7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Calcium channel blockers in the treatment of cardiac arrhythmias : Christopher Madias, MD : Mark S Link, MD : Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Dec 06, 2021. INTRODUCTION Calcium channel blockers (CCBs) are useful antiarrhythmic agents in the management of certain arrhythmias, primarily supraventricular tachyarrhythmias [1-3]. They have diverse electrophysiologic properties and are therefore of variable antiarrhythmic efficacy. The primary settings in which they are useful can be best appreciated from an understanding of their mechanism of action. This topic will review the electrophysiological properties of CCBs and their clinical indications in a variety of arrhythmias. More detailed discussions of the use of CCBs in specific arrhythmias, CCBs for nonarrhythmic conditions, and other treatment options for arrhythmias are presented separately. (See "Calcium channel blockers in the management of chronic coronary syndrome".) (See "Calcium channel blockers in heart failure with reduced ejection fraction".) (See "Choice of drug therapy in primary (essential) hypertension".) (See "Atrioventricular nodal reentrant tachycardia".) (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome".) (See "Wide QRS complex tachycardias: Approach to management".) (See "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".) (See "Control of ventricular rate in atrial flutter".) https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 1/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate ELECTROPHYSIOLOGIC PROPERTIES CCBs, considered class IV antiarrhythmic drugs ( table 1), preferentially affect myocardial tissue with a slow action potential that is mediated by calcium currents. The sinoatrial and atrioventricular nodes depend on calcium currents to generate slowly propagating action potentials. In contrast, fast response myocardial tissues (the atria, specialized infranodal conducting system, the ventricles, and accessory pathways) depend on sodium channel currents. (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".) CCBs block the slow calcium channel in a dose-dependent fashion, resulting in the following direct effects [3,4]: Slowing of phase 4 depolarization and the conduction velocity of the sinoatrial (SA) and atrioventricular (AV) nodes Lengthening the antegrade and retrograde refractory periods of the AV node Slowing of the sinus rate and increased PR interval on the electrocardiogram (ECG) via the slowing of conduction through the AV node Similar to sodium channel blockers, CCBs with antiarrhythmic activity (ie, verapamil and diltiazem) exhibit "use-dependence." This phenomenon is characterized by an increase in the extent of calcium channel blockade as the frequency of impulse generation and ventricular activation increases. CCBs can also cause significant peripheral vasodilation, an effect which can induce reflex activation of the sympathetic nervous system. As a result, the observed electropharmacologic and pharmacodynamic properties of CCBs represent a combination of direct effects and indirect sympathetic reflex actions. This is particularly important with dihydropyridines (ie, nifedipine), which are potent vasodilators and sympathetic activators. The serum concentration of dihydropyridine CCBs necessary to achieve electrophysiologic activity in humans is much higher than the concentration needed to induce potent vasodilation. Therefore, at prescribed doses, these agents do not exert measurable electrophysiologic effects and appear to be devoid of antiarrhythmic activity. In addition, the reflex activation of the sympathetic nervous system offsets any direct effect of the dihydropyridine CCBs on the sinoatrial and AV nodes. Among nondihydropyridine CCBs, the effect on vasodilation is more apparent with diltiazem than verapamil, which results in verapamil having a more pronounced effect on the SA and AV nodes as its action is not offset by vasodilatory activation of sympathetic activity. https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 2/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate CLINICAL USE Because verapamil and diltiazem primarily affect slow response tissues in the SA and AV nodes, these medications are primarily used for the management of supraventricular tachycardias dependent on conduction through the AV node (ie, atrioventricular nodal reentrant tachycardia and atrioventricular reentrant tachycardia) and for ventricular rate control in atrial fibrillation (AF), atrial flutter, and atrial tachycardia. They are largely ineffective for the direct prevention of most ventricular arrhythmias; however, there are some exceptions, such as the utility of verapamil for the treatment of idiopathic fascicular ventricular