ABSTRACT & COMMENTARY
Is There a Role for Routine Procainamide Infusion in the Evaluation of Patients with Cardiac Arrest?
By Edward P. Gerstenfeld, MD
Professor of Medicine, Chief, Cardiac Electrophysiology, University of California, San Francisco
Dr. Gerstenfeld does research for Biosense Webster, Medtronic, and Rhythmia Medical.
SOURCE: Somani R, et al. Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER). Heart Rhythm 2014;11:1047-1054.
The Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER) study evaluated the diagnostic utility of a procainamide infusion test in patients with unexplained cardiac arrest (UCA) or a family history of sudden death (FHSD). Patients with sudden death without any evidence of a Brugada pattern at baseline underwent procainamide testing (15 mg/kg to a maximum of 1 g at 50 mg/min). Patients were excluded if they had impaired left ventricular function (< 50%), any evidence of hypertrophic cardiomyopathy, any epicardial coronary stenosis > 50%, any anomalous coronary arteries, a prolonged QTc interval, or reversible cause of cardiac arrest. A test was considered positive for Brugada pattern if there was an increase in ST elevation > 1 mm or if there was > 1 mm of new ST elevation in leads V1 and/or V2. Procainamide testing was performed in 174 subjects (age 46.8 ± 15.4 years, 47% female), including 115 UCA survivors. A Brugada pattern was provoked in 12 subjects (6.9%), five of whom had no ST abnormalities at baseline. Ten of the 12 subjects were diagnosed clinically with the Brugada syndrome. Genetic testing was performed in 10 of the 12 procainamide-positive patients and one was positive for a mutation in the SCN5A gene. No subjects with a negative procainamide challenge were subsequently diagnosed with Brugada syndrome. The authors concluded that procainamide testing in subjects with UCA or a FHSD provoked the Brugada ECG pattern in a significant number of subjects, which facilitated the diagnosis of Brugada syndrome and should be recommended in the evaluation of patients with UCA.
The evaluation of sudden cardiac arrest varies among physicians, often leading to the common endpoint of placement of an implantable cardioverter defibrillator (ICD). In part, this common therapeutic endpoint has led many to limit the evaluation in such patients, since the diagnostic yield is low and therapeutic endpoint often not influenced by the evaluation. Most physicians I have encountered who evaluate a young sudden death survivor will perform an electrocardiogram, echocardiogram, evaluation of the coronary arteries, and then proceed to ICD placement. However, one should not minimize the importance of a more detailed electrophysiology evaluation in such patients. While inherited arrhythmia syndromes are rare, they will have implications not only for the cardiac arrest survivor, but his entire family. A diagnostic electrophysiology study is also imperative, in my opinion. Although uncommon, we have diagnosed several young cardiac arrest survivors with previously undiagnosed accessory pathways leading to rapid supraventricular tachycardia, and even several cases of rapid AV nodal reentry. In the current study, a procainamide infusion was performed in cardiac arrest survivors and their relatives. A Brugada pattern was evoked in 6.9% of patients, including five patients with a completely normal ECG. Although undoubtedly leading to ICD placement, this diagnosis would lead to genetic testing, further evaluation of first-degree relatives, and recommendations to avoid sodium channel blocking drugs such as tricyclic antidepressants and Class IC antiarrhythmics in the cardiac arrest survivor and diagnosed relatives. It seems reasonable that in addition to evaluation of the ECG and coronary arteries, routine electrophysiology study and procainamide infusion should be added to the diagnostic workup of the cardiac arrest survivor, even if the baseline ECG is normal.