Introduction: A number of patients present with recurrent palpitations and documented tachycardia where the P wave morphology on electrocardiogram (ECG) is similar to sinus P wave, making it difficult to distinguish between sinus or atrial tachycardia.
Case presentation: We present the case of a 22-year-old patient with incidental finding of incessant tachycardia and mild left ventricular systolic dysfunction, ejection fraction at 46% and no scar on cardiac magnetic resonance. ECG showed narrow complex tachycardia at 109 bpm with P wave axis similar to sinus rhythm but notched prolonged negative P wave in V1. She did not respond to trials with either bisoprolol or ivabradine. The differential diagnosis was inappropriate sinus tachycardia or atrial tachycardia (AT). However, in the absence of diurnal variation on Holter and the presence of systolic dysfunction, this was most likely AT and tachycardiomyopathy. She was listed for an electrophysiological study (EPS) and catheter ablation using 3D electroanatomical mapping (EAM) under general anaesthesia. ECG in pre-assessment showed a rate of 95 bpm and negative P waves in V1-3. On the day of the procedure, she was in narrow complex tachycardia with concentric coronary sinus activation (tachycardia cycle length [TCL] 530 ms). Ventricular entrainment showed VAAV response consistent with AT. During re-induction of AT, atrial flutter was induced. 3D EAM using Pentaray© and Carto 3 Coherent map confirmed cavotricuspid isthmus (CTI)-dependent flutter. Ablation using STSF DF catheter along CTI successfully resulted in bidirectional block. 3D EAM of sinus node was carried out. AT was re-induced and the 2 different TCLs (530 ms and 510 ms) mapped using Parallel mapping confirmed focal AT from the same focus in the anterolateral to basal right atrial appendage. Unipolar signals confirmed Qs morphology and catheter ablation was carried out. Another tachycardia was induced and mapped to the same focus, hence further ablation was carried out. Repeated EPS during the waiting period at baseline, on isoprenaline infusion and washout did not induce any tachycardia. Remapping on isoprenaline confirmed sinus tachycardia and CTI block.
Discussion and conclusion: Focal AT can result from automatic or triggered activity or micro-re-entry. Sometimes, it can be challenging to distinguish focal AT from inappropriate sinus tachycardia when P wave axis appears similar when the focus is close to the sinus node. However, the presence of negative P waves in the precordial leads would be more in keeping with an AT. The presence of systolic dysfunction in conjunction with the tachycardia was also more suggestive of AT and tachycardiomyopathy. Focal AT and sinus tachycardia are sometimes difficult to differentiate on Holter or ECG because of the similar morphology of the P-wave when focal AT originates from an area in proximity to the sinus node. EPS and EAM are critical in these cases as they can provide a more accurate diagnosis and can help locate the area of origin of the arrhythmia.
