With the development of advanced 3D mapping and ablation systems, catheter ablation procedures for arrhythmias have become routine in clinical practice and are strongly recommended by major guidelines. Although the current state-of-the-art systems have a high safety profile, complications can still arise from the thermal and/or electrical energy delivered. In this case report, we present a case of ST-segment elevation myocardial infarction with total occlusion of the right coronary artery, triggered by radiofrequency catheter ablation in the right atrium.

A 71-year-old male patient was referred to our center with a preliminary diagnosis of atrial tachycardia (AT) resistant to medical treatment (Figure 1). His medical history included hypertension, hyperlipidemia, and prior percutaneous coronary intervention (PCI) with coronary stent implantation in the left anterior descending artery (LAD). His current medications were acetylsalicylic acid 100 mg once daily, irbesartan/hydrochlorothiazide 300/25 mg once daily, metoprolol succinate 50 mg once daily, amiodarone 200 mg twice daily, and pitavastatin 2 mg once daily. With a resting heart rate of 62 BPM in sinus rhythm, medical therapy could not be further intensified, so radiofrequency ablation (RFA) of AT was planned.

Given the patient's complaints of angina during tachycardia episodes and his history of obstructive coronary artery disease, a diagnostic coronary angiography was performed before the AT ablation. It showed a patent LAD stent, a 40% narrowing in the mid-circumflex artery (Cx), and clinically insignificant plaques in the right coronary artery (RCA) (Figure 2).

Electroanatomical mapping of the AT was performed using the CARTO™ system and PENTARAY™ NAV eco catheter, which localized the AT focus between the tricuspid annulus and coronary sinus ostium. RFA was carried out with a Biosense-Webster Thermocool Smarttouch catheter at 35W power, 40°C cut-off temperature, and an irrigation speed of 15 cc/h. A successful ablation was indicated by an impedance drop of 10 Ω. After 14 ablation points, the AT was successfully terminated and could not be re-induced by subsequent tachycardia induction protocols (Figure 3). The patient was then transferred to the cardiology inpatient service for post-procedural monitoring.

A post-procedural electrocardiogram (ECG) revealed ST-segment elevation in leads II, III, and aVF (Figure 4). Upon questioning, the patient reported no angina, dyspnea, or other cardiac symptoms. The patient was urgently taken to the catheterization laboratory for a repeat coronary angiography, which revealed a 100% total occlusion in the distal RCA (Figure 5). The RCA was cannulated using a 6F JR-4 guiding catheter. Intracoronary nitroglycerin (100 μg and 200 μg) was administered, but without success. A floppy guidewire was then used to cross the lesion, and a 2.0 x 25 mm semi-compliant balloon was used for predilation.

Without access to intravascular imaging systems, the lesion was visually assessed with radiopaque injection, showing a hazy plaque. A 2.25 x 16 mm drug-eluting stent (DES) was implanted at nominal pressure. TIMI-3 flow was restored, and the patient was transferred to the coronary intensive care unit. A follow-up ECG showed >50% resolution of ST-segment elevations in leads II, III, and aVF (Figure 6). The patient was discharged the following day with the following medications: apixaban 5 mg twice daily, acetylsalicylic acid 100 mg once daily, clopidogrel 75 mg once daily, pitavastatin 2 mg once daily, irbesartan/hydrochlorothiazide 300/25 mg once daily, metoprolol succinate 50 mg once daily, and pantoprazole 40 mg once daily.

One of the typical locations for atrial tachycardia is adjacent to the coronary sinus ostium. This region provides easy catheter access but involves important anatomical structures. Aggressive ablation in this area may lead to inappropriate sinus tachycardia due to the proximity of the ganglion plexus at the junction of the inferior vena cava and left atrium.

Additionally, this region is near the circumflex artery (Cx) and right coronary artery (RCA). Ablation here may result in direct vascular damage or indirectly cause vasospasm due to thermal energy conduction. In our case, the distal RCA was likely damaged due to direct vascular injury.

Ablations in this area can also be painful. For this reason, pethidine hydrochloride was administered during the ablation procedure, which likely masked the pain of the subsequent myocardial infarction. Based on current knowledge, coronary vasospasm and plaque rupture can occur during ablation procedures.¹² This is usually caused by vasospasm, but rupture of vulnerable plaques may also occur.³⁴ If occlusion does not resolve with anti-vasospasm medications, percutaneous coronary intervention is required.⁵⁶⁷ It is crucial to closely monitor ECG changes during ablation in regions adjacent to coronary vessels, particularly in patients receiving sedation or analgesia.⁸