Cardiovascular system drugs
Antihypertensive drugs
Alpha-2 agonists
Angiotensin converting enzyme inhibitors (ACEIs)
Generic "-pril"
Angiotensin II receptor blockers (ARBs)
Generic "-sartan"
Calcium channel blockers (CCBs)
Beta blockers
Generic "-olol"
Alpha blockers
Generic "-osin"
Diuretics (water pills)
Direct vasodilators
Mechanism: Inhibit conversion from angiotensin I to angiotensin II. Reduce peripheral vessel resistance without causing reflex tachycardia.
Prescribe: High blood pressure, hear failure.
Side effect: Dry cough, hyperkalemia, angioedema, kidney disfunction.
Renin-Angiotensin-Aldosterone System (RAAS)
Renin
Function: initiate RAAS response when blood pressure dropped or reduced blood flow to kidneys
Action: converts angiotensinogen to angiotensin I
Angiotensin
Angiotensin I (Ang I) inactive precursor form
Angiotensin II (Ang II)
Function: active form of the angiotensin peptide
Action
Vasoconstriction
Stimulation of Aldosterone Release
Thirst and Antidiuretic Hormone (ADH) Release
Stimulation of Sodium Reabsorption
Promotion of Cardiac Hypertrophy
Aldosterone
Function: a hormone produced by the adrenal glands
Action: promote sodium reabsorption and potassium excretion
Captopril, enalapril, lisinopril, fosinopril, ramipril
Mechanism: Block effect of angiotensin II type 1 (AT1) receptors. Reduce peripheral vessel resistance without causing reflex tachycardia.
Prescribe: High blood pressure, hear failure.
Side effect: Mild effect like dizziness, fatigue, headache, hyperkalemia (rare).
Telmisartan, losartan, valsartan, candesartan, irbesartan.
Mechanism: Stimulate alpha-2 adrenergic receptors and reduce sympathetic nervous system activity.
Prescribe: High blood pressure, attention deficit hyperactivity disorder (ADHD).
Side effect: Drowsiness, depression, lethargy.
Clonidine, guanfacine, methyldopa.
Mechanism: Known as alpha-adrenergic antagonists as blocking alpha receptors' action. Have selective and non-selective but selective targets to blood vessels.
Prescribe: High blood pressure, BPH.
Side effect: Dizziness, fatigue, headache.
Doxazosin, terazosin, tamsulosin*.
Mechanism: Block effect of adrenaline (epinephrine) and norepinephrine on beta adrenergic receptors to reduce force of heart contraction. Have selective and non-selective.
Prescribe: High blood pressure, arrhythmias
Side effect: Dizziness, fatigue, bradycardia, hypotension, bronchoconstriction (non-selective), masking of hypoglycemia symptom in diabetics.
Selective (cardioselective): Metoprolol, atenolol, esmolol, bisoprolol, carvedilol.
Non-selective: propranolol, nadolol, timolol, acebutolol, nebivolol.
Mechanism: Block calcium ion Ca2+ into cells of heart and blood vessels to reduce contraction of smooth muscle such as heart, blood vessel wall and cardiac muscle cell.
Prescribe: High blood pressure, tachycardia, arrhythmias.
Side effect: Dizziness, flushing, headache; peripheral edema (dihydropyridines); constipation, bradycardia (non-dihydropyridines). Cannot use to patients with atrioventricular (AV) blocks by left ventricular failure.
Dihydropyridines: Amlodipine, nifedipine, felodipine, nicardipine.
Non-dihydropyridines: Verapamil, diltiazem.
Mechanism: Work directly on peripheral blood vessels without affecting autonomic nervous system activity on blood vessels.
Prescribe: High blood pressure, heart failure, angina*
Side effect: Tachycardia, headache, edema, hypotension, lupus like syndrome (hydralazine). Patients with coronary artery disease will be increase risk of coronary stealth phenomenon and myocardial infarction. Should not use nitroglycerin concomitantly with phosphodiesterase 5 inhibitors like sildenafil (Viagra) as increase risk of hypotension, myocardial infarction.*
Hydralazine (combine with nitrates), minoxidil.
Nitrates: nitroglycerin, isosorbide dinitrate, isosorbide mononitrate, sodium nitroprusside.
Mechanism: Promote diuresis, increase urine production then lead to reduce plasma volume and preload.
Potassium wasting: Thiazide diuretics, Loop diuretics work by block re-absorption of sodium, chloride and potassium.*
Potassium sparing diuretics work by blocking hormone aldosterone (aldosterone antagonists).
Prescribe: High blood pressure, heart failure, kidney disorder, edema.
Side effect: Hypokalemia (potassium wasting), hyperglycemia (thiazide), hyperuricemia (hydrochlorothiazide), ototoxicity (furosemide), hyperkalemia (potassium sparing), gynecomastia* (spironolactone), nausea, GIT disturbance.
Thiazide diuretics: Hydrochlorothiazide (HCTZ), chlorothiazide, chlorthalidone, hydroflumethiazide, indapamide (longer-acting), metolazone.
Loop diuretics: Furosemide, torsemide, bumetanide.
