A 72-year-old woman was referred for catheter ablation of persistent AF. Her chief complaint was mild dyspnoea and palpitations on effort. She had a history of hypertension for 5 years without anti-hypertensive drugs and AF for 12 months. Atrial fibrillation had persisted continuously for 5 months. Cardiac auscultation revealed increased intensity of the second heart sound (S2) but no murmurs or gallops. The remainder of the physical examination was unremarkable. A12-lead electrocardiogram (ECG) showed AF with negative T waves in leads I, aVL, and V3 to V6. An echocardiogram revealed normal left ventricular (LV) function with an ejection fraction of 66% and an enlarged left atrium (LA) with a volume of 80 mL. Her blood pressure at the outpatient clinic was 151/80 mmHg, and the beta blocker bisoprolol 2.5 mg was newly prescribed for rate control. A pre-procedural ECG-gated computed tomography (CT) scan using non-ionic contrast medium was performed without adverse events 1 week before catheter ablation to assess the left atrial and pulmonary venous anatomy. Catheter ablation was performed with conscious sedation using dexmedetomidine (0.7 mcg/kg/h) and fentanyl (20 mcg/kg/h). Throughout the procedure, arterial pressure was invasively measured using a 4 Fr sheath inserted in the femoral artery. After coronary angiography and pulmonary venography, antral pulmonary vein isolation was performed under the guidance of a three-dimensional electro-anatomical mapping system (CARTO, Biosense Webster, Diamond Bar, CA, USA). Although her blood pressure at presentation to the laboratory was 120/76 mmHg and the sedation was appropriate with a Ramsay sedation score of 4–5, her systolic blood pressure began to dramatically fluctuate within a range of 80–255 mmHg. The intravenous injection of nicardipine 0.5 mg was repeated, but its effect was transient, and the BP remained totally uncontrolled. Particularly after the direct cardioversion of AF, her blood pressure was markedly elevated despite the administration of thiamylal sodium 100 mg. This situation fulfilled the definition of a hypertensive crisis. A low-voltage area suggesting advanced structural remodelling was broadly observed in the LA, and pulmonary vein isolation was followed by linear ablation at the mitral isthmus and superior vena cava isolation. Although the procedure was completed without complications, the LV ejection fraction after ablation was significantly decreased to 48% compared with 66% before ablation. We speculated the presence of secondary hypertension, and her serum catecholamine levels measured 4 weeks after ablation were found to be clearly elevated [adrenalin 0.03 ng/mL (normal range = 0.00–0.10 ng/mL), noradrenalin 3.36 ng/mL (0.10–0.50 ng/mL), and dopamine <0.01 ng/mL (0.00–0.03 ng/mL)]. A 24-hour urine test revealed a normal level of metanephrines of 0.11 mg/day (0.04–0.18) but an increased level of normetanephrine of 1.40 mg/day (0.10–0.28). An enhanced magnetic resonance imaging showed a 2.8-cm right-sided adrenal mass, and 123I-metaiodobenzylguanidine scintigraphy showed high accumulation in association with the tumour. Pheochromocytoma was highly suspected and doxazosin 2 mg was immediately prescribed. To stabilize her blood pressure and increase the circulating plasma volume, additional phased prescriptions of doxazosin 16 mg, prazosin 6 mg, propranolol 30 mg, and nifedipine 80 mg were required. Finally, surgery was performed 11 months after the ablation, and an adrenal mass consistent with pheochromocytoma was successfully resected. Although a slow AT with an atrial cycle length of 300 ms was observed after ablation, it never recurred after postoperative stabilization of the blood pressure. Her serum noradrenalin and urine normetanephrine levels returned to values within normal limits. During a follow-up period of 35 months, the patient has remained free of any episodes of AF or AT without the need for antiarrhythmic drugs, and her LV function has completely normalized.