Calcium channel Blockers (FETT)

AMLODIPINE

Diltiazem

Verapamil

NIFEDIPINE

CCBs are classified into two major groups according to the main site of action: Dihydropyridines (e.g., nifedipine, amlodipine) are potent vasodilators, and nondihydropyridines (e.g., verapamil) are potent myocardial depressants.

• CCBs bind to and block L-type calcium channels in cardiac and vascular smooth muscle cells → decreased frequency of Ca2+ channel opening in response to cell membrane depolarization → decreased transmembrane Ca2+ current

• Vascular smooth muscle relaxation → vasodilation → decreased peripheral vascular resistance → decreased afterload → decreased blood pressure

• Decreased cardiac muscle contractility (negative inotropic action) → decreased cardiac output → decreased blood pressure

• Decreased SA node discharge rate (negative chronotropic action) → decreased heart rate (bradycardia) → decreased cardiac output → decreased blood pressure

• Decreased AV node conduction (negative dromotropic action) → termination of supraventricular arrhythmias

• Dihydropyridines act mainly on vascular smooth muscle. The order of potency is nifedipine/amlodipine followed by the nondihydropyridines verapamil and diltiazem.

• Nondihydropyridines act mainly on the heart. The order of potency is verapamil > diltiazem > amlodipine/nifedipine.

Dihydropyridine CCBs (nifedipine and amlodipine) primarily act on vascular smooth muscles. Nondihydropyridine CCBs (verapamil > diltiazem) primarily act on the heart.

Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.

• Arterial hypertension (esp. amlodipine )

• Stable angina: for patients with contraindications for beta blockers or who are not responsive to beta blockers

• Vasospastic angina (Prinzmetal angina)

• Achalasia

• Diffuse esophageal spasm

• Raynaud phenomenon (e.g., nifedipine, felodipine)

• Subarachnoid hemorrhage (e.g., nimodipine, nicardipine) to prevent secondary vasospasm

• Tocolysis

• Gestational hypertension

• Hypertensive urgency/hypertensive emergency (e.g., nicardipine, clevidipine)

• Thromboangiitis obliterans

• Supraventricular arrhythmias (verapamil and diltiazem )

  • Supraventricular tachycardia

  • Atrial fibrillation, atrial flutter

• Cardiomyopathy (hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy)

• Migraine

• Verapamil: cluster headache

• Effects due to vasodilation

  • Peripheral edema (esp. amlodipine)

  • Headaches, dizziness

  • Facial flushing, feeling of warmth

  • Reflex tachycardia: a condition of tachycardia secondary to a decrease in blood pressure (esp. nifedipine)

    • Vasodilation lowers the blood pressure, which stimulates baroreceptors of the sympathetic nervous system, resulting in reflex tachycardia. [7]

    • May worsen symptoms of angina

• Gingival hyperplasia

• Benzothiazepines: similar to those of the other CCB classes, but milder

• Phenylalkylamines

  • Reduced contractility

  • Bradycardia

  • AV block [8]

  • Gingival hyperplasia

  • Verapamil

    • Constipation

    • Hyperprolactinemia

• Allergy/hypersensitivity to CCBs

• Symptomatic hypotension [11]

• Acute coronary syndrome

• Hypertrophic obstructive cardiomyopathy (HOCM)

• Severe stenotic heart valve defects

• Preexisting cardiac conduction disorders

  • Wolff-Parkinson-White syndrome

  • Sick sinus syndrome

  • Systolic dysfunction (in congestive heart failure)

  • Bradycardia

  • 2° AV block/3° AV block

• Combination with beta blockers: risk of AV block, bradycardia, and/or decreased cardiac contractility