Flecainide toxicity in a 75-year-old female with acute kidney injury led to transient heart failure with reduced ejection fraction (35-40%) and QRS prolongation, which resolved upon drug cessation.
Case Report (n=1)
No
Clinicians must remain vigilant for flecainide-induced reversible HFrEF, particularly in patients with evolving renal function, even in the absence of traditional contraindications.
Flecainide, a class Ic antiarrhythmic, has been widely prescribed for managing cardiac arrhythmias. While effective in rhythm control, there is growing, albeit limited, evidence of its association with reversible heart failure with reduced ejection fraction (HFrEF), particularly under circumstances that may exacerbate drug toxicity. This case report presents a clinically significant episode of flecainide-induced HFrEF in a patient without structural heart disease, supported by a targeted review of the literature. The proposed mechanism involves QRS prolongation and impaired myocardial conduction due to sodium channel blockade, compounded by transient renal dysfunction. Clinicians must remain vigilant for cardiotoxic effects of flecainide, especially in patients with evolving renal function, even in the absence of traditional contraindications.
Wolchover et al. (Wed,) conducted a case report in Flecainide toxicity leading to transient heart failure with reduced ejection fraction (n=1). Flecainide was evaluated. Flecainide toxicity in a 75-year-old female with acute kidney injury led to transient heart failure with reduced ejection fraction (35-40%) and QRS prolongation, which resolved upon drug cessation.