Medical treatment of Acute Coronary Syndrome

Cardiovascular and circulatory diseases are yet the prominent causes of death in the world, responsible for more than 54 million deaths in 2013. The spectrum of ACS includes ST-segment elevation myocardial infarction (STEMI), and the non–ST elevation acute coronary syndromes (NSTE-ACS), which consist of non–ST elevation myocardial infarction (NSTEMI), and unstable angina (UA). Nearly all acute coronary syndromes result from coronary atherosclerosis, commonly with superimposed coronary thrombosis caused by rupture or erosion of an atherosclerotic lesion. Coagulation cascade and platelets activation play major roles in the formation of thrombus after plaque disruption.Therefore, basic pharmacologic treatment of acute coronary syndrome consists of anti- ischemic, antiplatelet and anticoagulant drugs. Anti-ischemics include Nitrates, Beta blockers, Morphine and Calcium Channel Blockers. Antiplatelets include ASA and Clopidogrel; and Anticoagulants include Unfractionated Heparin and Low Molecular Weight Heparins (LMWH).Nitrates are endothelium-independent vasodilators with peripheral and coronary vascular effects. By dilating the capacitance vessels, nitrates decrease cardiac preload and reduce ventricular wall tension.Beta blockers reduce heart rate, contractility, and BP, resulting in decreased MVO2.Morphine Sulfate has strong analgesic and anxiolytic effects, as well as hemodynamic actions, that are possibly beneficial in ACS. It causes venodilation and produces modest reductions in heart rate (through increased vagal tone) and systolic BP.Calcium channel blockers (CCBs) have vasodilatory effects and reduce arterial pressure.Aspirin (acetylsalicylic acid) irreversibly inactivates the cyclooxygenase activity of platelet prostaglandin Endoperoxide (PGH) synthase 1 (COX-1), thereby suppressing thromboxane A2 production throughout the platelet lifespan.Clopidogrel Irreversibly blocks ADP binding to the surface of the platelet P2Y12 receptor.Unfractionated Heparin is a combination of polysaccharide chains of various lengths that prevent coagulation by blocking thrombin (factor IIa) and factor Xa.LMWH has several advantages over UFH: (1) Greater anti–factor Xa activity (relative to factor IIa) that inhibits thrombin generation more efficiently; (2) Greater release of tissue factor pathway inhibitor than UFH, which is not neutralized by platelet factor 4; (3) Causing HIT less frequently; (4) High bioavailability of LMWH allows subcutaneous (SC) administration; (5) monitoring of the anticoagulation level is not necessary; and (6) less binding to plasma proteins than UFH and therefore and a more consistent anticoagulant effect.