Cardiovascular drugs are the most widely prescribed class of medications. They target hypertension, hyperlipidemia, heart failure, arrhythmias, and ischemic heart disease.

Prescription medication bottle for heart conditions — Cardiovascular drugs treat hypertension, heart failure, arrhythmias, and hyperlipidemia through diverse mechanisms. Source: Unsplash.

Antihypertensive Drugs

Hypertension affects 50% of adults over 45. The JNC 8 and ACC/AHA guidelines categorize four first-line antihypertensive classes.

Pills and capsules for cardiovascular medications — Antihypertensive drugs lower blood pressure through multiple mechanisms including ACE inhibition, angiotensin receptor blockade, calcium channel blockade, and diuresis. Source: Unsplash.

ACE Inhibitors and Angiotensin Receptor Blockers

ACE inhibitors (lisinopril, enalapril, ramipril, captopril) inhibit angiotensin-converting enzyme, reducing angiotensin II production and aldosterone secretion. ARBs (losartan, valsartan, irbesartan, olmesartan) block the angiotensin II AT1 receptor. Both classes lower blood pressure by vasodilation and reduced sodium and water retention. ACE inhibitors cause dry cough in 5-20% (due to bradykinin accumulation — ACE also degrades bradykinin). ARBs do not cause cough. Both classes can cause hyperkalemia and acute kidney injury in patients with renal artery stenosis, bilateral renal artery stenosis, or volume depletion. Angioedema is a rare but serious side effect (0.1-0.7%). ACE inhibitors and ARBs are teratogenic (contraindicated in pregnancy). They are first-line for hypertension in patients with CKD (proteinuria), heart failure, diabetes, and post-MI.

Calcium Channel Blockers

CCBs are divided into two subclasses. Dihydropyridines (amlodipine, nifedipine, felodipine) are primarily vasodilators — side effects include peripheral edema (5-15%, dose-dependent), headache, flushing, and gingival hyperplasia. Non-dihydropyridines (verapamil, diltiazem) have negative chronotropic and inotropic effects — they slow heart rate, reduce AV conduction, and are used for rate control in atrial fibrillation. Non-dihydropyridines should be avoided in heart failure with reduced ejection fraction and combined with beta-blockers only with caution (risk of heart block and bradycardia). All CCBs are metabolized by CYP3A4 and are subject to interactions (grapefruit juice increases levels).

Diuretics

Thiazide diuretics (hydrochlorothiazide, chlorthalidone) are first-line for hypertension (especially in African American patients). They inhibit the Na-Cl cotransporter in the distal convoluted tubule. Chlorthalidone is preferred over HCTZ in most guidelines due to longer duration and stronger evidence for cardiovascular event reduction. Side effects include hypokalemia, hyponatremia, hyperuricemia (gout), hyperglycemia, hypercalcemia, and dyslipidemia. Loop diuretics (furosemide, torsemide, bumetanide) are used for hypertension with CKD (GFR under 30 mL/min), volume overload (heart failure, cirrhosis), and edema. Potassium-sparing diuretics (spironolactone, eplerenone, amiloride) are used as add-on therapy for resistant hypertension and in heart failure (spironolactone and eplerenone reduce mortality in HFrEF).

Beta-Blockers

Beta-blockers are no longer considered first-line for uncomplicated hypertension (unless the patient has specific indications: CAD, prior MI, heart failure, atrial fibrillation, or migraines). Cardioselective beta-1 blockers (metoprolol, atenolol, bisoprolol) primarily affect the heart. Non-selective beta-blockers (propranolol, carvedilol, labetalol) block both beta-1 and beta-2 receptors. Carvedilol and nebivolol also have vasodilating properties. Side effects include bradycardia, fatigue, depression, sleep disturbances (especially lipophilic beta-blockers like propranolol and metoprolol), bronchospasm (in asthma/COPD — cardioselective agents are safer but not risk-free), masking of hypoglycemia symptoms, erectile dysfunction, and cold extremities.