tachycardia. (See 'Ventricular arrhythmia' below.) The antiarrhythmic effect of verapamil appears to be similar in adults and children, although less experience is available in children [1,2,5]. Verapamil and to a lesser degree diltiazem may be harmful in patients with hypotension or impaired ventricular function (especially those with a history of heart failure [HF]), and in general should not be used in patients with these conditions. In addition, CCBs should be used cautiously in patients already taking a beta blocker because of the combined negative inotropic and chronotropic effects of both classes of medications [5]. A brief review of these issues is provided here; the use of CCBs in the treatment of specific arrhythmias is discussed in detail elsewhere. Supraventricular tachycardia Both diltiazem and verapamil are accepted as treatments of choice for the termination of supraventricular tachycardias (SVT), such as AV nodal reentrant tachycardia and atrioventricular reciprocating tachycardia due to an accessory pathway. An important exception to the first-line use of these agents occurs in unstable patients with hemodynamic compromise. In an unstable patient with SVT, the preferred treatment is direct electrical cardioversion or intravenous adenosine, a very short-acting AV nodal blocking agent that rarely produces additional hypotension. (See "Atrioventricular nodal reentrant tachycardia".) Another situation in which CCBs should be avoided or used with caution is in the presence of a wide QRS complex tachycardia. If there is no doubt that a wide QRS complex tachycardia is supraventricular in origin, therapy directed at the AV node and the SVT may be given. In such cases, management is similar to that described above for SVT with a normal QRS duration. However, with a wide QRS complex tachycardia that is potentially ventricular tachycardia, CCBs blockers should be avoided, as there is a risk for hemodynamic deterioration following the administration of these medications. (See "Wide QRS complex tachycardias: Approach to management".) https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 3/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate CCBs appear to be of limited value in other forms of reentrant and automatic SVT [2,3,5,6]. Limited data exist concerning their role in SA nodal reentrant tachycardia or in atrial tachycardia due to an ectopic focus or intraatrial reentry (except for rate control by AV nodal blockade). However, oral verapamil may convert paroxysmal atrial tachycardia with block to sinus rhythm under certain circumstances, such as digoxin toxicity. Multifocal atrial tachycardia Either a non-dihydropyridine calcium channel blocker (ie, verapamil and diltiazem) or a beta blocker is usually the treatment of choice for multifocal atrial tachycardia. These drugs impair AV nodal conduction and will therefore slow the ventricular rate in this disorder; they do not usually reverse or prevent this arrhythmia. (See "Multifocal atrial tachycardia".) Atrial fibrillation and flutter Verapamil and diltiazem are used both acutely (via the intravenous route) and chronically (via the oral route) to slow the ventricular response in AF and atrial flutter. Their efficacy for rate control is due to their direct action to slow conduction and prolonged refractoriness in the AV node. Verapamil and diltiazem reduce both the resting and the exercise-induced increases in heart rate, whereas the major effect of digoxin (which works on the AV node via enhancing vagal tone) is on the resting rate. Therefore, verapamil and diltiazem are generally preferred to digoxin as monotherapy (in the absence of underlying HF) [7]. However, for patients with inadequate ventricular rate control with monotherapy, the concurrent use of digoxin or a beta blocker with verapamil or diltiazem has an additive depressant effect on the AV node. (See "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy" and "Control of ventricular rate in atrial flutter".) AV nodal blocking medications that are normally used to control the ventricular rate during AF (most importantly) or atrial flutter, including the CCBs verapamil and diltiazem, are contraindicated in patients with an accessory pathway and preexcitation. This is discussed in further detail in another topic. (See "Treatment of arrhythmias associated with the Wolff- Parkinson-White syndrome", section on 'When to avoid AV nodal blockers'.) CCBs also have a propensity to convert atrial flutter to fibrillation in a small number of patients, presumably due to a shortening of the atrial effective refractory period [8]. CCBs have been regarded as having little value in the termination and prevention of AF. However, verapamil may prevent the atrial electrical remodeling that occurs in AF, and the combination of verapamil with another agent has been shown to be effective in preventing AF recurrence [9]. