Table 3.

Overview of medications used for CAD.

Class	Indications	Mechanism	Drugs
Beta-adrenoceptor antagonists [28]	arrhythmia, hypertension, post-MI, angina pectoris, CAD	Act through the blockade of beta-adrenoceptors in cardiac muscle cells and vascular SMCs. Lead to decreased heart rate and cardiac output (CO). Secondarily, antagonism of β1-adrenoceptors will cause relaxation of vascular smooth muscle cells, induce vasodilation and lower total periphery resistance (TPR).	Metoprolol Propranolol Carvedilol Atenolol Nebivolol
Acetylsalicylic acid (ASA) [29]	acute MI, CAD, prevent re-thrombosis	Irreversible inactivation of cyclooxygenase (COX-1, -2) enzymes. This inhibition promotes a blockade of thromboxane synthesis, which decreases platelet activation.	Aspirin
Statins [30,31]	hyperlipidemia, dyslipidemia, post-MI	Inhibition of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase enzyme (HMG-CoA reductase), which catalyzes the transformation of HMG to mevalonic acid, thereby reducing intracellular cholesterol concentrations, which leads to the upregulation of LDL surface receptors. Eventually, plasma concentrations of LDL and total cholesterol fall with statin treatment.	Simvastatin Rosuvastatin Atorvastatin Pravastatin
Nitrates [32,33]	angina pectoris, CAD	Promote the release of nitric oxide (NO) in smooth muscle cells in blood vessels. High intracellular NO concentrations activate guanylyl cyclase (GC). Eventually, this results in decreased intracellular calcium concentrations. This causes dilatation of the coronary arteries, afterload reduction and increased angina threshold.	Glyceryl nitrate Isosorbide dinitrate Isosorbide mononitrate
Angiotensin-converting enzyme inhibitors (ACE-inhibitors) [34,35]	hypertension, LV heart failure (HF), heart failure post- MI, angina pectoris	The enzyme ACE hydrolyzes angiotensin I to the active form angiotensin II (Ang II). Effects carried out by Ang II are decreased by the inhibition of ACE. This promotes vasoconstriction, upregulation of aldosterone secretion in the kidneys and fibrosis in cardiac cells, resulting in vasodilation, reduced TPR and reduced preload and afterload.	Enalapril Captopril Ramipril Trandolapril
Calcium channel blockers [36]	hypertension, angina pectoris	Calcium channel blockers act through the blockade of L-type Ca2+ channels in vascular smooth muscle cells. The inhibition of voltage-gated calcium channels results in the decreased release of Ca2+ into the cytoplasm. This causes vasodilatation and a fall in TPR and blood pressure. Moreover, non-dihydropyridine derivatives (such as diltiazem and verapamil) have a direct effect on cardiac muscle cells. This leads to subsequent negative inotropy and negative chronotropy.	Diltiazem Verapamil Felodipin Amlodipin Lercadipin
Anti-anginal [37]	chronic angina pectoris	Acts through the inhibition of late influx sodium channels (INa) in cardiomyocytes. Thus, calcium overload is attenuated by reduced sodium/calcium exchange in cardiac myocytes. Subsequently, the oxygen demand is reduced and cardiac output improves.	Ranolazine
Anti-platelet medications [38]	MI, stroke, UAP, stent patients	The mechanism of action is carried out via the blockade of the Gi-protein coupled P2Y12 receptor. This causes inhibition of the intracellular PI3K pathway and diminished platelet activation and aggregation.	Clopidogrel Ticagrelor Prasugrel