Introduction:
Wolff-Parkinson-White syndrome is the most common form of ventricular preexcitation [1]. The prevalence of electrocardiographic preexcitation has been reported to be between 0.1 and 3.1 per 1000 persons [2 ]. WPW ECG pattern is caused by abnormal electrical conduction through an accessory pathway that bypasses the normal cardiac conduction system [3 ].
The definition of Wolff-Parkinson-White syndrome relies on the following electrocardiographic features: (1) a PR interval less than 0.12 seconds, (2) a slurring of the initial segment of the QRS complex, known as a delta wave, (3) a QRS complex widening with a total duration greater than 0.12 seconds, and (4) secondary repolarization changes reflected in ST segment-T wave changes that are generally directed opposite (discordant) to the major delta wave and QRS complex changes [4].
Only half the patients with electrocardiographic evidence of preexcitation are symptomatic at the time of diagnosis, with palpitations being the most common symptom. Other symptoms include dizziness, syncope, shortness of breath, and chest discomfort [2 ]. Patients with Wolff-Parkinson-White syndrome experience symptoms secondary to tachyarrhythmias, such as atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, and, rarely, ventricular fibrillation and sudden death [1]. The overall risk of sudden cardiac death in Wolff-Parkinson-White syndrome is estimated at 0.1% per year in asymptomatic patients and 0.3% per year in symptomatic patients [5].
This occurs due to rapid ventricular rates in conditions with rapid atrial depolarization, such as atrial fibrillation (AF) or atrial flutter. These fast ventricular rates can degenerate into ventricular fibrillation (VF) and cardiac arrest [2,3,6,7].
PLSVC is the most common congenital anomaly of the thoracic venous system; it occurs in 0.3% to 0.5% of the general adult population and accounts for 10% of cases of congenital heart disease (CHD). PLSVC results when the left superior cardinal vein caudal to the innominate vein fails to regress.
PLSVC is most commonly observed as an isolated finding, but it can also be associated with other cardiovascular abnormalities, including atrial septal defect, bicuspid aortic valve, coarctation of the aorta, coronary sinus ostial atresia, and cortriatriatum. In the absence of other congenital abnormalities, PLSVC draining into the coronary sinus is an asymptomatic condition with no hemodynamic significance [8,9,10].