3. 1.Introduction
Angina pectoris is the chief
symptom of ischemic heart disease
(IHD) characterized by sudden,
severe, pain which may radiate to
the left shoulder and surface of the
left arm.
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4. 1.Introduction
• Myocardial oxygen
consumption depends
on preload afterload
and heart rate.
• When the oxygen
supply to the
myocardium is
insufficient for its
needs, myocardial
ischemia develops.
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6. 2.Type of angina
1. Classical angina
(stable angina):
• Pain is induced by
exercise or emotion,
both of which increase
myocardial oxygen
demand.
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7. 2.Type of angina
• In such patients there is
narrowing of the coronary
arteries due to atherosclerosis
and therefore the coronaries
cannot dilate to increase the
blood supply during exercise.
• Hence there is an imbalance
between oxygen supply and
demand.
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8. 2.Type of angina
2.Unstable angina:
• Unstable angina is classified between stable
angina and Myocardial infraction.
• What cause unstable angina- this atheroma
plague rapture and blood clot may form and
decrease blood flow in the artery.
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8
9. 2.Type of angina
• 3.Variant angina
• angina that occurs at rest
and is due to coronary
artery spasm.
• Symptoms are caused by
decreased blood flow to
the heart muscle from the
spasm of the coronary
artery.
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13. 1. Nitrates
• They are converted to
nitric oxide.
• Activates vascular guanylyl
cyclase which increases
the synthesis of cGMP.
• This cGMP catalases the
phosphorylation of protein
kinases causing relaxation
of the smooth muscles.
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14. 1. Nitrates
• Pharmacokinetics :-
• Organic nitrates are lipid-soluble: well absorbed
from buccal mucosa. Action occur 5-7 min.
• Half life 2-5 hr.
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17. 2.Calcium channel blockers
• Ex - Verapamil, Diltiazem, Amlodipine,
Nifedipine, Nicardipin.
• MOA:
• The intracellular concentration of calcium
plays an important role in maintaining the
tone of smooth muscle and in the
contraction of the myocardium.
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18. 2.Calcium channel blockers
• Calcium enters muscle cells through special
voltage sensitive calcium channels.
• This triggers release of calcium from the
sarcoplasmic reticulum and mitochondria, which
further increases the cytosolic level of calcium.
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19. 2.Calcium channel blockers
• Calcium channel blocker block L-type calcium
channels in the heart and in smooth muscle of
the coronary and peripheral arteriolar.
• This causes vascular smooth muscle to relax,
dilating mainly arterioles
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20. 2.Calcium channel blockers
• Pharmacokinetic action :
• Most of these agents have short half-lives (3 to 8
hours)
• Metabolized in liver
• Excreted in urine
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21. 2.Calcium channel blockers
• ADR:
• Dizziness, headache, and a feeling of fatigue
caused by a decrease in blood pressure
• Peripheral edema is another commonly reported
side effect of this class.
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23. 3.β-blockers
• Ex- Propranolol, Atenolol, Metoprolol.
• MOA:
• Blockade of cardiac β1 receptors results in
decreased myocardial contractility and cardiac
output.
• They reduce the BP due to a fall in the cardiac
output.
• They also lower plasma renin activity and have
an additional central antihypertensive action.
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32. 5.References:
• Essentials Of Medical Pharmacology 8th Edition
2018 By KDTripathi
• Lippincott's pharmacology
• Padmaja Uday Kumar Professor and Head
Department of Pharmacology Fr. Muller Medical
College, Mangalore Karnataka India
• Goodman and Gilman’s The Pharmacological Basis of
Therapeutics, 11th -Edition 2006
• Rang & Dale’s Pharmacology, Eighth edition
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