Safety of Outpatient Initiation of Disopyramide for Obstructive Hypertrophic Cardiomyopathy Patients

Abstract

Background: Disopyramide is effective in ameliorating symptoms in patients with hypertrophic cardiomyopathy; however, its potential for proarrhythmic effect has raised concerns about its use in the ambulatory setting. The risk of initiating disopyramide in this manner has never been evaluated.

Methods and results: All charts of patients seen in the outpatient hypertrophic cardiomyopathy clinic between 2010 and 2014 were screened for initiation of disopyramide and data were extracted. Disopyramide in our clinic is usually initiated at a dose of 300 mg daily and titrated during follow-up. A total of 2015 patients were seen in the clinic, including 168 who were started on disopyramide. There were no cardiac events within 3 months of disopyramide initiation. During long-term follow-up (255 patient-years; mean, 447 days; interquartile range, 201-779), only 2 patients developed cardiac events (syncope of unknown cause in both). Thirty-eight patients (23%) developed side effects of disopyramide and 18 (11%) stopped the drug because of these side effects. Of the patients continuing disopyramide long term, 63% remained free of septal reduction interventions at end of follow-up. Disopyramide at a dose of 300 mg prolonged the mean QTc interval by 19±23 ms; however, increasing the dose to 600 mg had no further significant effect.

Conclusions: Initiation of disopyramide in the outpatient setting is safe and the risk of subsequent sudden cardiac death is low. Because of its QT-prolonging effect, precautions may be necessary in patients at higher risk of torsades de pointes.

Keywords: acquired long QT syndrome; disopyramide; hypertrophic cardiomyopathy; sudden cardiac death.

Figure 1

Disopyramide‐induced electrocardiographic changes. Electrocardiograms of a 53‐year‐old man with hypertrophic cardiomyopathy and left ventricular outflow tract gradients of up to 90 mm Hg. He suffered from exertional shortness of breath despite trials of beta‐blockers and calcium‐channel blockers. After initiation of disopyramide and increase in dose to 600 mg daily, his symptoms resolved and gradients diminished to 15 mm Hg. Electrocardiograms were recorded before disopyramide and while on 300 and 600 mg daily. Heart rate and QRS interval showed no significant change after disopyramide initiation. The PR interval was 180 ms at baseline, prolonged minimally on 300 mg and to 200 ms on 600 mg. The corrected QT interval was 378 ms at baseline, prolonged to 426 ms on 300 mg and remained without significant change (419 ms) after dose increase to 600 mg. Note the change in T‐wave morphology with a more‐rounded peak on disopyramide.