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Classification of Cardiovascular Drugs

Cardiovascular drugs are grouped by their primary therapeutic use and mechanism of action. The major classes are outlined below.

1. Antihypertensive Drugs

These are the largest and most clinically used group. They are sub-classified by mechanism:
SubclassMechanismExamples
Thiazide diureticsInhibit NaCl reabsorption in distal tubuleHydrochlorothiazide, Chlorthalidone
Loop diureticsBlock Na-K-2Cl cotransporter in loop of HenleFurosemide, Bumetanide
Potassium-sparing diureticsAntagonize aldosterone or block ENaCSpironolactone, Amiloride
ACE inhibitors (ACEi)Block angiotensin-converting enzymeEnalapril, Lisinopril, Captopril
Angiotensin receptor blockers (ARBs)Block AT1 receptorLosartan, Valsartan
Beta-blockers (β-blockers)Block β-adrenergic receptorsMetoprolol, Atenolol, Carvedilol
Calcium channel blockers (CCBs)Block L-type Ca²⁺ channelsAmlodipine, Nifedipine, Verapamil, Diltiazem
Alpha-1 blockersBlock α1 receptors on vascular smooth musclePrazosin, Doxazosin
Central alpha-2 agonistsReduce sympathetic outflow centrallyClonidine, Methyldopa
Direct vasodilatorsDirectly relax vascular smooth muscleHydralazine, Minoxidil
Neprilysin inhibitors (ARNi)Block angiotensin + neprilysinSacubitril/Valsartan
From Katzung's Basic and Clinical Pharmacology, 16th Edition and Goodman & Gilman's Pharmacological Basis of Therapeutics

2. Antiarrhythmic Drugs (Vaughan-Williams Classification)

The Vaughan-Williams scheme classifies antiarrhythmic drugs (AADs) by their predominant effect on the cardiac action potential. Note that many agents have overlapping actions across classes - this is an important limitation of the classification.
ClassMechanismExamplesKey Adverse Effects
IANa⁺ channel block (intermediate kinetics) - slows Phase 0, prolongs repolarizationQuinidine, Procainamide, DisopyramideQT prolongation, torsades de pointes, lupus-like syndrome (procainamide), cinchonism (quinidine)
IBNa⁺ channel block (rapid kinetics) - shortens Phase 3 repolarizationLidocaine, MexiletineSeizures, CNS toxicity, tremor, ataxia
ICNa⁺ channel block (slow kinetics, high potency) - markedly slows Phase 0Flecainide, PropafenoneBradycardia, proarrhythmia, bronchospasm (propafenone)
IIβ-adrenergic receptor blockade - inhibits Phase 4 spontaneous depolarizationMetoprolol, Atenolol, EsmololBradycardia, heart block, bronchospasm, fatigue
IIIK⁺ channel block - prolongs action potential duration and refractory periodAmiodarone, Sotalol, Dofetilide, IbutilideQT prolongation, torsades; amiodarone: multiorgan toxicity (pulmonary, thyroid, hepatic)
IVCa²⁺ channel block (non-dihydropyridines) - slows SA/AV nodal conductionVerapamil, DiltiazemBradycardia, AV block, constipation
OthersMultiple/miscellaneous mechanismsAdenosine, Digoxin, RanolazineAdenosine: transient asystole; Digoxin: arrhythmias, GI toxicity
Note: Amiodarone has actions across all four classes (I, II, III, IV), which makes it uniquely effective but also uniquely toxic. - Harrison's Principles of Internal Medicine, 22nd Edition

3. Drugs for Heart Failure

Drug ClassExamplesMechanism
ACE inhibitors / ARBs / ARNiLisinopril, Valsartan, Sacubitril-ValsartanReduce preload and afterload, reverse remodeling
Beta-blockersCarvedilol, Metoprolol succinate, BisoprololReduce sympathetic stimulation, reverse remodeling
DiureticsFurosemide, SpironolactoneReduce volume overload
SGLT2 inhibitorsEmpagliflozin, DapagliflozinNatriuresis, anti-fibrotic, metabolic benefits
Cardiac glycosides (positive inotropes)DigoxinInhibit Na⁺/K⁺-ATPase → increased intracellular Ca²⁺ → stronger contraction; also slows AV conduction
Other inotropesDobutamine, Milrinone, LevosimendanUsed in acute decompensated heart failure
Hydralazine + NitratesHydralazine + Isosorbide dinitrateAlternative vasodilator combo (especially in African Americans)
Katzung's Basic and Clinical Pharmacology, 16th Edition

4. Antianginal Drugs

ClassExamplesMechanism
NitratesNitroglycerin, Isosorbide mononitrateDonate NO → venodilation → reduce preload; also dilate coronary arteries
Beta-blockersMetoprolol, AtenololReduce heart rate and oxygen demand
Calcium channel blockersAmlodipine, Verapamil, DiltiazemReduce coronary vasospasm, reduce afterload
RanolazineRanolazineBlocks late Na⁺ current → reduces intracellular Ca²⁺ overload

5. Lipid-Lowering Drugs (Antidyslipidemics)

ClassExamplesMechanism
Statins (HMG-CoA reductase inhibitors)Atorvastatin, Rosuvastatin, SimvastatinReduce hepatic cholesterol synthesis → upregulate LDL receptors
EzetimibeEzetimibeBlocks intestinal cholesterol absorption (NPC1L1 inhibitor)
PCSK9 inhibitorsAlirocumab, EvolocumabPrevent LDL receptor degradation → increase LDL clearance
FibratesFenofibrate, GemfibrozilActivate PPARα → reduce triglycerides, increase HDL
Bile acid sequestrantsCholestyramine, ColesevelamBind bile acids → force hepatic use of cholesterol to make new bile
Nicotinic acid (Niacin)NiacinReduces VLDL synthesis; raises HDL (less used now due to side effect profile)

6. Anticoagulant / Antiplatelet / Thrombolytic Drugs

ClassExamplesMechanism
AntiplateletsAspirin, Clopidogrel, Ticagrelor, AbciximabBlock platelet aggregation via COX-1, ADP receptors (P2Y12), or GP IIb/IIIa
HeparinsUnfractionated heparin, EnoxaparinActivate antithrombin III → inhibit thrombin and Factor Xa
Vitamin K antagonistsWarfarinInhibit factors II, VII, IX, X (vitamin K-dependent)
Direct oral anticoagulants (DOACs)Rivaroxaban, Apixaban (anti-Xa); Dabigatran (anti-IIa)Direct inhibition of specific clotting factors
ThrombolyticsAlteplase (tPA), StreptokinaseConvert plasminogen to plasmin → lyse clots

Summary Overview

CARDIOVASCULAR DRUGS
├── 1. Antihypertensives (diuretics, ACEi, ARBs, CCBs, beta-blockers, vasodilators)
├── 2. Antiarrhythmics (Vaughan-Williams Class I-IV + others)
├── 3. Heart Failure drugs (ACEi/ARB/ARNi, beta-blockers, diuretics, SGLT2i, inotropes)
├── 4. Antianginals (nitrates, beta-blockers, CCBs, ranolazine)
├── 5. Lipid-lowering agents (statins, PCSK9i, fibrates, ezetimibe)
└── 6. Antithrombotic agents (antiplatelets, anticoagulants, thrombolytics)

Sources: Lippincott Illustrated Reviews: Pharmacology | Harrison's Principles of Internal Medicine, 22nd Ed. | Katzung's Basic and Clinical Pharmacology, 16th Ed. | Goodman & Gilman's Pharmacological Basis of Therapeutics
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