This document discusses angina pectoris, its types and treatment. It defines angina as chest pain due to insufficient blood supply to the heart. There are three main types - stable angina, unstable angina and vasospastic angina. Treatment focuses on reducing oxygen demand on the heart and increasing oxygen supply. The main drug classes used are organic nitrates, beta blockers, and calcium channel blockers. Nitrates provide quick relief of chest pain while beta blockers and calcium channel blockers are used long-term to prevent angina episodes.

1. ANGINA PECTORIS AND ITS
TREATMENT
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2. ANGIAN PECTORIS
• Angina pectoris is characteristic sudden,
severe, pressing chest pain radiating to the
neck, jaw, back and arms. It is due to cardiac
ischemia(insufficient blood supply to meet
the O2 demand of cardiac tissues).
• It is generally due to the obstruction or
spasm of coronary arteries(arteries supplying
blood to the heart) which results in less O2
supply than the demand of heart muscles.
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3. ANGIAN PECTORIS
• Angina is not a disease. It is a symptom of an
underlying heart problem known as Ischemic
Heart Disease(IHD).
• Transient, self-limited episodes (15 seconds to
15 minutes) of myocardial ischemia do not
result in cellular death.
• If angina remains more than 20 min. it leads
to Myocardial Infarction (Death of Cardiac
tissues).
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4. TYPES OF ANGINA PECTORIS
1. STABLE ANGINA:
• Also known as typical, classical or
atherosclerotic angina.
• It is associated with coronary atherosclerosis
plaques that partially obstruct one or more
coronary arteries.
• It usually occurs with exertion or emotional
excitement.
• Rest is usually leads to complete relief of the
pain with in 15 min.
• It constitute about 90% of angina cases.
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5. TYPES OF ANGINA PECTORIS
2. UNSTABLE ANGINA:
• It lies between stable angina and myocardial
infarction.
• It is also known as acute coronary syndrome,
characterized by increased frequency and severity
of attacks.
• Result from the combination of atherosclerotic
plaques, platelet aggregation and vasospasm.
• These attacks can be precipitated by progressively
less physical effort.
• Can’t be relieved by rest or Nitroglycerin.
• It is treated by medical emergency.
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6. TYPES OF ANGINA PECTORIS
3. VASOSPASTIC ANGINA:
• Also known as rest, variant or Prinzmetal angina.
• It is associated with reversible coronary artery
spasm usually at the site of atherosclerotic
plaque.
• Spasm may occur even during sleep.
• Vasospastic angina may deteriorate into Unstable
angina.
• It is responsible for less than 10% of cases.
• It promptly responds to coronary vasodilators
such as Nitroglycerin & Calcium Channel Blockers.
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7. TYPES OF ANGINA PECTORIS
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8. PATHOPHYSIOLOGY
DECREASED O2 SUPPLY
Coronary
• Atherosclerosis
• Vasospasm
• Thrombosis
INCREASED O2 DEMAND
• Increase in Heart Rate
• Increased contractility
of Heart
• Increase in wall
tension
• Increase in Preload
• Increase in After load.
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9. TREATMENT OF ANGINA PECTORIS
Drugs used in angina
exploit two main
strategies:
• Reduction of Oxygen
demand.
• Increase of oxygen
supply to myocardium.
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10. ANTIANGINAL DRUGS
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11. ANTIANGINAL DRUGS
ORGANIC NITRATES
• Organic nitrates(and nitrites) used in treatment of
angina pectoris are simple nitric and nitrous acid
esters of glycerol.
• All the nitrates share the same mechanism of action,
differs only in their time course.
• Only major action is direct relaxation of smooth
muscles.
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12. ANTIANGINAL DRUGS
CLASSIFICATION OF NITRATES
1. SHORT ACTING NITRATES:
• Used to terminate acute attack of angina.
• Nitroglycerin (GTN) and Amyl nitrate.
• Usually administered sublingually.
• Onset of action 1 min.
• Short Duration 15 min.
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13. ANTIANGINAL DRUGS
2. INTERMEDIATE ACTING NITRATES
• Isosorbide mononitrate, isosorbide dinitrate oral.