Antiarrhythmic Drugs

The Vaughan Williams classification groups antiarrhythmics by mechanism. Class I (sodium channel blockers) includes Ia (quinidine, procainamide, disopyramide) — moderate Na+ block, prolong repolarization; Ib (lidocaine, mexiletine) — weak Na+ block, shorten repolarization; Ic (flecainide, propafenone) — strong Na+ block, minimal effect on repolarization. Class I drugs are used for various supraventricular and ventricular arrhythmias — the Cardiac Arrhythmia Suppression Trial (CAST) demonstrated increased mortality with Ic agents (flecainide, encainide) in post-MI patients, limiting their use. Class II (beta-blockers) are used for rate control in atrial fibrillation and prevention of SCD post-MI. Class III (potassium channel blockers) — amiodarone, sotalol, dofetilide, ibutilide — prolong repolarization. Amiodarone is the most effective antiarrhythmic but has significant extracardiac toxicity: pulmonary fibrosis (1-10%), thyroid dysfunction (15-20%), corneal deposits (90%+ with chronic use), hepatitis, photosensitivity, and peripheral neuropathy. Sotalol has beta-blocking properties and carries risk of torsades de pointes. Class IV (calcium channel blockers — verapamil, diltiazem) are used for rate control in atrial fibrillation.

⚠ Caution

Amiodarone accumulates extensively in tissues (Vd ~5,000 L, half-life 40-60 days). Because of its high iodine content (37% by weight) and long half-life, toxicity can develop months to years after starting therapy and may persist for months after discontinuation. Required baseline tests: chest X-ray, PFTs (DLCO), LFTs, TSH, and eye exam. Follow-up monitoring: chest X-ray and PFTs annually (or sooner if symptoms — cough, dyspnea), LFTs every 6 months, TSH every 6 months, and eye exam annually. Amiodarone should be used at the lowest effective dose (typically 100-200 mg/day for maintenance). The risk of pulmonary toxicity increases with cumulative dose, age over 60, pre-existing lung disease, and recent pulmonary procedures. Any new cough or dyspnea in a patient on amiodarone requires prompt evaluation. Amiodarone also inhibits CYP2C9 (increases warfarin levels) and inhibits digoxin clearance.

Lipid-Lowering Agents

Statins (HMG-CoA reductase inhibitors) are the cornerstone of lipid management. They inhibit the rate-limiting enzyme in cholesterol synthesis, reducing LDL cholesterol by 30-55% depending on potency and dose. Atorvastatin 10-80 mg and rosuvastatin 5-40 mg are high-potency statins. Simvastatin 20-40 mg and pravastatin 40-80 mg are moderate-potency. Side effects include myalgia (5-10%), transaminase elevation (1-3%), and rarely rhabdomyolysis (0.1%). Statins reduce cardiovascular events in both primary prevention (20-25% relative risk reduction per mmol/L LDL reduction) and secondary prevention (20-30% RRR). Ezetimibe inhibits intestinal cholesterol absorption, lowering LDL by 15-20% as monotherapy or 20-25% added to a statin. PCSK9 inhibitors (evolocumab, alirocumab) are monoclonal antibodies that increase LDL receptor recycling, lowering LDL by 50-60%. They are reserved for patients with heterozygous familial hypercholesterolemia, clinical ASCVD not at LDL goal on maximally tolerated statin + ezetimibe, or statin intolerance.

Heart Failure Medications

Guideline-directed medical therapy for heart failure with reduced ejection fraction includes four pillars: beta-blocker (bisoprolol, carvedilol, metoprolol succinate), ACE inhibitor or ARB (with ARNI — sacubitril/valsartan — preferred in NYHA II-III), aldosterone antagonist (spironolactone, eplerenone), and SGLT2 inhibitor (dapagliflozin, empagliflozin). Diuretics (loop diuretics) are used for symptom control (volume overload) but do not improve survival. Digoxin is used for rate control in atrial fibrillation and as an add-on in HFrEF — it reduces hospitalizations but does not improve survival. The combination of hydralazine plus isosorbide dinitrate is used as an alternative or addition to renin-angiotensin system inhibition, with particular benefit in African American patients.

Summary

Cardiovascular drugs include antihypertensives (ACE inhibitors/ARBs, CCBs, diuretics, beta-blockers), antiarrhythmics (sodium channel blockers, beta-blockers, potassium channel blockers, CCBs), lipid-lowering agents (statins, ezetimibe, PCSK9 inhibitors), and heart failure medications (beta-blockers, RAS inhibitors, aldosterone antagonists, SGLT2 inhibitors). Statins are the most effective class for reducing cardiovascular events. Amiodarone is effective but requires careful toxicity monitoring. Heart failure therapy targets four neurohormonal pathways.