Potassium sparing diuretics: Amiloride, spironolactone, triamterence*.
Antiarrhythmics
Class I - Sodium channel blockers
Class II - Beta blockers #
Class III - Potassium blockers
Class IV - Calcium channel blockers: Non-dihydropyridines #
Class V - Others
Mechanism: Block sodium ion into cells of heart to reduce rate of depolarization, conduction velocity and repolarization. Increase refractory period. Stabilize abnormal rhythms.
Prescribe: Ventricular arrhythmias, atrial fibrillation/flutter in short-term.
Side effect: Constipation, dry mouth, proarrhythmia, nausea, dizziness, cardio toxicity, arterial embolism.
Class Ia: Quinidine, procainamide, disopyramide.
Class Ib: Lidocaine, mexiletine.
Class Ic: Flecainide, encainide.
Ranolazine.
Mechanism: Block potassium channel in-out cardiac muscle cells. Prolong action potential duration. Recue AV and SA node conduction. Increase refractory period. Stabilize heart electrical activity.
Prescribe: Ventricular arrhythmias, atrial fibrillation/flutter.
Side effect: Bradycardia, heart block, photosensitivity, constipation, photodermatitis, blue skin syndrome (amiodarone), dizziness, hepatotoxicity.
Amiodarone, sotalol, dofetilide, dronedarone.
Digoxin
Adenosine
Magnesium
Mechanism: Cardiac glycoside that inhibit sodium-potassium (Na+/K+) pump in cardiac cells that lead to increase calcium level in intracellular. Enhance myocardial contractility and slow down electrical conduction of AV node.
Prescribe: Atrial fibrillation/flutter, hear failure.
Mechanism: A natural occurring nucleoside act as potent vasodilator and slow down hear electrical conduction through AV node that interrupting pathway of tachycardia.
Prescribe: Supraventricular tachycardia.
Mechanism: Stabilize cell membranes and inhibit calcium influx into cardiac cells. Also modulating potassium channel and Na+/K+ pump activity.
Prescribe: Arrhythmias, hypomagnesemia, Torsades de Pointes, prolong QT interval.
Antiplatelets
COX-1 inhibitors
Adenosine diphosphate (ADP) receptor inhibitors
Glycoprotein IIb/IIIa inhibitors
Thromboxane inhibitors
Thrombolytics
Streptokinase
Recombinant tissue plasminogen activators (rtPA)
Anticoagulants
Vitamin K antagonists - Warfarin
Heparin
Factor IIa/Xa inhibitors
Mechanism: Irreversibly inhibit COX-1 enzyme which produce TXA2 that promote platelet aggregation and vasoconstriction.
Prescribe: Myocardial infarction, stroke. Also used to relive pain, fever, inflammation.
Side effect: GI irritation, bleeding, flatulence, diarrhea, tinnitus, blurred vision.
Aspirin (ASA), triflusal, salsalate.
Mechanism: Irreversibly inhibit P2Y12 receptors on platelets that play an important role of platelet activation and aggregation.
Prescribe: High risk of blood clot formation like after stent placement, myocardial infarction, stroke, peripheral artery disease (PAD).
Side effect: Bleeding, GI irritation, rashes, neutropenia (ticlopidine) - decrease of white blood cells.
Clopidogrel, prasugrel, ticlopidine, ticagrelor, tragrelor.
Mechanism: Bind to glycoprotein IIb/IIIa (GP IIb/IIIa) on platelet surface and prevent the binding of fibrinogen (I) that promote platelet aggregation and turn to fibrin (Ia).
Prescribe: High risk of blood clot formation like coronary angioplasty (balloon) and stent (wire mesh tube) placement, acute coronary syndrome.
Side effect: Bleeding, bradycardia, hypotension
Reversible biding: Abciximab, eptifibatide.
Irreversible binding: Tirofiban.
Mechanism: Prevent action of thromboxane synthase and block TXA2 receptors on platelet. Reduce platelet activation and aggregation.
Prescribe: After stent placement, myocardial infarction, stroke.
Side effect: Bleeding, GI irritation, rash, hypotension.
Ifetroban: thromboxane receptor antagonist.
Dipyridamol: Phosphodiesterace inhibitor with antiplatelet properties due to its effect on cAMP levels and indirectly influence TXA2.
Picotamide: dual antiplatelet agent that inhibit both TXA2 synthesis and ADP-mediated platelet activation pathway.
Mechanism: Bacterial enzyme binds to plasminogen and convert it to active plasmin that responsible for breaking down fibrin fibrinogen in blood clots. Dissolving the blood clot within blood vessels.
Prescribe: Myocardial infarction, stroke, pulmonary embolism, deep vein thrombosis.
Side effect: Bleeding, hypotensive, rashes, flushing.
Mechanism: Tissue plasminogen activators (tPA) are natural enzyme facilitate conversion from plasminogen to plasmin that responsible for breaking down fibrin in blood clots. Recombinant tissue plasminogen activators (rtPA) are synthetic version. Dissolving the blood clot within blood vessels.
Prescribe: Myocardial infarction, stroke, pulmonary embolism, deep vein thrombosis, arterial thrombosis.
