This document discusses angina pectoris, or chest pain caused by reduced blood flow to the heart. It defines three main types of angina - stable, unstable, and Prinzmetal's variant - based on the characteristics and triggers of the chest pain. The document then reviews several classes of drugs used to treat angina, including nitrates, beta-blockers, calcium channel blockers, and nicorandil. It provides details on the pharmacological mechanisms and clinical uses of individual drugs within these classes, such as nitroglycerin, metoprolol, verapamil, and nicorandil. Adverse effects are also outlined for each medication.

1. PREPARED BY: JEGAN. S. NADAR

2.  Angina=pain , pectis=chest
 Ischemic heart disease
 Generally described as pain
arising in the substernal region
(below the sternum) or region of
chest
 Pain radiates
 Left Arm ,neck, jaw, teeth,
fingers , below the abdomen
What is Angina??
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5.  Stable:
 Typical angina
 caused by stable plaque
 Attacks of pain= physical activity
 Relieved by rest
 Unstable: cresendo- pain at regular intervals
 Pre-infarction angina
 caused by unstable plaque
 Serious pattern
 Frequent onset of pain
 Pain for long intervals
 Prinzmetal’s: variant
 caused by unstable plaque
 occurs at rest
 unpredictable
 pain can increase for no obvious reason
TYPES OF ANGINA
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9. ANGINA
PECTORIS
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14.  Nitrates cause a
rapid reduction
in myocardial
oxygen demand
followed by rapid
relief of
symptoms
 They are effective
in all form of
angina
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17. Pharmacokinetics
 Organic nitrates are lipid soluble: well absorbed from buccal mucosa,
intestines and skin.
 Ingested orally, all except isosorbide mononitrate undergo extensive and
variable first pass metabolism in liver.
 They are rapidly denitrated by a glutathione reductase and a
mitochondrial aldehyde dehydrogenase.
 The partly denitrated metabolites are less active, but have longer t½.
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18. ADVERSE EFFECTS
These are mostly due to vasodilatation.
 Fullness in head, throbbing headache; some degree of tolerance develops
on continued use.
 Flushing, weakness, sweating, palpitation, dizziness and fainting; these
are mitigated by lying down.
 Erect posture and alcohol accentuate these symptoms.
 Rashes are rare, though relatively more common with pentaerythritol
tetranitrate
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19. Dependence
 Organic nitrates is now well recognized.
 Sudden withdrawal after prolonged exposure has resulted in spasm
of coronary and peripheral blood vessels.
 MI and sudden deaths have been recorded.
Interactions
 Sildenafil causes dangerous potentiation of nitrate action: severe
hypotension, MI and deaths are on record
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21. β-blockers
Blocks β1 receptor
Decreases Cardiac output, heart rate, contractility and BP
Decrease in Myocardial oxygen demand
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22.  The nonselective β blockers have an unfavourable effect on lipid
profile (raise triglyceride level and LDL/HDL ratio).
 They have also fared less well on quality of life parameters like
decreased work capacity, fatigue, loss of libido and subtle
cognitive effects (forgetfulness, low drive), nightmares and
increased incidence of antidepressant use.
 Many of these drawbacks are minimized in the β1 selective agents
and in those which penetrate brain poorly
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23.  Advantages of cardio-selective over non-selective:
 In asthma
 In diabetes mellitus
 In peripheral vascular disease
 Drawbacks (side effects):
 Fatigue, – decreased work capacity
 Loss of libido – impotence
 Cognitive defects – forgetfulness
 Difficult to stop suddenly
 Therefore cardio-selective drugs are preferred now
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26.  Calcium is essential for muscular contraction
 Calcium influx is increased in ischemia because of membrane
depolarization that hypoxia produces
 In turn, this promotes the activity of several adenosine triphosphate
consuming enzymes, thereby depleting energy stores and worsening
ischemia
 Thus calcium channel blocker protect the tissue by inhibiting
entrance of calcium into cardiac and smooth muscle of coronary and
systemic arterial blood. Jegan

27.  Calcium channel blockers are arteriolar vasodilator that causes
decrease in smooth muscle tone and vascular resistance
 It reduces total peripheral resistance , blood pressure, cardiac output
and heart rate
 Therefore decrease in myocardial oxygen demand
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29. Verapamil
 It slows cardiac AV conduction directly and decreases heart rate ,
contractility, and blood pressure.
 It dilates arterioles and has some α adrenergic blocking activity.
 Dose: 40-160mg TDS
Interaction
• Verapamil should not be given with β blockers
• It increases plasma digoxin level by decreasing its
excretion: toxicity can develop.
• It should not be used along with other cardiac
depressants like quinidine and disopyramide.
Adverse effect
• Nausea
• Constipation
• Headache
• Hypotension
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30. Diltiazem
 It is somewhat less potent vasodilator than nifedipine and verapamil,
direct depression of SA node and A-V conduction are equivalent to
verapamil.
 Usual clinical doses produce consistent fall in BP with little change or
decrease in HR.
 Dose: 30–60 mg TDS
Side effects
• Side effects are milder, but the profile is similar to
verapamil.
• Like verapamil, it also increases plasma digoxin
level.
• Diltiazem should not be given to patients with
preexisting myocardial disease. Jegan

31. Nifedipine
 It is the prototype DHP with a rapid onset and short duration of action.
 The overriding action of nifedipine is arteriolar dilatation → t.p.r.
decreases, BP falls.
 Coronary flow is increased.
 Dose- 5-20mg TDS
Adverse effects
Frequent side effects are
• Palpitation,
• Flushing,
• Ankle edema,
• Hypotension,
• Headache,
• Drowsiness and Nausea.
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32. Nicorandil
 This dual mechanism antianginal drug activates ATP sensitive K+ channels
(KATP).
 Opening these channel causes potassium ion to leak out from the cell.
 This action hyperpolarises and stabilises the cell membrane of the
vascular smooth muscle and prevents its contraction, leading to its
relaxation. Thus they act as arterial vasodilator.
 In heart they reduce the excitability of cell and show protective effect
against ischemia. Jegan

33.  Like nitrates it also acts as a NO donor—relaxes blood vessels by
increasing cGMP.
 Thus, arterial dilatation is coupled with venodilatation
 Coronary flow is increased
 No significant cardiac effects on contractility and conduction have been
noted.
 Dose:5-20mg BD
Adverse effect
• Palpitation
• Weakness
• Vomiting
• Large ulcers in mouth
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