Late Onset of Wolff-Parkinson-White Syndrome in a 72-year-old Man

Abstract

We encountered a case of wide QRS tachycardia with chronic atrial fibrillation in Wolff-Parkinson-White syndrome. Unique features were late onset of syncope attacks associated with this tachycardia at an advanced age of 72 years old without previous documentation of WolffParkinson-White syndrome on electrocardiogram. He had a high likelihood of sudden cardiac death. Catheter ablation using CARTO TM system easily led to a successful ablation of the accessory pathway. The mechanism of late onset of the wide QRS tachycardia was attributed to possible changes of electrophysiologic properties including the atrio-ventricular node and/or the accessory pathway, and the unique location of the accessory pathway. Case ReportA 72-year-old man was admitted for evaluation of frequent syncope or fainting attacks which had suddenly begun 1 month before admission in May 2002. He easily experienced syncope attacks on exercise. Thus, his daily life activities were limited. He was taking antihypertensive drugs (5 mg of enalapril and 25 mg of atenolol), digitalis glycosides (0.125 mg of digoxin) and warfarin potassium as anticoagulant therapy for~10 years because of a history of cerebral infarction associated with hypertension and non-valvular chronic atrial fibrillation (Af). An electrocardiogram (ECG) taken 1 year prior to the admission was Af with narrow QRS complex ( Fig. 1A) with no evidence of tachycardia and delta waves (mean heart rate; 64 beats per minute, QRS; 82 msec). While the ECG taken 2 months prior to the admission showed Af with intermittent delta waves (mean heart rate; 60 beats per minute) ( Fig. 2A).On admission, his blood pressure was 102/64 mmHg and pulse rate was 124 beats per minute and irregular. When his heart rate was over 150 beats per minute on exercise, his systolic blood pressure dropped under 70 mmHg with manifestation of fainting. There were no murmurs on cardiac auscultation. Routine blood test results were almost normal except for a coagulation time. An ECG (Fig. 1B) showed wide QRS complex tachycardia (mean heart rate; 138 beats per minute, QRS; 134 msec) with a slur at the initial portion of the QRS complex. This tachycardia was suppressed by an intravenous administration of procainamide, which is known to depress the conduction of the accessory pathway (1), and resulted in a dramatic decrease of the wide QRS complex (Fig. 2B). By contrast, the tachycardia was accelerated by an intravenous application of verapamil or digitalis glycosides (Fig. 2C), which are reported to depress the conduction of the atrio-ventricular (AV) node (2, 3). With this change of ECG, the patient experienced symptoms of hypotension and notable fainting. These findings suggested that this patient might have Wolff-Parkinson-White (WPW) syndrome. A chest radiograph showed a mild increase of the cardiothoracic ratio (CTR; 54%) and two-dimensional echocardiography revealed no evidence of cardiac abnormalities except for mild dilatation of the left atrium, such as Ebstein's anomaly and mitral leaflet prolapse which are...

Rapid Recovery from Congestive Heart Failure Following Successful Radiofrequency Catheter Ablation in a Patient with Late Onset of Wolff-Parkinson-White Syndrome

“…In the present case, we encountered a late-onset manifestation of an accessory pathway in a patient with long-standing persistent AF. Takemoto et al reported a similar case of late onset WPW syndrome in a patient with long-standing persistent AF (2). They suggested that the presumed mechanism of late onset WPW syndrome is the decrease in the capability of conduction via the atrioventricular (AV) node which may progress with age, leading to pre-excitation of the ventricles through the anterograde conduction over the accessory pathway.…”