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Antianginal drugs (VK)
The document discusses various types of angina and treatments for restoring the balance between oxygen supply and demand in the heart. It describes 3 main types of angina - chronic stable angina, unstable angina, and vasospastic angina. The goal of antianginal drug therapy is to increase blood flow to the heart and decrease myocardial oxygen demand. The major antianginal drug classes discussed are nitrates, beta-blockers, calcium channel blockers, and potassium channel openers. Specific drugs within each class are also named and their mechanisms and uses summarized within 3 sentences.
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Antianginal drugs (VK)
- 2. When the supplyof oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle aches. The heart demands a large supply of oxygen to meet the demands placed on it.
- 7.
- 8. Chronic stable angina (alsocalled classic or effort angina) Unstable angina (also called preinfarction or crescendo angina) Vasospastic angina (also called Prinzmetal’s or variant angina)
- 10. The goal oftherapy with antianginal agents is to restore the balance between oxygen supply and demand in the ischemic region of the myocardium.
- 11. CLASSIFICATION 1.Nitrates Short acting:Glyceryl trinitrate (GTN, Nitroglycerine) Long acting: Isosorbide dinitrate (short acting by S.L route), Isosorbide mononitrate, Erythrityl tetranitrate, Pentaerythritol tetranitrate 2.β-Blockers Propranolol, Metoprolol, Atenolol and others. 3.Calcium channel blockers Phenyl alkylamine : Verapamil Benzothiazepine : Diltiazem Dihydropyridines : Nifedipine, Felodipine, Amlodipine, Nitrendipine, Nimodipine, Lacidipine, Benidipine
- 12. 4.Potassium channel opener Nicorandil,Pinacidil 5.Others Dipyridamole, Trimetazidine, Oxyphedrine Clinical Classification (A)Used to abort or terminate attack GTN, Isosorbide dinitrate (sublingually). (B)Used for chronic prophylaxis All other drugs.
- 13. Therapeutic Objectives Increase bloodflow to ischemic heart muscle and/or Decrease myocardial oxygen demand Minimize the frequency of attacks and decrease the duration and intensity of anginal pain Improve the patient’s functional capacity with as few side effects as possible Prevent or delay the worst possible outcome, MI
- 14. Available forms: Sublingual Ointments Buccal Transdermal patches Chewabletablets Inhalable sprays Capsules Intravenous solutions
- 15. Nitrates Nitrates Denitrated in thesmooth muscle cell Release nitric oxide Release nitric oxide Stimulate Guanylyl cyclase Stimulate Guanylyl cyclase Increased cGMP Increased cGMP Dephosphorylation of myosin light Dephosphorylation of myosin light chain (reduced ca+ conc in the cytosol) chain (reduced ca+ conc in the cytosol) Relaxation of vascular Relaxation of vascular smooth muscle fibres smooth muscle fibres Mainly vasodilatation Mainly vasodilatation Arterial dilatation Arterial dilatation Dila of coronary vessels Dila of coronary vessels
- 16. Cause vasodilation dueto relaxation of smooth muscles Potent dilating effect on coronary arteries Used for prophylaxis and treatment of angina
- 17. Nitroglycerin Prototypical nitrate Large first-passeffect with PO forms Used for symptomatic treatment of ischemic heart conditions (angina) I.V form used for BP control in perioperative hypertension, treatment of CHF, ischemic pain, and pulmonary edema associated with acute MI
- 18. isosorbide dinitrate (Isordil, Sorbitrate,Dilatrate SR) isosorbide mononitrate (Imdur, Monoket, ISMO) Used for: Acute relief of angina Prophylaxis in situations that may provoke angina Long-term prophylaxis of angina
- 19. Side Effects Headache Usually diminishin intensity and frequency with continued use Tachycardia, postural hypotension Tolerance may develop (Monday disease)
- 20. Isosorbide dinitrate Isosorbide dinitratehas active initial metabolites. This drug is administered orally or sublingually; it has better oral BA and a longer half-life (up to 1 h) than nitroglycerin. Timed-release oral preparations are available with durations of action up to 12 hours.
- 21. Therapeutic uses 1. Sublingual nitroglycerinis most often used for severe, recurrent Prinzmetal's angina. 2. Continuous infusion or slowly absorbed preparations of nitroglycerin (including the transdermal patch) or derivatives with longer half-lives have been used for unstable angina and for CHF in the presence of MI.
