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Adverse cardiac effects are a known, albeit infrequent, complication of azole antifungal drug therapy. Most often, cardiotoxicity is the result of drug–drug interactions due to azole inhibition of CYP3A4, but also of CYP2C19 and CYP2C9, leading to increased serum levels of concomitantly administered medications that require hepatic metabolism. Adverse interactions of azole antifungal drugs with digoxin or terfenadine are well known. Cytochrome P450 inhibition may also result in reduced activity of prodrugs that require hepatic metabolism to be converted to active metabolites. Apart from the potential impact of altered drug metabolism, azole antifungal agents also exhibit direct pharmacologic actions that may result in adverse cardiac proarrhythmic effects. Most important of these is moderate QT-interval prolongation principally attributed to azoleinduced blockade of the rapid component of delayed rectifier potassium current IKr and possibly the ultrarapid activating component of delayed rectifier potassium current IKur. 13 In the ventricle, IKr block may increase the risk of torsades de pointes polymorphic ventricular tachycardia. In the atrium, IKr and IKur blockade is expected to result in prolongation of action potential duration. The latter effect may be expected to delay onset of intrinsic cellular pacemaker function, resulting in bradycardia. The report presented here describes a case of development of symptomatic sinus bradycardia and chronotropic incompetence in a patient with normal cardiac function being administered oral therapy with the azole antifungal drug

Sinus bradycardia and chronotropic incompetence associated with single-agent itraconazole antifungal therapy: A case report