
A Brief History of the WPW Syndrome.
David A. Ciraulo, M.D., F.A.C.C., Associate Professor, UCLA School of Medicine.
In 1893, the Oxford physiologist AF (Albert Frank) Stanley Kent was first to describe vestigial heart muscle fibers that seemed to connect the myocardium of the right atrium with that of the right ventricle in lab animals (mice, rabbits, et al.) and humans (on postmortem exams). In this pre-ECG era, Kent theorized that these embryological bypass track anomalies might provide an alternate route of myocardial activation between the right atrium and right ventricle which might thereby bypass the normal atrial-ventricular (AV) nodal transit route.
Fifteen years after his discovery, Kent resigned his post as a Professor of Physiology at Oxford to become the Director of Industrial Organization studies at the Manchester Municipal College of Technology. During WW2, Kent was by then an 80-year-old retired teacher who volunteered to serve in Britain’s Home Guard as a weapons quartermaster. Kent died in 1958 at the age of 95 and, though the implications of his accessory conduction pathway were not understood at that time, his right-sided bypass track is still known as the “Bundle of Kent.”
A decade after Kent wrote about his anomalous cardiac muscle bundle, the German physiologist Wilhelm Einthoven introduced his Electrokardiogram (EKG), a device that could record electromagnetic waves to reflect the phases of contraction and relaxation in the heart’s chambers. 1 Einthoven’s original EKG contraption weighed about 600 lbs. and was therefore only available for experimental investigations in university research laboratories. 2
In 1914, a young physiology genius named George Ralph Mines began to study cardiac arrhythmias at Cambridge and later at the McGill University research labs in Toronto. There Mines demonstrated that atrial tachyarrhythmias could be based on a reentry electrical circuit which could be interrupted by a second shock timed to occur during the study animal’s ventricular contraction. Mines was therefore the first to recognize the phenomenon of reentry electrical activation that might travel along the accessory muscle AV activation pathways that Kent had described. 3 Mine’s also showed that ventricular fibrillation could be induced by an electrical shock delivered during the recovery phase of the heart’s normal activation sequence.
Ironically, Mines was found one morning lying unconscious on his laboratory floor, still attached to his lab’s electrical wires for cardiac monitoring and electrical excitation. At the hospital, Mines was briefly semi-conscious but then died. He was only 28 years old. Perhaps Mines had tried to self-induce an arrhythmia, probably persistent ventricular tachycardia (VT), explaining his semi-conscious state before his death from ventricular fibrillation (VF).
Mines’ unexpected death was thought to have been accidental. Little was then known about the dangers of electrocution. In that era, there was also a common research ethical tradition in which medical investigators tried dangerous experiments on themselves before applying them to groups of volunteer human research subjects. 3
In the early 1920s, America’s Sanborn Company was first to market a commercial electrocardiogram (ECG) machine as a compact device weighing less than 30 lbs. and portable enough for hospital and office use. Using such a device, cardiologists Louis Wolff, John Parkinson, and Paul D. White studied 11 patients (aged 11 to 55 with an average age of 27.6) with histories of palpitations for years or decades. These attacks were described as sudden and sustained bursts of rapid heart action associated with symptoms of marked light-headedness which could be partially relieved by bending forward. In each case, ECGs showed a shortened PR interval and a prolonged QRS (>120 msec), both of which normalized during exercise. 4
This widening of the QRSs in these patients was a slurring of that deflection’s initial phase which the three WPW authors mistook for a “bundle branch block” pattern. Today we know that this initial QRS slurring represents the activation of a WPW accessory pathway, which on the left side of the heart represents a type A pathway and on the right a type B pathway. Also, the shortened PR interval (<120 msec) reflects accelerated AV conduction. The authors also thought that the youth of these WPW patients suggested that their condition was due to a congenital cardiac anomaly and indeed WPW is often associated with other cardiac anomalies. 4
This condition is still recognized as the Wolff, Parkinson, White (WPW) Syndrome, though these original authors made no mention of accessory conduction pathways, reentry excitation, or the condition’s risk of sudden cardiac death (SCD). In the 1951 fourth edition of Dr. White’s book Heart Disease however, he mentions a woman with WPW syndrome who died suddenly, having had a heart rate of nearly 300 beats per minute (BPM) before she expired. 5
By the late 1960s, cardiologists became aware that certain WPW patients (those at risk of atrial fibrillation or with rapid atrial tachycardias) died suddenly. For these patients at high risk, surgical interruption of WPW conduction pathways obviated their risk of SCD. By 1991, accurate electrophysiologic mapping of accessory pathways and radiofrequency ablation provided a safe and effective non-surgical prevention of SCD in vulnerable WPW patients. 6, 7
WPW is the second most common cause of paroxysmal supraventricular tachycardia, being present in 1-3 per 1000 people. Despite the commonality of WPW syndrome, SCD in WPW cases is rare, occurring at an estimated 3.6 to 26 per 10 million people-years and about 50% of WPW/SCD victims had no prior symptoms of WPW syndrome during their lifetime. 8


References:
1. Cadogan, M. (2025 July 16). AF Stanley Kent. Life in the Fastlane.
2. Brusco S. (2015 September 16). MedTech Memoirs: The Electrocardiograph (EKG).
3. DeSilva RA. George Ralph Mines, Ventricular Fibrillation and the Discovery of the Vulnerable Period. J Am Cardiol. 1997:29:1397-402.
4. Wolff L, Parkinson J, White PD. Bundle-branch Block with Short P-R Interval in Healthy Young People Prone to Paroxysmal Tachycardia. J Am Heart J. 1930; 5:685-704.
5. Moss AJ. History of Electrocardiology. History of Wolff-Parkinson-White Syndrome: Introductory Note to a Classic Article by Louis Wolff, M.D. John Parkinson, M.D., and Paul D. White, M.D. Ann Noninvasive Electrocardiol. 2006:11:338-9.
6. Scheinman MM. The History of the Wolff-Parkinson-White Syndrome. Pioneers of Modern Medicine. Rambam Maimonides Medical Journal. 2012; 3:e0019.
7. Jackman WM, Wang X, Friday KJ, et al. Catheter Ablation of Accessory Atrioventricular Pathways (Wolff-Parkinson-White Syndrome) by Radiofrequency Current. NEJM 1991; 324:1605-1611.
8. Vatasescu RG, Paja CS, Sus I, et al. Wolf-Parkinson-White Syndrome: Diagnosis, Risk Assessment, and Therapy-An Update. Diagnostics. 2024; 14:296.