- 22. Adverse ef fects Nitratesand nitrites produce vasodilation, which can lead to orthostatic hypotension, reflex tachycardia, throbbing headache (may be dose limiting), blushing, and a burning sensation. Tolerance. Large doses produce methemoglobinemia and cyanosis.
- 23. Atenolol (Tenormin) Metoprolol (Lopressor) Propranolol(Inderal) Nadolol (Corgard)
- 24. Mechanism of Action Decreasethe HR, resulting in decreased myocardial oxygen demand and increased oxygen delivery to the heart Decrease myocardial contractility, helping to conserve energy or decrease demand
- 25.
- 26. Side Effects Body System Effects Cardiovascular bradycardia,hypotension second- or third-degree heart block heart failure Metabolic Altered glucose and lipid metabolism
- 27. Side Effects Body System Effects CNS dizziness,fatigue, mental depression, lethargy, drowsiness, unusual dreams Other impotence wheezing, dyspnea
- 28.
- 29. Mechanism: Calcium channel-blockingagents produce a blockade of L-type (slow) calcium channels, which decreases contractile force and oxygen requirements. Agents cause coronar y vasodilation and relief of spasm they also dilate peripheral vasculature and decrease cardiac afterload. Preload refers to total volume of blood in the left ventricle of the heart and the pressure it exerts before the left ventricle contracts. Afterload then is the amount of pressure exerted by the left ventricle when it does contract.
- 31. Pharmacologic proper ties CC blocking agents can be admi orally. When admi intravenously, they are effective within minutes. The therapeutic use of these drugs in angina is generally reserved for instances in which nitrates are ineffective or when β-Blks C/I. Serum lipids are not increased. These drugs produce hypotension.
- 32. Verapamil Verapamil produces slowedconduction through the AV node (predominant effect); this may be an unwanted effect in some situations (especially in the treatment of hypertension). Verapamil may produce AV block when used in combination with β-blks.
- 33. The toxic effectsof verapamil include myocardial depression, heart failure, and edema. Verapamil also has peripheral vasodilating effects that can reduce afterload and BP The peripheral effects of verapamil can produce headache, reflex tachycardia, and fluid retention.
- 34. These dihydropyridine CCBlshave predominant actions in the peripheral vasculature; they decrease afterload and to a lesser extent preload and lower blood pressure. These drugs have significantly less direct ef fect on the hear t than verapamil.
- 35. Diltiazem Diltiazem, a benzothiazepine,is intermediate in properties between verapamil and the dihydropyridines. Diltiazem is used to treat variant (Prinzmetal's) angina, either naturally occurring or drug-induced and stable angina.
- 36. Bepridil Bepridil blocks bothslow and fast sodium channels and both voltage-dependent and receptor-mediated calcium channels. Bepridil is used only when other agents have failed or have elicited intolerable A/E. Bepridil may cause ventricular arrhythmias.
- 37. Therapeutic Uses First-line agentsfor treatment of angina, hypertension, and supraventricular tachycardia Short-term management of atrial fibrillation and flutter Several other uses
- 38. Their efficacy issimilar to nitrates, beta blockers, CCBs Main advantages of Nicorandil, it has longer DOA and does not cause tolerance Administered orally
- 39. Nicorandil & Nicorandil & Pinacidil Pinacidil OpenATP-dependent K+ channels Open ATP-dependent K+ channels K+ efflux K+ efflux Hyperpolarization of the membrane Hyperpolarization of the membrane Venodilators Venodilators Arterial dilators Arterial dilators ↓Preload ↓Preload ↓ Afterload ↓ Afterload
- 40.
Editor's Notes
- #31 In cardiac physiology, preload is the end volumetric pressure that stretches the right or left ventricle of the heart to its greatest geometric dimensions under variable physiologic demand. [1] In other words, it is the initial stretching of the cardiomyocytes prior to contraction; therefore, it is related to the sarcomere length at the end of diastole. Parameters such as ventricular end diastolic volume or pressure are used to measure preload since the ideal length of the cardiac sarcomere cannot be measured. Passive filling of the (heart) ventricle and subsequent atrial contraction thus allows an echocardiographically volumetric measurement. Preload is theoretically most accurately described as the initial stretching of a single cardiomyocyte prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation may be inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged. The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the strict definition of preload. Atrial pressure is a surrogate for preload.