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials", section on 'Verapamil'.) https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 4/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate Ventricular arrhythmia The role of CCBs in ventricular arrhythmias is less well defined [10- 15]. CCBs inadequately suppress ventricular premature beats in patients with structurally normal or abnormal hearts. They also have no significant effect on arrhythmia frequency or arrhythmic mortality in patients with hypertrophic cardiomyopathy, dilated cardiomyopathy, or mitral valve prolapse [1,2,16]. As a class, CCBs have a limited role in the treatment of ventricular tachycardia (VT) or ventricular fibrillation (VF) in the setting of organic heart disease. They do not suppress nonsustained VT, nor do they prevent the inducibility of VT/VF after programmed electrical stimulation. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".) However, calcium blockers may have a role in the following clinical settings: They are often effective when ventricular tachycardia or fibrillation is due to transient coronary artery spasm [17]. (See "Vasospastic angina".) They may have a role for polymorphic VT in the structurally normal heart or in those with familial catecholaminergic polymorphic VT that is due to a RyR2 or calsequestrin gene mutation [18]. (See "Catecholaminergic polymorphic ventricular tachycardia".) Exercise-triggered VT (called repetitive monomorphic VT) having the morphologic pattern of left bundle branch block and an inferiorly directed axis deviation (right ventricular outflow tract tachycardia) or a pattern of right bundle branch block and rightward axis (left ventricular outflow tract tachycardia) may respond predictably and promptly to intravenous verapamil. Such an arrhythmia may occur in patients without identifiable cardiac disease [12,19,20]. (See "Ventricular tachycardia in the absence of apparent structural heart disease".) A relatively rare, sustained VT that occurs in patients without evidence of structural heart disease has the morphologic pattern of right bundle branch block with left axis deviation [21-23]. This arrhythmia, which is called an idiopathic fascicular ventricular tachycardia (primarily of the left posterior fascicle), verapamil sensitive tachycardia, or Belhassen tachycardia, appears to be a distinct clinical entity and, in most cases, responds to intravenous verapamil [21,24]. (See "Ventricular tachycardia in the absence of apparent structural heart disease".) Arrhythmia mortality after myocardial infarction Routine treatment of the post-MI patient with a calcium channel blocker is not justified. It is possible that CCBs might benefit selected https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 5/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate patients after MI, particularly those with a non-Q wave infarct, without HF, and who are unable to take a beta blocker [25-27]. However, the level of benefit, if present, is small. Additionally, there are subsets of patients in whom certain CCBs may increase mortality (see "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of ST-elevation myocardial infarction", section on 'Calcium channel blockers' and "Major side effects and safety of calcium channel blockers" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction", section on 'Calcium channel blockers'). CCBs reverse coronary vasospasm and attenuate myocardial ischemic damage following experimental coronary occlusion [28]. These observations led to clinical studies assessing if these drugs might increase survival in patients with acute myocardial infarction (MI). Numerous randomized controlled trials of CCBs (diltiazem, verapamil, and nifedipine) have been analyzed [29,30]. No agent was found to unequivocally and decisively decrease mortality; in fact, pooled data for five CCBs suggested an unfavorable trend in total mortality, particularly with the short-acting dihydropyridines ( figure 1). This is in contrast to the clear benefit associated with other drugs such as beta blockers, statins, aspirin, and angiotensin converting enzyme inhibitors. