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Antianginal Drugs

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Antianginal Drugs Antianginal drugs Antianginal drugs are drugs used for the treatment of ischemic heart disease (coronary heart disease). Ischemic heart disease (IHD) is characterized by disbalance between myocardium oxygen demand and coronary blood supply. FACTORS DETERMINING MYOCARDUM OXYGEN DEMAND: 1. contractility of myocardium 2. heart rate (HR) 3. tension of myocardium wall at the end of diastole (preload), and its` maximal tension during systole (afterload). FACTORS DETERMINING MYOCARDIAL BLOOD SUPPLY 1. perfusion pressure that ensures movement of blood through coronary vessels, it is the difference between the pressures in coronary sinuses (intramyocardial pressure) and aorta. The higher is the intramyocardial pressure (for example preload increase), the lower is the perfused pressure and the worse is the myocardial blood supply. 2. resistance and diameter of coronary arteries, which depends on the external factors (which bring to passive changes of resistance and diameter of coronary vessels), internal factors (which cause active changes in them) and blood viscosity. 2.1. To the external factors belongs extravascular myocardial compression (the compression of coronary vessels due to the heart contraction during systole), especially intramural coronary vessels. In these vessels, blood supply nearly completely ceases during systole. So, 67-90% of the heart blood supply is realized during diastole, especially at its beginning, when the myocardium is fully relaxed. In this case subendocardial arteries become mainly compressed (picture 1). 2.2. To the internal factors belongs local-self –regulating mechanisms (due to pO2 and/or pCO2 level changes), nervous (activation of α-adrenorecpetors causes vasoconstriction and stimulation of M-cholino- and β2-adrenoreceptors brings to vasodilation of coronary arteries) and humoral factors (EDRF, prostacycline etc.). 1 Picture 1: Extravascular myocardial compression of coronary arteries 3. Passability of coronary arteries( the existence of atherosclerotic plugs and/or thrombs). There are the following types of IHD. 1.Sudden coronary death 2.Angina pectoris 2.1. Exertional angina 2.2. Vasospastic angina or Prinzmetal`s angina 3. Myocardial infarction 4. Postinfarction cardiosclerosis 5.Arrhyhtmias 6.Heart failure During exertional angina the attacks can be precipitated during physical or emotional loading, which can lead to increase in oxygen demand, because coronary vessels have atherosclerotic plug, they can`t be adequately dilated and support adequate blood flow. In vasospastic angina attacks can be precipitated due to vasospasm of vessels. 2 Based on the above mentioned, we can state that the main goal of IHD treatment is a restoration of the balance between oxygen requirement and blood supply of myocardium, which can be achieved by the: 1. improvement of blood supply 2. reduction of myocardium oxygen demand 3. improvement of blood supply and at the same time reduction of the myocardium oxygen demand. The main goals of the angina pectoris treatment are: 1. Elimination of angina attacks 2. Prevention of angina attack development, which supposes the long-term treatment of the patients. Classification of antianginal drugs 1. Drugs reducing heart oxygen demand, simultaneously improving blood supply: Organic nitrates L-type Ca2+ -channel blockers K+-channel activators 2. Drugs predominantly reducing oxygen demand: 2.1. β-adrenoblockers 2.2. Bradycardic drugs 3. Drugs improving myocardial blood supply: Spasmolytic drugs Drugs removing coronary spasm by reflex mechanism Drugs, which are included in the complex treatment of IHD, but aren`t considered to be antianginal drugs: 1. cardioprotectors 2. antiaggregants 3. anticoagulants 4. fibrinolytics 5. hypolipidemic drugs – statins. 3 1. Drugs decreasing the heart oxygen demand and simultaneously improving blood supply Organic nitrates Nitroglycerin was for the first time synthesized in 1846 by Ascanio Sobrero. He found out that the sublingual usage of small doses of nitroglycerin causes headache. A year later, Konstantin Hering determined the curing doses of nitroglycerin and obtained nitroglycerin tablets. At the present three groups of organic nitrates are used: 1. Nitroglycerin 2. Isosorbide dinitrate derivatives-Isomac, Isodinit, Cardicet 3. Isosorbide 5- mononitrate derivatives-Olicard, Monochinkve, Mono Rom retard Practically, it is more convenient to classify them according to the duration of their action 1. nitrates with short duration of action (the duration is up to 1 hour), 2. nitrates of moderate duration of action (1-6 hours), 3. nitrates with long duration action (6-24 hours). Pharmacodynamics. Hemodynamic effects of nitrates are similar to those of the endothelial vasodilator NO. In the arteries and veins endothelium NO is produced during L-arginin metabolism, with participation of NO-synthatase. In arteries NO is produced more than in veins, though guanylate cyclase in veins is much more sensitive towards NO. There are known two varieties of NO synthetase - the structural (constitutive, endothelial) and inducible ones. The structural NO-synthetase is endothelial Ca2+-calmadulin-dependent enzyme, which is present also in thrombocytes, neurons, and is characterized by a low degree of activation. The inducible NO synthetase is produced under the influence of immunogenic and pre- inflammatory factors (γ-interferon, interleukin-1). 