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Description : Check out this medical presentation on Pharmacology, which is titled "Antianginal Drugs", to know about the antianginal drugs.

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Published on : Jul 18, 2021 | Views : 4201 | Downloads : 18

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Assoc. Prof. Ivan Lambev (www.medpharm-sofia.eu) ANTIANGINAL DRUGS
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Angina pectoris is a symptom of reversible myocardial ischaemia and is most frequently experienced as chest pain on exertion, which is relieved by rest. Pain is the consequence of an imbalance between oxygen supply and oxygen demand in the ischaemic area of myocardium.
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This imbalance results from an inability of the coronary blood flow to meet the metabolic demands of the heart, due to a fixed atheromatous narrowing of coronary artery. Usually reversible coronary artery spasm participates too.
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ECG Stress Test (10–20 min) Non- Invasive method
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ECG Stress Test: Recordings
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Iopramide (Ultravist®) in a. femoralis Invasive method
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X-ray a. femoralis
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They can be given to relieve rapidly the ischaemia during an acute attack, or as prophylaxis to reduce the risk of subsequent episodes. Antianginal drugs increase oxygen supply by improving coronary blood flow or reduce oxygen demand by decreasing cardiac work.
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Major sites of actions of antianginal drugs
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Glyceryl- 3-nitrate Isosorbide dinitrate Organic nitrates – indirect donors of NO
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Organic nitrates are vasodilators which relax vascular smooth muscle. They connect with thiol groups (-SH) and release nitric oxide (NO). NO combines with thiol groups in vascular endothelium to form nitrosothiol (R-SNO). Nitrosothiol activates guanylate cyclase which raises the concentration of cyclic GMP. This reduces the availability of intracellular calcium and produces vasodilation in three main vascular beds.
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Ca2+ Organic nitrate (R-ONO2) Endothelium Smooth muscle Celullar action of nitrates SR – sarcoplasmatic reticulum GTP – guanosine triphosphate GMP – guanosine monophosphate
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Organic nitrates dilate: Venous capacitance vessels and lower left ventricular filling pressure (“preload”) Arterial resistance vessels and reduce ventricular emptying (“afterload”). This is less important than venodilation during long treatment but it lowers blood pressure, decreases cardiac work and contributes to reduced oxygen demand.
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Coronary arteries. Nitrates have little effect on the total coronary flow but they improve the blood flow through collateral vessels. Nitrates also relieve coronary artery spasm. The net effect is increased blood flow supply to ischaemic areas of the myocardium.
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Glyceryl trinitrate is the most widely used organic nitrate. It is well absorbed orally but undergoes extensive first-pass metabo- lism in the liver to inactive metabolites. Usually glyceryl trinitrate is given by one of three routes to avoid first-pass effect and hence increases its bioavailability: Sublingually (as a tablets). Its effect begins after 1-2 min and lasts 18–20 min. Tablets lose their potency with prolonged storage.
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Glyceryl trinitrate Nitrolingual® spray: 0.4 mg/dose Nitroglycerin®: ling. 0.5 mg Nitroderm® TTS Perlinganit® - i.v. inf. (+ Heparin)
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Isosorbide dinitrate (prodrug) Isoket®: spray and tabl. (sub linguam) Isodinit®: tablets 20 mg Kardiket®: tabl. 20 mg Isosorbide-5-mononitrate t1/2 4–5 h (Olicard® 40 retard: 12 h)
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Adverse reactions of nitrates: Venodilation may lead to postural hypo- tension, dizziness, syncope, tachycardia. Arterial dilation causes throbbing headache and flushing, but tolerance is common during treatment with long-acting nitrates (retard tablets). Tolerance to the therapeutic effects. This may be due to depletion of vascular thiol groups. It can be avoided by a “nitrate-low” period of 10-12 h each day.
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II. Beta-adrenoceptor antagonists (b-blockers) (1) (b1 & b2 ) Propranolol Oxprenolol Pindolol Carvedilol (antioxidant) (b & a ) Atenolol Acebutolol Bisoprolol Celiprolol Metoprolol
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VDCC ROCC Receptor AP Ca2+ Ca2+ Sarcoplasmatic reticulum Cell wall (–) Beta-blockers AP – action potential, NA – noradrenaline VDCC – voltage dependent calcium channels ROCC – receptor operating calcium channels (–)
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All b-blockers act as competitive antagonists of catecholamines at beta-adrenoceptors: decrease heart rate; reduce the force of cardiac contraction; lower blood pressure; reduce oxygen demand. Lipophilic -blockers (e.g. propranolol) are well absorbed from the gut, but undergo extensive first-pass metabolism in the liver, with considerable variability among individuals.