• Used in Prophylaxis of Angina.
• Slow onset of action and duration of action is 2-4
hours.
3. LONG ACTING NITRATES
• Used to prevent an attack of angina.
• Isosorbide dinitrate, Isosorbide mononitrate
Erythritryl tetranitrate.
• Administered topically (Transdermal).
• Slow onset and duration of action is 10 hours.
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14. MECHANISM OF ACTION OF NITRATES
Nitrates(Denitrated in smooth muscle cell)
↓
Release NO (Nitric Oxide)
↓
Increase in Guanylyl Cyclase
↓
↑ cGMP*→ Dephosphorylation of MLCK (Myosin Light
chain Kinase)
↓
Relaxation of vascular smooth muscles
(*Cyclic Guanosine Mono Phosphate)
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15. ANTIANGINAL DRUGS
ORGANIC NITRATES:
• Veins express greater amount of the enzymes that
generate NO from GTN than arteries.
• Which results in more Venodilation & less
arteriodilation by Nitrates.
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16. ANTIANGINAL DRUGS
1. EFFECTS ON CARDIOVASCULAR SYSTEM:
• Smooth muscle relaxation by Nitrates leads to
Venodilation → reduced preload.
• Relaxation of arterial smooth muscles results in
decreased after load → decreased peripheral
resistance → decrease in Blood Pressure.
• Decrease in myocardial fiber tension → decrease in
oxygen demand.
2. EFFECTS ON OTHER ORGANS:
• Nitrates relax the smooth muscles of bronchi, GIT,
urinary tract.
• Effects are too small to be clinically useful.
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17. ANTIANGINAL DRUGS
CLINICAL USES OF ORGANIC NITRATES
1. ANGINA PECTORIS: Effective in stable as well as
Prinzmetal angina.
2. ACUTE CORONARY SYNDROME
3. MYOCARDIAL INFRACTION
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18. ANTIANGINAL DRUGS
PHARMACOKINETICS OF ORGANIC NITRATES:
• Organic nitrates are lipid soluble.
• Absorbed through buccal mucosa, skin & GIT.
• All except Isosorbide mononitrate undergo
extensive first pass metabolism.
• SL route produces rapid onset 1-2 Min, but shorter
duration of action.
• Absorption through skin is slow.
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19. ANTIANGINAL DRUGS
ADVERSE EFFECTS:
• Headache
• Postural hypotension
• Reflex tachycardia
• Sildenafil potentiate the effect of nitrates and may
produce dangerous hypotension, hence this
combination is contraindicated.
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20. ANTIANGINAL DRUGS
TOLERANCE:
• Tolerance to the action of enzymes develops
rapidly.
• Enzymes which convert the nitrates into NO,
stop working.
• Blood vessels become desensitized to
vasodilation.
• It can be overcome by providing daily a
“Nitrate free interval”.
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21. ANTIANGINAL DRUGS
BETA BLOCKERS
• The drugs used to antagonize the effects of beta
adrenergic receptors are called as beta blockers.
• β- Blocking agents decrease the oxygen demand of
heart muscles by lowering both rate and contraction
of heart muscles through:
• -ve Chronotropic (Heart rate)
• -ve Dromotropic (Velocity of conduction)
• -ve Inotropic (Force of cardiac muscle contraction)
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22. ANTIANGINAL DRUGS
CLASSIFICATION OF β- BLOCKERS:
1. NON SELECTIVE β- BLOCKING AGENTS:
• Propranolol, Timolol, Pindolol, Sotalol.
2. SELECTIVE β1 BLOCKING AGENTS:
• Atenolol, Bisoprolol, Esmolol, Metoprolol,
Acebutolol.
• All the β blockers are Non-selective at high doses.
• Propranolol is the prototype drug of this class.
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23. ANTIANGINAL DRUGS
MECHANISM OF ACTION OF β- BLOCKERS
Decrease heart rate & Contractility
↓ ↓
Increase duration of diastole Decrease workload
↓ ↓
Increase coronary blood flow Decrease O2 demand
↓
Increase oxygen supply
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24. ANTIANGINAL DRUGS
EFFECTS AND CLINICAL USES
• β1 antagonists reduce the frequency and severity of
anginal episodes.