Side effect: Bleeding, shock sepsis.
Alteplase, reteplase, tenecteplase.
Mechanism: Inhibit the synthesis of vitamin K that essential for production of clotting factors (II, VII, IX, X) in the liver.
Prescribe: For long-term maintenance therapy to treat high risk of thrombosis include atrial fibrillation/flutter, deep vein thrombosis, pulmonary embolism.
Side effect: Bleeding, manifest as intracranial hemorrhage (bleeding in skull) and hemorrhagic stroke (bleeding in brain).
Require regular monitoring by International Normalized Ratio (INR) test.
Manage with dietary if contain high Vitamin K.
Mechanism: Bind to and hasten function of antithrombin III, a natural anticoagulant protein in blood that inhibit action of clotting factors (IIa - thrombin, IXa, Xa).
Prescribe: Treat high risk of thrombosis include deep vein thrombosis, pulmonary embolism, intravenous catheter maintenance.
Side effect: Bleeding, GI irritation, osteoporosis (bone loss), flatulence.
Patients required monitoring such as activated partial thromboplastin (aPTT) or anti-factor Xa activity.
Mechanism: Inhibit factors Xa or IIa - thrombin in the coagulant cascade.
Prescribe: Treat high risk of thrombosis include atrial fibrillation/flutter, deep vein thrombosis, pulmonary embolism.
Side effect: Bleeding, GI irritation.
Mild side effect than warfarin or heparin.
Not effect by diet and do not require INR blood test.
Xa inhibitors: Oral administration: Apixaban, betrixaban, rivaroxaban ;
Subcutaneous: Fondaparinux
IIa inhibitors: Oral administration: Dabigatran;
Intravenous: Argatroban, lepitrudin.
Cholesterol medications
HMG-CoA reductase inhibitors "-statin"
Ezetimibe
PCSK9 inhibitors
ACL inhibitors
Bile acid sequestrants
Fibrates
Niacin
Omega-3-fatty acid
Mechanism: Inhibit enzyme HMG-CoA reductase in liver to reduce production of cholesterol.
Prescribe: Treat hypercholesterolemia, prevent cardiovascular disease, manage post cardiovascular event.
Side effect: Muscle pain, myopathy, GI irritation, diarrhea, constipation, increase blood sugar level, elevation of liver enzyme.
Rare serious side effect include: rhabdomyolysis (muscle breakdown) lead to kidney failure, liver toxicity.
Atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin.
Mechanism: Block action of protein NPC1L1 to inhibit the absorption of cholesterol in the small intestine.
Prescribe: Treat hypercholesterolemia, combine with other cholesterol medications.
Side effect: GI irritation, muscle soreness, fatigue, flatulence.
Mechanism: Bind to and block action of PCSK9 proprotein on LDL receptors in liver's surface. PCSK9 promote the degradation of LDL receptors and lead to reduce of LDL clearance from plasma.
Prescribe: Treat hypercholesterolemia, prevent myocardial infarction, stroke.
Side effect: Itchy, swelling, pain, bruising at injection site, back pain, flu-like symptoms.
Alirocumab, evolocumab.
Mechanism: Block action of ACL enzyme. ACL enzyme involve in conversion from citrate to acetyl-CoA.
Prescribe: Treat hypercholesterolemia.
Side effect: Cold-like/flu-like symptoms, muscle spasm, GI irritation, high level of uric acid in blood that can lead to gout, anemia.
Bempedoic acid.
Mechanism: Form insoluble complexes with bile acid in the intestines to reduce fat dietary digestion. The insoluble complexes will be excreted into feces lead to decrease of body's bile acid pool, therefore liver need to use cholesterol to produce new bile acid. The LDL level in blood stream also be reduced.
Prescribe: Treat hypercholesterolemia.
Side effect: GI irritation, constipation, heartburn, deficiencies of fat soluble vitamins include A, D, E, K.
Cholestyramine, colestipol, coleseverlam.
Mechanism: Reduce production of triglyceride in the liver. Increase clearance of triglyceride-rich lipoprotein. Mild LDL lowering.
Prescribe: Treat dyslipidemia.
Side effect: GI irritation, runny nose, back pain, headache, muscle injury lead to kidney injury, kidney disfunction, abnormal laboratory test of liver function.
Gemfibrozil, fenofibrate, fenofibric acid.
Mechanism: Known as vitamin B3 or nicotinic acid that increase HDL level, lower LDL and triglyceride levels.
Prescribe: Treat dyslipidemia.
Side effect: Flushing, GI irritation, rashes, elevated of blood sugar level, liver enzyme abnormalities.
Mechanism: Particularly EPA, DHA. Reduce production of triglyceride in the liver. Increase clearance of triglyceride-rich lipoprotein. Have antiplatelet effect that cardiovascular benefit.
Side effect: Burping, joint or muscle pain, constipation, upset stomach, bleeding.
Prescribe: Treat hypercholesterolemia.
Omega-3-acid ethyl ester, icosapent ethyl.
Side effect: CNS and GI toxicities, anorexia (loss appetite), visual disturbance.
Enoxaparin