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Hydrophilic beta-blockers (e.g. atenolol) are less completely absorbed from the gut and are eliminated unchanged by the kidney. The dose range to maintain effective plasma concentrations is narrower than that for drugs which undergo metabolism and the clinical response in angina pectoris is more predictable. Adverse reactions of beta-blockers Blockade of beta1-receptors may cause bradycardia, AV block, heart failure.
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Blockade of beta2-receptors may cause bronchospasm, intermittent claudication (reducing peripheral blood flow) and hypoglycemia. CNS effects: sleep disturbance, dreams and hallucinations (more common with lipophilic drugs which cross the BBB). Most β-blockers raise the plasma concentration of triglycerides and lower the concentration of HDL. Induratio penis pastica (fibrosis …) Sudden withdrawal syndrome: Beta-blockers should be stopped gradually.
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III. Calcium antagonists Calcium is essential for excitation and contraction in muscle cells. Free calcium must either enter the cell or be released from intracellular stores (e.g. SR). Calcium antagonists have widely different chemical structures.
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Calcium antagonists block predominantly L-type calcium channels, localized in myocardium and myocytes of blood vessels. L-type channels are connected to the plateau of the AP. Plateau phase of AP
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VDCC ROCC Receptor AP Ca2+ Ca2+ Sarcoplasmatic reticulum Cell wall NA (–) Calcium antagonists AP – action potential, NA – noradrenaline VDCC – voltage-dependent calcium channels ROCC – receptor operating calcium channels
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Calcium antagonists cause a reduction in coronary and peripheral resistance, lower the blood pressure and oxygen demand. Dihydropyridine derivatives (e.g. amlodipine, felodipine, nifedipine, nisoldipine) have no negative chronotropic effect and do not impair myocardial contractility.
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(Tipathy, 2003)
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Calcium antagonists Amlodipine normal frequently dihydropyridine t1/2 31–47 h, 55–91% p.o. bioavailability 5–10 mg/24 h p.o. (once daily) Nifedipine (tachycardic dihydropyridine) – effective in vasospastic angina Diltiazem (in SR dosage forms) Verapamil (Isoptin SR® – tabl. 120 mg) (22% p.o. bioаvailability, first pass effect – extensive liver metabolism)
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ADRs of calcium antagonists Arterial dilation: headache, flush, dizziness, ankle swelling (resistant to treatment with diuretics but not with ACE inhibitors). Bradycardia and AV block (verapamil). Verapamil + beta-blockers: potentiate cardiodepression. Tachycardia (nifedipine, nisoldipine). Constipation (verapamil 8%, nifedipine 3%) Haemorrhagic gingivitis (inhibition of collagen synthesis)
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4. Metabolic cardioprotective agents Trimetazidine (Preductal MR®) has prolonged concentration plateau lasting up to 11 h. It increases ATP synthesis and decreases acidosis in ischemic tissues. Trimetazidine supplies energy for the Na+/K+ transmembrane pump, but can cause parkinsonism.
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Angiotensinogen Angiotensin I Angiotensin II AT1- receptor AT2- receptor ACE Enalapril (-) Kinins PGs: vasodilation (kininase II) (-) ACE 5. ACE inhibitors: Enalapril, Lisinopril Ramipril, Trandolapril …
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6. If-blockers delays pulse rate with
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IV. OTHER DRUGS USED IN CORONARY HEART DISEASE (CHD) Platelet antiaggregants Antifibrinolytics (Alteplase - t-PA) Antidyslipidemic drugs Anxiolytics, etc.
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V. ALTERNATIVE METHODS FOR TREATMENT OF ISCHAEMIC HEART DISEASE
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Rotational atherectomy (Rotablation) – Chronic narrowing's or blockages may become calcified or have a lot of atheroma in them making them very difficult to treat with just a balloon. Rotablation is a procedure where, once again, a very fine wire is guided through the narrowing and then a catheter with a small device called a burr, similar to drill, mounted at its tip is guided to the beginning of the narrowing. The burr is connected to an external device which when activated by the cardiologist causes the burr to spin at very high speeds inside the narrowing, thereby creating a channel wide enough for a balloon or stent to then be used.
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ANGIOGENESIS PDGF TGF- TNF- (+) (+) (-) VEGF (+)
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Regenerative medicine
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BMI > 30: >>> saturated fatty acids >>> salt and >>> sugar >>> alcohol <<< fruits and vegetables Smoking Lipid status Stress 2/3 of the risk Risk factors for CVD Chomocysteine > 15 mmol/l  Diabetes mellitus Metabolic syndrome Sedentary life style Tachycardia
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Никотинът е и ензимен индуктор.
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“The heart never stops. When it stops, it stops forever”. Leonardo da Vinci Modern medicine often disproves this saying.