Cardiovascular/Non-dihydropyridine CCB

Non-dihydropyridine CCBs

also: rate-limiting CCB · verapamil · diltiazem

Overview

Rate-limiting calcium-channel blockers — act on cardiac conduction as well as vessels. Used for rate control and angina, NOT routine first-line hypertension.

Mechanism

Block L-type Ca²⁺ channels in cardiac myocytes and the SA/AV node → negative chronotropy, negative dromotropy (slows AV conduction) and negative inotropy, plus vasodilation. Class IV antiarrhythmic (Vaughan-Williams).

Indications

AF / SVT rate control
Stable angina
Hypertension (when β-blocker unsuitable)

The agents

Verapamilmost cardioselective

CYP3A4

Strongest AV-node effect + negative inotrope; marked constipation.

Diltiazemintermediate

CYP3A4

Balanced rate + vasodilator; better tolerated than verapamil.

Adverse effects

Bradycardia / heart blockserious

Constipationclassic

Verapamil especially.

Worsening heart failureserious

Negative inotropy.

Ankle oedemacommon

Cautions & contraindications

Concurrent beta-blockerall

Additive AV-node suppression → severe bradycardia, asystole. Verapamil + β-blocker is the classic dangerous combination.

2nd/3rd-degree heart blockall

Heart failure with reduced EF (HFrEF)all

Negative inotropy worsens it.

AF with WPW / pre-excitationall

AV-node block promotes conduction down the accessory pathway → VF.

Interactions

Verapamil + β-blocker → bradycardia/asystole (avoid)
CYP3A4 inhibitor — raises simvastatin, digoxin, ciclosporin levels

Monitoring & kinetics

Heart rate, ECG (PR interval),BP

Oral / IV. Hepatic CYP3A4. IV verapamil never with a β-blocker.

Source: BNF — Calcium-channel blockers