A man in his 50s with a history of hypertension, New York Heart Association stage III heart failure with reduced ejection fraction (<25%) from polysubstance abuse, and 2 prior strokes presented with bilateral scrotal and lower extremity edema for 10 days. He did not have chest pain, shortness of breath, or dyspnea on exertion but noted scrotal pain. Findings from a heart and lung examination were notable for mild wheezing. A chest radiograph revealed no acute cardiopulmonary processes. The initial electrocardiogram (ECG) is shown in Figure 1.
Question: What is the rhythm?
The ECG demonstrates sinus tachycardia at a rate of 100 with alternating QRS complex morphologic characteristics (Figure 2). QRS complex A has a PR interval of approximately 180 milliseconds (ms) with left axis deviation while QRS complex B has a PR interval of approximately 120 ms with normal axis with repolarization abnormalities. Other features of this ECG, including broad P-wave in II and QRS voltages in the precordial leads, suggest left atrial enlargement and ventricular hypertrophy consistent with the patient’s history of hypertension and heart failure. This ECG was initially interpreted as electrical alternans vs ventricular bigeminy. Further investigation demonstrated that QRS complex B included a delta wave (Figure 3) while QRS complex A did not. This pattern demonstrated normal conduction along the AV node-His-Purkinje system (QRS complex A) alternating with conduction along a preexcitation accessory pathway (QRS complex B).
Positive delta wave in QRS complex B. Appx indicates approximately; ms, milliseconds.
Arrowheads indicate delta waves.
The patient was found to have a troponin level of 0.12 and brain natriuretic peptide score of 328. Along with his examination findings, he was diagnosed as having a heart failure exacerbation. Measurements of the patient’s pulse and blood pressure did not reveal alternation that would be compatible with end-stage heart disease, nor was there paradoxical pulse or blood pressure that suggested a hemodynamically significant pericardial effusion with tamponade. The patient had a transthoracic echocardiogram that showed no pericardial effusions but did demonstrate a left ventricular ejection fraction of less than 25% and global hypokinesis. He was treated with diuretics and discharged with his home medications to follow up with his local physician.
Wolff-Parkinson-White (WPW) syndrome was first described in 1930 in a series of 11 patients with paroxysmal tachycardia and short PR intervals on ECG.1 In 1943, the delta wave of WPW pattern was correlated with anatomic anomalous bundles of connecting tissue, the bundle of Kent, which bypassed the AV node-His-Purkinje system.2 The WPW pattern can be seen in about 0.2% of the general population.3 Patients with both evidence of an accessory pathway on ECG and symptomatic tachyarrhythmias are considered to have WPW syndrome.
In the WPW pattern, the PR interval is shorter owing to ventricular preexcitation through the accessory pathway, compared with PR intervals observed during normal AV node-His-Purkinje conduction. The QRS duration can be at the upper end of normal range in preexcited beats and when a delta wave is present. QRS complexes in the WPW pattern are typically fusion complexes representing ventricular depolarization over the accessory pathway and normal AV node-His-Purkinje system. The degree of ventricular preexcitation often depends on the relative refractoriness of the available pathways, which leads to intermittent conduction through alternate (accessory) pathways. It can be characterized as concealed pathway (the delta wave is absent despite the existence of an accessory pathway), minimal preexcitation, and maximal preexcitation. The varying degrees of preexcitation result in different PR intervals and appearances of the delta waves.
In this particular case, preexcitation occurs in a 2:1 fashion owing to long refractory period of the accessory pathway, such that it does not occur with every sinus beat at a rate of 100. The PR interval in normally conducted beats (QRS complex A) is approximately 190 ms compared with approximately 120 ms for those beats conducted through the accessory pathway (QRS complex B). The delta waves in QRS complex B are positive in all precordial leads except for V3, with an R/S ratio greater than 1 in V1. Discordant ST segment and T-wave changes in the precordial leads are observed only in QRS complex B. The finding of a positive delta wave in V1 suggests a left-sided bundle of Kent. Of note, the discordant ST-segment and T-wave changes seen with positive delta waves are commonly misinterpreted as a posterior myocardial infarction. In contrast, the right-sided bundle of Kent WPW pattern that feature negative delta waves in V1 and V2 is commonly mistaken for the Q waves of an anterior myocardial infarction.
Although this ECG was initially interpreted as electrical alternans vs ventricular bigeminy, it is not consistent with either of these diagnoses. Premature ventricular beats in bigeminy have aberrant-appearing wide QRS complexes without delta waves. This ECG is not consistent with electrical alternans because the PR interval is not constant between QRS complexes of different morphologic characteristics. Of note, electrical alternans is specific for large pericardial effusions—the timely recognition of this pattern should prompt an investigation to confirm the diagnosis. One final interpretation of this ECG not initially considered is premature atrial depolarizations with aberrant conduction, or Ashman phenomenon, which occurs when His-Purkinje fibers receive a new impulse before they have fully repolarized.4 The consistency of the PP intervals suggests against this interpretation.
Asymptomatic patients presenting with the WPW pattern can undergo exercise testing to determine whether the accessory pathway has a long refractory period—if so, the pathway is unlikely to conduct rapidly enough during atrial tachyarrthymias to cause ventricular tachyarrthymias. Patients with high-risk findings, however, could undergo further risk stratification and potential treatment with an electrophysiological study.5
A WPW pattern with long refractory period could be easily misinterpreted as electrical alternans, ventricular bigeminy, premature atrial depolarizations with aberrant conduction, or myocardial infarction.
A WPW pattern features different PR intervals between the QRS complexes of differing morphologic characteristics with a constant PP interval.
The QRS complex conducted by an accessory pathway in a WPW pattern features a delta wave with discordant ST-segment and T-wave changes.
In a WPW pattern, the delta wave’s directionality suggests the anatomical location of the bundle of Kent, but definition of the precise pathway requires an electrophysiological study.
Corresponding Author: Jin Ge, MD, MBA, Department of Medicine, University of California San Francisco, 505 Parnassus Ave, Room M-987, San Francisco, CA 94143-0119 (email@example.com).
Published Online: November 28, 2016. doi:10.1001/jamainternmed.2016.7231
Conflict of Interest Disclosures: None reported.
Ge J, Groh C, Goldschlager N. Alternating QRS Complex Morphologic Characteristics in a Man Presenting With Scrotal Edema. JAMA Intern Med. 2017;177(1):120-122. doi:10.1001/jamainternmed.2016.7231