4 Due to the participation of endothelial glutathione – S - transferase sulfydryl groups, nitrates are transformated into nitrite form, after which, reactive, free-radical NO is formed, which, as a lipophylic compound quickly penetrates into the smooth muscles, where activates cytoplasmic guanylate cyclase. As a result, the quantity of cGMP increases. By activation of special protein kinases cGMP brings to dephosphorylation of myosin light chains, preventing formation of actomyosin. So relaxation of smooth muscles occurs. Besides, the increased quantity of cGMP may restrict penetration of Ca2+ into the cell. Besides above mentioned vasodilating effect, NO also stimulates prostacycline and PgE synthesis, which possess vasodilative and antiaggregant properties. Half life of NO is 6-30 sec. Systemic effects of organic nitrates Cardiovascular system Mechanisms of antianginal effect of nitrates are: 1. Decrease in preload. In low therapeutic doses, nitrates mainly dilate veins. Dilation of veins results in their increased capacity, due to which the reverse blood flow to the heart and also preload becomes decreased. Decreased preload results in lowering of the enddiastolic pressure of ventricles that reduces the heart oxygen requirement. Moreover decreased enddiastolic pressure of ventricles brings to the improvement of blood supply in subendocardial part of myocardium. 2. Decrease in afterload. Nitrates in the middle therapeutic doses dilate arterioles, resulting in a reduction of general peripheral resistance and afterload. In this case systolic BP is mainly reduced. 3. Dilation of coronary vessels. As it is known, ischemia stimulates dilation of coronary vessels. In the conditions of myocardial ischemia acidosis develops which brings to dilation of coronary vessels by compensatory mechanism, meanwhile the vessels with atherosclerosis cannot be dilated. Nitrates mainly dilate large coronary vessels of epicardium, in a result of which in the vessels with atherosclerotic affection pressure gradient for blood supply of ischemia area becomes increased (improved). Moreover, nitrates also eliminate spasms of coronary vessels, so they are effective also in treatment of vasospastic angina (picture 2). 5 4. Nitrates improve collateral blood supply directly as well as indirectly. Nitrates can directly dilate collateral coronary vessels, increasing the quantity of functioning collateral vessels. Besides, by reducing the intraventricular pressure and volume, and decreasing myocardial wall tension, they indirectly decrease the external compression of collateral vessels. 5. Antiaggregant action. Nitrates increasing the quantity of cGMP in thrombocytes, inhibit thrombocyte aggregation preventing a thrombus formation in the coronary artery lumen. Picture 2. Action of organic nitrates on coronary blood flow Smooth muscles Organic nitrates relax all smooth muscles-bronchi, esophagus, biliary ducts, gall bladder, Ody’s sphincter, urethra, also uterus. Pharmacokinetics Organic nitrates differ from each other mainly by their pharmacokinetic properties. Nitroglycerin. During oral rout of administration nitroglycerin and its depot preparations with gradually dissolving active substance (Sustak forte, Nitrong forte) have an insignificant antianginal effect. It is explained by the fact that nitroglycerin, being a lipophylic drug is completely absorbed from intestines, and in the liver with participation of nitrate reductase undergoes to biotransformation, in a result of which 80-90% of the drug becomes neutralized. 6 Depot drug forms of the nitroglycerine have more bioavailability and duration of action (up to the 6 hours). That is why nitroglycerin preparations are mainly used by sublingual rout with the purpose to stop angina attacks. In this case half - life is 1-3 min and duration of action is 15-20 min. Nowadays there are available another drug forms of nitroglycerin-buccal polymeric films (which are applied on the upper jaw gum), ointments, patches etc. having a longer duration of action and can be used for prevention of angina attacks. Nitroglycerin can be used also by intravenous injections. Isosorbide dinitrate preparations
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