A 28-year-old pregnant woman at 37 gestational weeks was admitted to the hospital for childbirth. She experienced palpitations since her 5th gestational month, and her ECG revealed atrial tachycardia with a rate of 134 bpm (Fig. 1a). Negative P wave in lead D1 and positive P wave in lead V1 suggested a left atrial origin. She showed no clinical signs of heart failure. Her transthoracic echocardiogram revealed global left ventricular systolic dysfunction with an ejection fraction of 45%. She was hemodynamically stable. However, we could manage the arrhythmia neither with medical therapy nor with electrical cardioversion. Our obstetricians decided to perform vaginal delivery, and the baby was in well condition.
Figure 1.
(a) Focal atrial tachycardia (AT). This 12-lead ECG demonstrating atrial tachycardia at a rate of 134 bpm. Negative P wave in lead D1 and positive P waves in inferior leads suggest a left atrial origin. (b) Electroanatomic activation map of the left atrium appendage (LAA). The color bar shows the progression of activation times during AT (from red through green, blue, and purple). The earliest endocardial activation was located at the base of LAA 36 ms ahead of P wave onset. Red dots indicate ablation sites
LA - left atrium
One week after the childbirth, the patient underwent a transseptal puncture and a left atrial mapping using MicroPort Columbus™ 3D Navigation System. The earliest endocardial activation was located within the base of the left atrial appendage (LAA) 36 ms ahead of P wave onset (Fig.1b). Ablation using an irrigated catheter (25 w) was applied, and sinus rhythm was restored. Before discharge, an ACE inhibitor and a beta-blocker were added to the treatment.
After 1 year of follow-up, routine echocardiograms revealed complete improvement in LV systolic function, and the patient was still in sinus rhythm.
In this case, we illustrated the focal AT from an uncommon origin in pregnancy. Catheter ablation led to the restoration of sinus rhythm and made a crucial contribution to the improvement of LV systolic function.
Footnotes
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