
Potential Deleterious Effects

23. ROUTES OF ADMINISTRATION
1. Sublingual route – rational and effective for the
treatment of acute attacks of angina pectoris. Half-life
depend only on the rate at which they are delivered to
the liver.
2. Oral route – to provide convenient and prolonged
prophylaxis against attacks of angina
3. Intravenous Route – useful in the treatment of
coronary vasospasm and acute ischemic syndrome.
4. Topical route – used to provide gradual absorption of
the drug for prolonged prophylactic purpose.

24. Drug Usual single dose Route of
administration
Duration of action
Short acting
Nitroglycerin
0.15-1.2 mg sublingual 10 - 30 min
Isosorbide dinitrate 2.5-5 mg sublingual 10 – 60 min
Amyl nitrite 0.18 – 3 ml inhalation 3 – 5 min
Long acting
Nitroglycerin sustained
action
6.5 – 13 mg q 6-8 hrs oral 6 – 8 hrs
Nitroglycerin 2%
ointment
1 – 1.5 inches q hr topical 3 – 6 hrs
Niroglycerin slow
released
1 –2 mg per 4 hrs Buccal mucosa 3 – 6 hrs
Nitroglycerin slow
released
10 – 25 mg /24hrs (one
patch/day}
transdermal 8 –10 hrs
Isosorbide dinitrate 2.5 – 10 mg per 2 hrs sublingual 1.5 – 2 hrs
Isosorbide dinitrate 10 –60 mg per 4-6 hrs oral 4 – 6 hrs
Isosorbide dinitrate
chewable
5 – 10 mg per 2-4 hrs oral 2 – 3 hrs
Isosorbide mononitrate 20 mg per 12 hrs oral 6 –10 hrs

25. Adverse Effects
Throbbing headache
Flushing of the face
Dizziness
Postural Hypotension – due to pooling of
blood in the dependent portion of the body

26. Contraindication
Renal ischemia
HOCM
Acute MI
Patients receiving other antihypertensive
agent

27. B-Blockers
Hemodynamics Effects
Decrease heart rate
Reduced blood pressure and cardiac
contractility without appreciable decrease
in cardiac output

29. B-Blockers
Decrease heart rate & Contractility
Increase duration of diastole
Decrease workload
Increase coronary blood flow
Decrease O2 consumption
Increase oxygen supply

30. Contraindication
Congestive heart failure
Asthma
Complete heart block

31. Ca - Channel Blockers
Effects
Coronary artery dilatation
Reduction on peripheral arterial
resistance – decrease after load

32. Ca Channel Blockers
Coronary artery dilatation
Decrease coronary bed resistance
(Relieved coronary vasospasm)
Increase coronary blood flow
Increase oxygen supply

33. Ca channel Blockers
Reduction on peripheral resistance
(Secondary to dilatation of aorta)
Decrease blood pressure
Decrease after load
Decrease workload
Decrease oxygen consumption

34. Pharmacokineticss
Drugs Onset of action Peak of action Half-life
Nifedipine 20 minutes 1 hour 3-4 hours
Verafamil 1-2 hours 5 hours 8-10 hours
Diltiazem 15 minutes 30 minutes 3-4 hours
Nicardifine 20 minutes 45 minutes 2-4 hours
Felodipine 2-5 hours 6-7 hours 11-16 hour

36. Side effect
• Nausea and vomiting
• Dizzyness
• Flushing of the face
• Tachycardia – due to hypotension
Contraindications
• Cardiogenic shock
• Recent myocardial infarction
• Heart failure
• Atrio-ventricular block

37. Combination Theraphy
Nitrates and B-blockers
* The additive efficacy is primarily a result
of one drug blocking the adverse effect of
the other agent on net myocardial oxygen
consumption
* B-blockers – blocks the reflex
tachycardia associated with nitrates
* Nitrates – attenuate the increase in the
left ventricular end diastolic volume
associated with B-lockers by increasing
venous capacitance

38. Ca channel blockers and B-blockers
* useful in the treatment of exertional
angina that is not controlled adequately
with nitrates and B-blockers
* B-blockers – attenuate reflex tachycardia
produce by nifedipine
* These two drugs produce decrease
blood pressure

39. Ca channel blockers and Nitrates
* Useful in severe vasospastic or
exertional angina (particularly in patient
with exertional angina with congestive
heart failure and sick sinus syndrome)
* Nitrates reduce preload and after load
* Ca channels reduces the after load
* Net effect is on reduction of oxygen
demand

40. Triple drugs – Nitrate + Ca channel
blockers + B-blockers
*Useful in patients with exertional angina
not controlled by the administration of
two types of anti-anginal agent
* Nifidipine – decrease after load
Nitrates – decrease preload
B-blockers – decrease heart rate &
myocardial contractility

41. Type of
Angina
Other Names Description Drug Therapy
STABLE Classic
Exertional
Fixed
Atherosclerotic
Obstruction
coronary artery
Nitrates
CCB
B-blockers
VARIANT Prinzmetal’s
Vasospasmic
Vasospasm at
any time
Nitrates
CCB
UNSTABLE Crescendo Combined effect
Pre= MI
Nitrates
CCB

43. DIPYRIDAMOLE:-
It inhibits platelet aggregation by potentiating
PGI2 and increasing cAMP in platelets.
It is not useful as an anti-anginal drug (“coronary
steal”) but is being employed for prophylaxis of
coronary and cerebral thrombosis in post-MI and
post-stroke patients, as well as to prevent
thrombosis in patients with prosthetic heart
valves.

44. CORONARY STEAL PHENOMENON

45. TRIMETAZIDINE
an add on medication to conventional therapy in
angina and post-MI patients.
Mechanism of action
It causes inhibition of mitochondrial enzyme long
chain 3-ketoacyl thiolase (LC-3KAT)  Reduces fatty
acid metabolism in myocardium and increases
glucose metabolism  Shift back of substrate to
glucose decreases oxygen demand.

46. .RANOLAZINE
It is a newer antianginal drug used in prophylaxis of
angina
Mechanism of action-It acts by reducing a late
sodium current (INa) that facilitates calcium entry via
the sodium-calcium exchanger  Decreased
intracellular calcium concentration  Decreased
cardiac contractility and work
It also inhibits LC-3KAT

47. IVABRADINE
Mechanism of action-Relatively selective If
sodium channel blocker that reduces cardiac
rate by inhibiting the hyperpolarization-
activated sodium channel in the sinoatrial node