Pharmacotherapy of angina pectoris

Angina pectoris develops as a result of an imbalance between the oxygen supply and the
oxygen demand of the myocardium. It is a symptom of myocardial ischemia. When the increase
in coronary blood flow is unable to match the increased oxygen demand, angina develops. It
has become apparent that spasm of the coronary arteries is important in the production of
angina.
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Drugs used in angina pectoris
Organic nitrates e.g. nitro-glycerine, isosorbide dinitrate, etc.
Beta adrenergic blocking agents e.g. propranolol, atenolol, etc.
Calcium channel blocking agents e.g. verapamil, nifedipine, etc.
Miscellaneous drugs e.g. aspirin, heparin, dipyridamole.

  • Organic nitrates: organic nitrates are potent vasodilators and successfully used in therapy of
    angina pectoris for over 100 years.
    The effects of nitrates are mediated through the direct relaxant action on smooth muscles.
    Nitrates are believed to act by mimicking the vasodilator action of endothelium derived relaxing
    factor (EDRF) identified as nitric oxide. Vasodilating organic nitrates are reduced to organic
    nitrites, which is then converted to nitric oxide.
    The action of nitrates begins after 2-3 minutes when chewed or held under tongue and action
    lasts for 2 hours. The onset of action and duration of action differs for different nitrates and
    varying pharmaceutical preparations.
    Adverse effects include flushing, weakness, dizziness, tachycardia, palpitation, vertigo,
    sweating, syncope localized burning with sublingual preparation and contact dermatitis with
    ointment.
    Therapeutic uses: prophylaxis and treatment of angina pectoris, post myocardial infarction,
    coronary insufficiency, acute LVF (left ventricle failure)
  • Adrenergic blocking agents
    Exercise and emotional excitement induce angina in susceptible subject by the increase in heart
    rate, blood pressure and myocardial contractility through increased sympathetic activity.
    Beta receptor blocking agents prevent angina by blocking all these effects. In most patients the
    net effect is a beneficial reduction in cardiac workload and myocardial oxygen consumption e.g.
    atenolol, propranolol metoprolol, labetolol.
    Adverse effects: Lethargy, fatigue, rash, cold hands and feet, nausea, breathlessness,
    nightmares and bronchospasm. Selective beta blockers have relatively lesser adverse effects.
    Therapeutic uses other than angina include hypertension, Cardiac arrhythmias, post
    myocardial infarction and pheochromocytoma.
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  • Calcium channel blockers: calcium is necessary for the excitation contraction coupling in
    both the cardiac and smooth muscles. Calcium channel blockers appear to involve their
    interference with the calcium entry into the myocardial and vascular smooth muscle, thus
    decreasing the availability of the intracellular calcium e.g. nifedipine, felodipine, verapamil and
    diltiazem.
    Other therapeutic uses: hypertension, acute coronary insufficiency, tachycardia,
    Adverse effects: flushing nausea/vomiting, headache, Ankle swelling, dizziness, constipation,
    etc.

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