Intermittent WPW Pattern in a Heart Transplant Recipient with Normal Donor Electrocardiogram

Abstract

<h3>Introduction</h3> The use of a heart from donors with symptomatic Wolff-Parkinson-White (WPW) syndrome has been previously described in few case reports. However, intermittent pre-excitation (IPX) is a rare variant of WPW that can make the diagnosis and treatment challenging. <h3>Case Report</h3> A 53-year-old male with chronic non-ischemic cardiomyopathy and ventricular tachycardia, experienced an out-of-hospital (OOH) cardiac arrest secondary to ventricular fibrillation (VF) and a second VF arrest while hospitalized necessitating temporary mechanical circulatory support. He was stabilized and subsequently listed for a heart transplant (HT). A donor became available whose cause of death was an OOH cardiac arrest presumably due to drug overdose. Immediately post HT, the recipient was noted to have a classic WPW pattern on his electrocardiogram (EKG) with short PR interval and a delta wave axis compatible with a right anterior accessory pathway (AP). The only available donor EKG was normal. Two days later the recipient EKG normalized. Post-operative changes or ionic disturbances were postulated to have caused this IPX and an outpatient electrophysiology study (EPS) was recommended. Two weeks later, while still hospitalized, the WPW pattern reappeared and remained persistent without tachyarrhythmias (Figure). An inpatient EPS indicated that this was a high-risk pathway and successful radiofrequency ablation was performed. <h3>Summary</h3> Few reported cases of donor hearts with pre-existing AP amenable to ablation suggest that this is an acceptable approach to expanding the donor pool. However, IPX with normal donor EKG is less well described. IPX conveys the same risk of life-threatening arrhythmias as persistent pre-excitation. Cardiac denervation in HT recipients can make the approach to IPX challenging in the early post-operative period. Our case highlights the importance of early risk stratification of IPX pathways in HT recipients with otherwise limited historical information about arrhythmias in the donor.