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].