A 37-year-old man was admitted to our cardiology department with sustained palpitations for 36 hours. He had suffered from paroxysmal palpitations for five years. This had happened one to three times per month, especially in the six months before admission and syncope occurred occasionally. The most useful way to terminate the acute episode of palpitations was a loading dose of propafenone (up to 210 mg). The patient had been diagnosed with dilated cardiomyopathy seven years ago by an ultrasound examination. The onset electrocardiogram (ECG) was a fast and regular rhythm with wide QRS complexes (174 beats/min). During the administration of propafenone, the following ECG was documented (figure 1).
What is your diagnosis?
Answer
Figure 1.
A) 12-lead surface ECG during the administration of propafenone.The paper speed is as usual (25 mm/s). B) ECG enlargement by 100% (only V1 lead) during the administration of propafenone. The paper speed is as usual (25 mm/s).
The 12-lead ECG shows an atrial flutter (AF) rhythm with a horizontal axis; the AF waves are very clear in the V1 lead and the rate is 348 beats/ min (figure 2A, thin black arrows). Initially, the onset ECG was a fast and regular rhythm with wide QRS complexes (via left accessory pathway as 2:1, not printed). However, after use of propafenone, the ECG showed the intermittent Wolff-Parkinson-White (WPW) syndrome (figure 2A, thick black arrow: delta wave) with two different QRS complexes (figure 2A, thick red arrow: the wide one; thin red arrow: the narrow one). So the diagnosis is pre-excited atrial flutter in intermittent WPW syndrome; the AF waves conduct in a different ratio (2:1, 3:1 and 4:1).
Sinus rhythm was recovered by direct synchronised cardioversion and the patient underwent an electrophysiological study (figure 3). The pre-excitation was still present (figure 3, thin red arrow). However, an orthodromic supraventricular tachycardia with a cycle length of 410 ms, which the impulse conducted retrogradely through the accessory pathway, could be evoked with programmed right ventricular apex stimuli. The earliest retrograde atrial activation was at coronary sinus (CS) 3-4 (figure 3, thick red arrow: CS3-4). So the accessory pathway was located at 2:30 o’clock of the mitrial valve annulus (the same as CS3-4) and successfully ablated with radiofrequency. The drawing shows the two different ways of conduction (figure 4). He is asymptomatic after one year of follow-up.
Figure 2.
A) Twelve-lead surface ECG during use of propafenone. The three top arrows=AF waves; thick black arrow=delta wave; left arrow: the narrow QRS complex, second left arrow: the wide QRS complex. B) The enlargement of 100% of ECG (only V1lead) during use of propafenone. Thin black arrows=AF waves.
Figure 3.
Electrophysiologial study. The orthodromic circus movement tachycardia (cycle length 410 ms) is evoked with programmed right ventricular apex stimuli. Thin arrow=the delta wave is still present; thick arrow=the earliest retrograde atrial activation is at CS3-4. Paper speed is 50 mm/s.
Figure 4.
The two different ways of conduction (left panel). The orthodromic circus movement tachycardia (right panel).