• β1 antagonists improve survival in post MI patients
and decrease the risk of subsequent cardiac events &
complications.
• β-Blockers in combination with nitrates can be quite
effective because undesirable compensatory effects
evoked by nitrates (tachycardia) are reduced by β
blockers.
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25. ANTIANGINAL DRUGS
EFFECTS AND CLINICAL USES
• β blockers are only used for prophylactic therapy of
angina, no use in acute attack of angina.
• Effective against exercise induced angina but are
ineffective in vasospastic angina.
• β blockers are routinely used in unstable angina.
• All the β blockers are equally effective in classical
angina but Cardioselective agents are preferred.
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26. ANTIANGINAL DRUGS
PHARMACOKINETICS
• Most of the systemic agents developed for chronic
oral use.
• Bioavailability and half life vary greatly.
• Esmolol is short acting (10 min) β-antagonist used
only parenterally.
• Nadolol is longest acting(14-24 hours) β-antagonist.
• Acebutolol, Atenolol are less lipid soluble and enter
in CNS to a lesser extent.
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27. ANTIANGINAL DRUGS
CONTRAINDICATIONS
β blockers are contraindicated in following conditions;
• Prinzmetal Angina
• COPD, Asthma (β2 in lungs)
• Diabetes Mellitus(β2 in liver & pancreas)
• Bradycardia (β1 in heart)
ADVERSE EFFECTS
• Excessive β blockade → Bronchospam → Fatal for asthmatics
• AV blockade → Heart Failure
• CNS sedation
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28. ANTIANGINAL DRUGS
CALCIUM CHANNEL BLOCKERS(CCB)
• CCB inhibit the entry of Ca2+ in smooth muscle or
cardiac muscles → prevent them from contraction.
• All the CCB are arteriodilators and vasodilator to less
extent, hence reduce the peripheral resistance.
• Some agents have more effect on cardiac muscle
than others but all serve to lower blood pressure.
• They are useful in Prinzmetal angina in conjunction
with nitrates.
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29. ANTIANGINAL DRUGS
CLASSIFICATION OF CCB
CCB are classified into three chemical classes;
1. DIPHENYLALKYLAMINES:
• Verapamil is only member of this class.
• Significant effect on cardiac and vascular smooth
muscles cells.
2. BENZOTHIAZEPINES:
• Diltiazem is the only member of this class.
3. DIHYDROPYRIDINES :
• 1st Generation is Nefidipine
• 2nd Generation are Amlodipine, Felodipine,
Isradipine, Nicardipine, Nisolodipine.
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30. ANTIANGINAL DRUGS
MECHANISM OF ACTION
Block Voltage sensitive L-Type Ca2+ channels
↓
Prevent entry of calcium into the cell
↓
No excitation contraction coupling in the heart and
vascular smooth muscles
↓
• Relaxation of vascular smooth muscles→ Decreased
Afterload → Less peripheral resistance.
• Decreased myocardial contractility → Less O2 demand.
• Coronary Vasodilation
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31. ANTIANGINAL DRUGS
PHARMACOKINETICS OF CCB
• All the CCB are 90-100% orally absorbed.
• High first pass metabolism.
• Peak plasma conc. Occurs in 1-3 hours except
Amlodipine 6-9 hours.
• All are highly bound with plasma proteins.
• >90% of the drug is metabolized in liver and excreted
via urine.
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32. ANTIANGINAL DRUGS
ADVERSE EFFECTS
• Constipation in 10% patients taking Verapamil.
• Dizziness, headache and fatigue.
• Flushing of face.
• AV blockade.
• Heart failure.
• Tachycardia due to hypotension.
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33. COMBINATION OF DRUGS IN ANGINA
Nitrates + β blocker
• Reflex tachycardia by nitrates ↓ by β-blockers.
Nifedipine + β blocker
• Reflex tachycardia countered by β-blockers.
Nitrates + calcium channel blockers
• Nitrates ↓ preload, CCBs ↓ afterload
CCB + β-Blocker + Nitrates
• If not controlled by 2 drugs
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