Abnormal Lead V1 Tracing

The patient is a 74-year-old male with a history of persistent atrial fibrillation (AF); s/p pulmonary vein isolation (PVI) and cavotricuspid isthmus (CTI) dependent atrial flutter (AFL) ablation 2 years ago; aortic stenosis; s/p mechanical aortic valve replacement (AVR); coronary artery disease; s/p coronary artery bypass graft (CABG); obstructive sleep apnea (OSA) on continuous positive airway pressure (CPAP); hypertension; and body mass index (BMI) at 27.4 kg/m2; who is seen at the antiarrhythmic clinic for his routine 3-month follow-up.

He has been feeling fair with frequent episodes of exertional shortness of breath, fatigue, malaise, and exercise intolerance, which has affected his regular moderate intensity exercise activity. He does not drink alcohol and eats a Mediterranean diet.

His rhythm control strategy of AF started 9 years ago, when he underwent an electrical cardioversion followed with an initiation of sotalol, which sustained sinus rhythm for 7 years. However, persistent AF breakthrough required another cardioversion and initiation of amiodarone, that caused the patient significant tremor necessitating lowering the dose. AF recurrence led to initiation of dofetilide and AF and AFL ablation 2 years ago. Post-ablation, he felt great, and his 30 days mobile cardiac telemetry showed sinus rhythm with 2% atrial tachyarrhythmia.

He is on warfarin, dofetilide, potassium chloride, magnesium oxide, metoprolol, and losartan. His lab data showed serum potassium at 4.3, serum magnesium at 1.9, serum creatinine at 0.97, and glomerular filtration rate (GFR) at 76.

Recent 30 days mobile cardiac telemetry showed 63% atrial tachyarrhythmia.

An electrocardiogram (ECG) (Figure 1) is performed and shows the following:

Figure 1

What is the most appropriate next step?

Show Answer