From the Guidelines
Calcium channel blockers prolong AV node repolarization in atrial fibrillation by blocking L-type calcium channels in the AV nodal tissue, which slows conduction and increases refractoriness. Medications like diltiazem (starting at 120-360 mg daily in divided doses) and verapamil (120-360 mg daily in divided doses) are commonly used for this purpose, as recommended by the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation 1. These non-dihydropyridine calcium channel blockers specifically target the AV node, reducing the number of atrial impulses that can be conducted to the ventricles, thereby controlling ventricular rate in atrial fibrillation. The mechanism involves inhibiting calcium influx during phase 2 of the cardiac action potential, which extends the effective refractory period of the AV node, as described in the 2006 ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation 1. This prolongation of repolarization means fewer atrial fibrillation impulses can pass through to the ventricles, resulting in better rate control. Some key points to consider when using calcium channel blockers for atrial fibrillation include:
- They should be used cautiously in patients with heart failure with reduced ejection fraction, hypotension, or significant bradycardia, as noted in the 2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy 1.
- Dose adjustments may be necessary in patients with hepatic or renal impairment.
- Side effects may include hypotension, bradycardia, heart failure exacerbation, and constipation.
- The choice of medication should be individually determined according to age, lifestyle, and heart failure symptoms, and the dose modulated to avoid symptomatic bradycardia but to achieve a resting heart rate < 100 BPM, as recommended by the 2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy 1. Overall, calcium channel blockers are a useful treatment option for controlling ventricular rate in patients with atrial fibrillation, but their use requires careful consideration of the individual patient's characteristics and medical history, as emphasized in the 2001 ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation 1 and the 2006 ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation 1.
From the FDA Drug Label
Electrical activity through the AV node depends, to a significant degree, upon calcium influx through the slow channel By decreasing the influx of calcium, verapamil hydrochloride prolongs the effective refractory period within the AV node and slows AV conduction in a rate-related manner.
Calcium Channel Blockers like verapamil hydrochloride prolong AV node repolarization by decreasing the influx of calcium, which in turn slows AV conduction. This effect is rate-related and can help control heart rate in conditions like atrial fibrillation 2.
- The effective refractory period within the AV node is prolonged, reducing the likelihood of rapid ventricular response.
- AV conduction is slowed, allowing for more controlled electrical activity through the AV node.
From the Research
Mechanism of Action
- Calcium channel blockers (CCBs) such as verapamil and diltiazem work by suppressing conduction through the atrio-ventricular (AV) node, making them effective in treating AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT) 3.
- CCBs also reduce ventricular response during atrial fibrillation/flutter by prolonging AV node repolarization 3, 4.
Effects on Atrial Fibrillation
- Atrial fibrillation is a common symptomatic sustained arrhythmia, and controlling heart rate is crucial to prevent cardiac symptoms 4.
- CCBs such as diltiazem and verapamil can be used to achieve acute slowing of the ventricular response in atrial fibrillation 4.
- However, the use of CCBs may be limited by their short duration of action and potential hypotension 4, 5.
Pharmacologic Properties
- Verapamil and diltiazem are vasodilators with negative inotropic, chronotropic, and dromotropic effects, which can be beneficial in treating supraventricular tachycardia 6.
- Nifedipine, on the other hand, is a vasodilator with no clinical effects on cardiac conduction or contractility 6, 7.
Clinical Implications
- CCBs may have a role in the acute reduction of ventricular response in patients with atrial fibrillation complicated by congestive heart failure, but their safety in chronic heart rate control remains to be proven 5.
- The combination of CCBs and beta blockers may be beneficial in treating chronic stable angina pectoris, but caution is advised in patients with impaired left ventricular function 7.