Class Ic antiarrhythmic agents are effective in the treatment of various atrial tachyarrhythmias. They are known to cause rate-related QRS widening in the presence of structural heart disease, which can lead to life-threatening arrhythmias. The role of routine exercise electrocardiography in patients without structural heart disease is unknown. All patients initiated on class Ic antiarrhythmic agents and who had exercise electrocardiography performed from June 2009 to June 2013 were included. Symptom-limited treadmill electrocardiography was performed to detect significant QRS widening at peak exercise (defined as an increase of >25% of baseline QRS). Fifty-six patients were included in the study. All patients were screened for structural heart disease before initiation of the medication. Significant QRS widening and atrial tachycardia occurred in a single patient, which terminated with cessation of exercise. This patient had a history of tachycardia-mediated cardiomyopathy with normalization of ejection fraction 3 years before being placed on flecainide. In conclusion, routine exercise testing to detect QRS widening is not warranted in patients with no structural heart disease.
Class Ic antiarrhythmic drugs are used for rhythm control in the management of paroxysmal and persistent atrial fibrillation. However, these agents possess proarrhythmic potential because of the widening of the QRS complex, potentially leading to ventricular tachycardia, fibrillation, and torsades de pointes. Evidence suggests that these proarrhythmic events occur when the sinus rates are high, suggesting a use-dependent sodium channel blockade as the mechanism for arrythmogenesis. Because the results of the Cardiac Arrhythmia Suppression Trial (CAST) have been published, these agents have been contraindicated in patients with known structural heart disease. Patients are screened for underlying ischemic and structural heart disease before initiation of these drugs. Despite such meticulous screening, expert opinion suggests performing exercise stress testing in patients on IC agents to monitor for exercise-induced QRS widening and proarrhythmia. However, there is little evidence demonstrating the clinical utility and cost-effectiveness of this strategy especially in the current era when the drug is no longer used in patients with structural heart disease. We hypothesized that routine exercise stress testing would not be necessary to monitor all patients on class Ic antiarrhythmic drugs and conducted the study with the following specific aims: (1) to assess the frequency of exercise-induced QRS widening in patients who have already been screened for heart disease and (2) to identify high-risk subgroups within this cohort where exercise testing would be useful.
Methods
Patients >18 years on class Ic antiarrhythmic agents for treatment of atrial arrhythmias and who underwent exercise stress testing at the University of Arkansas for Medical Sciences from January 2008 to June 2013 were identified. This retrospective study was approved by the institutional review board. The current practice in our cardiac electrophysiology service is to use class Ic agents in patients who have no history of myocardial infarction, normal LV systolic function by echocardiogram or nuclear imaging, absence of significant LV hypertrophy (<1.5 cm), and absence of myocardial ischemia by stress testing or significant (>50%) coronary artery disease by angiography. Treadmill ECG is performed on all patients who are on a daily dose of at least 200 mg of flecainide or 300 mg of propafenone. We collected data on age, gender, race, diabetic status, left ventricular systolic function, indication for antiarrhythmic therapy, duration of antiarrhythmic therapy, dosage of the drug, QRS width on a 12-lead electrocardiogram (ECG) before initiation therapy, QRS width on a 12-lead ECG on the day of the exercise stress test, maximum QRS width documented during the exercise stress test, maximum metabolic equivalents achieved, arrhythmic events during the exercise stress test, and treatment decisions made based on the findings of the stress test (dose changes and/or discontinuation). QRS width was measured with electronic calipers in a computerized ECG reporting system (MUSE; GE, Waukesha, Wisconsin). The longest QRS width in a given lead was chosen at baseline, and the maximum QRS width at peak exercise was chosen in the same lead. QRS widening was defined as an increase in exercise QRS that is >25% of baseline QRS. Arrhythmic events that occurred during stress testing were categorized based on the interpretation of the rhythm strips. Cost per exercise test performed was calculated based on billing data. Descriptive statistics were used to report results.
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