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".) SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Cardiac implantable electronic devices" and "Society guideline links: Supraventricular arrhythmias".) SUMMARY AND RECOMMENDATIONS In addition to adenosine, the calcium channel blockers (CCBs) diltiazem and verapamil are treatments of choice for the termination of supraventricular tachycardia. (See 'Supraventricular tachycardia' above and "Atrioventricular nodal reentrant tachycardia".) Diltiazem and verapamil can be used both acutely (via the intravenous route) and chronically (via the oral route) to slow the ventricular response in atrial fibrillation (AF), atrial tachycardia, and atrial flutter. (See 'Atrial fibrillation and flutter' above.) https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 6/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate In patients with hypotension or impaired ventricular function, especially those with a history of heart failure, diltiazem and verapamil may be harmful, and are relatively contraindicated. (See 'Clinical use' above.) CCBs should be used cautiously in patients already taking a beta blocker because of the combined negative inotropic and chronotropic effects of both classes of medications. (See 'Clinical use' above.) In a patient with a wide QRS complex tachycardia that is potentially ventricular tachycardia, CCBs should be avoided, as there is a risk for hemodynamic deterioration following the administration of these medications. (See 'Supraventricular tachycardia' above and "Wide QRS complex tachycardias: Approach to management".) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Haines DE, DiMarco JP. Current therapy for supraventricular tachycardia. Curr Probl Cardiol 1992; 17:411. 2. Singh BN, Ellrodt G, Peter CT. Verapamil: a review of its pharmacological properties and therapeutic use. Drugs 1978; 15:169. 3. Singh BN, Hecht HS, Nademanee K, Chew CY. Electrophysiologic and hemodynamic effects of slow-channel blocking drugs. Prog Cardiovasc Dis 1982; 25:103. 4. Cranefield PF, Aronson RS, Wit AL. Effect of verapamil on the noraml action potential and on a calcium-dependent slow response of canine cardiac Purkinje fibers. Circ Res 1974; 34:204. 5. Singh BN, Nademanee K, Baky SH. Calcium antagonists. Clinical use in the treatment of arrhythmias. Drugs 1983; 25:125. 6. Boriani G, Bertaglia E, Carboni A, et al. A controlled study on the effect of verapamil on atrial tachycaarrhythmias in patients with brady-tachy syndrome implanted with a DDDR pacemaker. Int J Cardiol 2005; 104:73. 7. Tsuneda T, Yamashita T, Fukunami M, et al. Rate control and quality of life in patients with permanent atrial fibrillation: the Quality of Life and Atrial Fibrillation (QOLAF) Study. Circ J 2006; 70:965. 8. Singh BN. Control of cardiac arrhythmias by modulation of the slow myocardial channel. In: Calcium channels, their properties, functions, regulation, and clinical relevance, Horowitz L, Partridge LD, Leach JK (Eds), CRC Press, Boca Raton 1991. p.327. https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 7/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate 9. De Simone A, De Pasquale M, De Matteis C, et al. VErapamil plus antiarrhythmic drugs reduce atrial fibrillation recurrences after an electrical cardioversion (VEPARAF Study). Eur Heart J 2003; 24:1425. 10. Belhassen B, Horowitz LN. Use of intravenous verapamil for ventricular tachycardia. Am J Cardiol 1984; 54:1131. 11. Wellens HJ, B r FW, Lie KI, et al. Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia. Am J Cardiol 1977; 40:579. 12. Gill JS, Blaszyk K, Ward DE, Camm AJ. Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology. Am Heart J 1993; 126:1126. 13. Sung RJ, Shapiro WA, Shen EN, et al. Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity. J Clin Invest 1983; 72:350. 14. Sclarovsky S, Strasberg B, Fuchs J, et al. Multiform accelerated idioventricular rhythm in acute myocardial infarction: electrocardiographic characteristics and response to verapamil. Am J Cardiol 1983; 52:43. 15. Grenadier E, Alpan G, Maor N, et al. Polymorphous ventricular tachycardia in acute myocardial infarction. Am J Cardiol 1984; 53:1280. 16. McKenna, WJ, Harris, et al. Hypertrophic cardiomyopathy: Comparison of verapamil and amiodarone in the treatment of arrhythmia. Br Heart J 1980; 45:354. 17. Kimura E, Tanaka K, Mizuno K, et al. Suppression of repeatedly occurring ventricular fibrillation with nifedipine in variant form of angina pectoris. Jpn Heart J 1977; 18:736. 18. Swan H, Laitinen P, Kontula K, Toivonen L. Calcium channel antagonism reduces exercise- induced ventricular arrhythmias in catecholaminergic polymorphic ventricular tachycardia patients with RyR2 mutations. J Cardiovasc Electrophysiol 2005; 16:162. 19. Palileo EV, Ashley WW, Swiryn S, et al. Exercise provocable right ventricular outflow tract tachycardia. Am Heart J 1982; 104:185. 20. Wu D, Kou HC, Hung JS. Exercise-triggered paroxysmal ventricular tachycardia. A repetitive rhythmic activity possibly related to afterdepolarization. Ann Intern Med 1981; 95:410. 21. Lin FC, Finley CD, Rahimtoola SH, Wu D. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties. Am J Cardiol 1983; 52:95. 22. German LD, Packer DL, Bardy GH, Gallagher JJ. