Cardizem (Diltiazem) 30–360 mg Tablets and Extended-Release Capsules: Prescription Non-Dihydropyridine Calcium Channel Blocker for Hypertension, Angina, and Heart Rate Control in Atrial Fibrillation — Generic Available

Information last reviewed: May 2026 — for educational purposes only.

Diltiazem is a benzothiazepine-class non-dihydropyridine (non-DHP) calcium channel blocker available under the brand name Cardizem and several extended-release formulations including Cardizem CD, Cartia XT, and Dilacor XR. It is a prescription medication that reduces blood pressure by relaxing arterial smooth muscle and also exerts clinically significant effects on the heart's electrical conduction system.

Uses of Diltiazem

Diltiazem is used for hypertension, chronic stable angina, and vasospastic (Prinzmetal) angina. Importantly, it is also widely used for rate control in atrial fibrillation and atrial flutter, given its ability to slow conduction through the AV node. Its dual cardiovascular profile — antihypertensive and antiarrhythmic — makes it particularly useful in patients with both hypertension and supraventricular tachyarrhythmias.

Mechanism, Warnings, and Key Interactions

Diltiazem blocks L-type calcium channels in both vascular smooth muscle and cardiac tissue, producing negative chronotropy (heart rate reduction) and negative inotropy (reduced contractile force). Diltiazem must not be used in patients with heart failure with reduced ejection fraction (HFrEF) — its negative inotropic effect worsens outcomes in this population, unlike the dihydropyridine amlodipine which is safe in HF. It is also contraindicated in second- or third-degree AV block (without a functioning pacemaker) and should not be combined with beta-blockers due to additive risk of severe bradycardia and AV block. Diltiazem is a moderate CYP3A4 inhibitor, meaning it raises plasma levels of many co-administered drugs. Simvastatin must be limited to 10 mg per day when used with diltiazem to reduce myopathy risk. Common side effects include constipation, peripheral oedema, and headache.

Available Strengths and Formulations

Diltiazem IR tablets come in 30 mg, 60 mg, 90 mg, and 120 mg strengths, dosed four times daily. Extended-release capsules (Cardizem CD, Cartia XT, Dilacor XR) range from 120 mg to 360 mg and are taken once daily. SR (sustained-release) formulations of 60–120 mg are taken twice daily. The appropriate formulation depends on the indication — once-daily ER is preferred for hypertension and chronic angina management.

Pricing Overview

Generic diltiazem IR and ER formulations are widely available at low cost. Extended-release brands may carry higher prices. Patients requiring multiple daily dosing of IR formulations generally find the cost manageable, while the convenience of ER once-daily dosing is a significant adherence advantage. Contact Lucas Clinic for current pricing and product availability.

Frequently Asked Questions

Why can't diltiazem be used in heart failure with reduced ejection fraction?

Diltiazem reduces the heart's contractile force (negative inotropy) through its calcium channel blocking effect on cardiac muscle. In HFrEF, the heart is already struggling to pump effectively, and further reducing contractility can precipitate worsening heart failure, decompensation, and increased mortality. This contrasts with amlodipine, a dihydropyridine CCB that acts primarily on vascular smooth muscle and is considered safe in heart failure patients.

What is the significance of diltiazem's CYP3A4 inhibition?

Diltiazem moderately inhibits the CYP3A4 enzyme, which metabolises a large number of commonly prescribed drugs. This inhibition raises blood levels of co-administered CYP3A4 substrates, potentially causing toxicity. The most clinically important example is the statin simvastatin, which must be capped at 10 mg/day to avoid serious myopathy or rhabdomyolysis. Other affected drugs include certain immunosuppressants, benzodiazepines, and anticoagulants.

Can diltiazem be combined with a beta-blocker?

This combination is generally avoided due to the risk of additive bradycardia and AV conduction block. Both drug classes independently slow the heart rate and impair AV nodal conduction, and their effects are synergistic in a dangerous way. If combined inadvertently or out of necessity, close monitoring of heart rate and ECG is required. In most cases, an alternative strategy, such as switching to a dihydropyridine CCB, is preferred when a patient already takes a beta-blocker.

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