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease. Am J Cardiol 1983; 52:1202. https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 8/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate 23. Belhassen B, Shapira I, Pelleg A, et al. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-electrophysiologic entity. Am Heart J 1984; 108:1034. 24. Nogami A. Idiopathic left ventricular tachycardia: assessment and treatment. Card Electrophysiol Rev 2002; 6:448. 25. Verapamil in acute myocardial infarction. The Danish Study Group on Verapamil in Myocardial Infarction. Eur Heart J 1984; 5:516. 26. Effect of verapamil on mortality and major events after acute myocardial infarction (the Danish Verapamil Infarction Trial II DAVIT II). Am J Cardiol 1990; 66:779. 27. Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltiazem on mortality and reinfarction after myocardial infarction. N Engl J Med 1988; 319:385. 28. Singh BN, Nayler WG. The role of calcium antagonists in acute myocardial infarction. In: Earl y interventions in acute myocardial infarction, Rapaport E (Ed), Kluwer Academic Publication s, Boston 1989. p.123. 29. Held PH, Yusuf S. Impact of calcium channel blockers on mortality. In: Cardiovascular pharm acology and therapeutics, Singh BN, Dzau VJ, Vanhoutte PM, Woosley RL (Eds), Churchill Livi ngtion, New York 1993. p.525. 30. Yusuf S, Held P, Furberg C. Update of effects of calcium antagonists in myocardial infarction or angina in light of the second Danish Verapamil Infarction Trial (DAVIT-II) and other recent studies. Am J Cardiol 1991; 67:1295. Topic 951 Version 26.0 https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 9/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate GRAPHICS Revised (2018) Vaughan Williams classification of antiarrhythmic drugs abridged table Class 0 (HCN channel blockers) Ivabradine Class I (voltage-gated Na+ channel blockers) Class Ia (intermediate dissociation): Quinidine, ajmaline, disopyramide, procainamide Class Ib (rapid dissociation): Lidocaine, mexilitine Class Ic (slow dissociation): Propafenone, flecainide Class Id (late current): Ranolazine Class II (autonomic inhibitors and activators) Class IIa (beta blockers): Nonselective: carvedilol, propranolol, nadolol Selective: atenolol, bisoprolol, betaxolol, celiprolol, esmolol, metoprolol Class IIb (nonselective beta agonists): Isoproterenol Class IIc (muscarinic M2 receptor inhibitors): Atropine, anisodamine, hyoscine, scopolamine Class IId (muscarinic M2 receptor activators): Carbachol, pilocarpine, methacholine, digoxin Class IIe (adenosine A1 receptor activators): Adenosine Class III (K+ channel blockers and openers) Class IIIa (voltage dependent K+ channel blockers): https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 10/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate Ambasilide, amiodarone, dronedarone, dofetilide, ibutilide, sotalol, vernakalant Class IIIb (metabolically dependent K+ channel openers): Nicorandil, pinacidil Class IV (Ca++ handling modulators) Class IVa (surface membrane Ca++ channel blockers): Bepridil, diltiazem, verapamil Class IVb (intracellular Ca++ channel blockers): Flecainide, propafenone Class V (mechanosensitive channel blockers): No approved medications Class VI (gap junction channel blockers) No approved medications Class VII (upstream target modulators) Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Omega-3 fatty acids Statins HCN: hyperpolarization-activated cyclic nucleotide-gated; Na: sodium; K: potassium; Ca: calcium. Graphic 120433 Version 3.0 https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 11/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate Calcium channel blockers do not change mortality after acute myocardial infarction (MI) A meta-analysis of controlled trials of calcium channel blockers in post-myocardial infarction patients failed to show any effect on mortality. However, the agents that reduce heart rate, particularly verapamil, showed a trend toward an improved survival while nifedipine, which increases heart rate, showed a trend toward an increased mortality. Data from Held PH, Yusuf S. In: Cardiovascular Pharmacology and Therapeutics, Singh BN, Dzau V, Vanhoutte PM, Woosley RL (Eds), Churchill Livingstone, New York, 1993, p. 525. Graphic 74199 Version 3.0 https://www.uptodate.com/contents/calcium-channel-blockers-in-the-treatment-of-cardiac-arrhythmias/print 12/13 7/5/23, 8:20 AM Calcium channel blockers in the treatment of cardiac arrhythmias - UpToDate Contributor Disclosures Christopher Madias, MD No relevant financial relationship(s) with ineligible companies to disclose. Mark S Link, MD No relevant financial relationship(s) with ineligible companies to disclose. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. 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