Acute coronary occlusion following radiofrequency catheter ablation has previously been reported as a very rare complication in the treatment of accessory pathways.1 We report a case of acute coronary occlusion following a routine atrial flutter ablation. Previously, there has been only one case of acute coronary occlusion following atrial flutter ablation reported in the literature.4 To our knowledge, such a case has never been reported in a patient without known prior coronary disease. Case Report. A 70-year-old male with a history of hypertension and remote benign cerebral tumor was referred to the Winthrop Pacemaker-Arrhythmia Center for ablation of paroxysmal atrial flutter that had been documented on a 12-lead electrocardiogram. He was a remote smoker, but had no other known coronary risk factors. Several months prior to this admission, the patient underwent exercise SPECT myocardial perfusion imaging which revealed no abnormalities. An electrocardiogram done on routine pre-operative testing revealed a normal sinus rhythm at 70 bpm with first degree AV block and an isolated Q-wave in lead III. At the onset of the procedure, the patient had normal sinus rhythm. Using a 20-pole isthmus mapping catheter, a clockwise typical atrial flutter pattern was observed spontaneously. A separate 8 mm peanut ablation catheter was placed within the cavotricuspid isthmus near the tricuspid annulus. Bidirectional isthmus block was achieved via spot welding with multiple applications of RF energy at 30 Watts for 45 seconds. Immediately following RF ablation, the patient complained of mild chest discomfort. ST-segment elevation was noted in leads II, III, and aVF. He immediately received 325 mg of aspirin, two sublingual nitroglycerins, and was emergently transferred to the catheterization lab, where coronary angiography revealed an occlusion of the right coronary artery in its distal portion (Figure 1). The remainder of the right system and the left system were free of disease. Primary angioplasty and stenting of the right coronary artery lesion was performed with an excellent result (Figure 2). The patient remained asymptomatic and the echocardiogram performed post-procedure and prior to discharge revealed a normal LVEF (56-59%) with no apparent wall motion abnormalities. The patient s peak Troponin I was 9 mg/dl. Discussion. This is the second reported case of right coronary artery (RCA) occlusion secondary to radiofrequency ablation of atrial flutter at the cavotricuspid isthmus. Review of the literature revealed only seven case reports with any reference to acute coronary occlusion secondary to radiofrequency catheter ablation.3-9 Of these, only one was related to RF ablation of atrial flutter.4 In the Multicentre European Radiofrequency Survey of radiofrequency catheter ablation of arrhythmias,2 arterial thrombosis was extremely rare following this procedure, on the order of 0.1-0.7%, and most of these events involved ablation of accessory pathways or ventricular tachycardia. Transient myocardial ischemia was reported in 1 of 141 patients who underwent catheter ablation of atrial tachycardia or atrial flutter.2 The effects of RF ablation on coronary vessels has been studied previously in an animal model using young pigs.11 Involvement of the main RCA was documented histologically in three of eight animals, one year after RF application to the right atrium. Previous studies have also shown edema and lymphocytic infiltration of the coronary arteries in three of five pigs at 48 hours.12 Bokenkamp et al.11 postulated that several factors affect lesion characteristics after RF ablation in pigs: 1) small heart size; 2) long energy exposure; and 3) short distance between the ablation site and the right coronary artery. Various small, long-term studies in human subjects failed to show any altered angiographic coronary artery anatomy.10 The inferior right atrial isthmus has been described anatomically.14 The anterior sector of this area is located adjacent to the hinge of the tricuspid valve. This is a smooth vestibule of the tricuspid valve that is made up of a thin layer of myocardium (0.5-5.0 mm thick). The RCA and small nerve bundle are found at the epicardial surface of this vestibule within the tissues of the atrioventricular groove. Lesions up to 7 mm deep can be observed using catheters with an 8 mm tip,15 as was used in this case. In our case, this patient had normal perfusion on a recent exercise stress test. The absence of atherosclerosis elsewhere on the angiogram, as well as the location of the occlusion, suggest that the occlusion was associated with the RF ablation. Whether a previous non-obstructive lesion that was not hemodynamically significant was present previously cannot be excluded. We believe there are two possible explanations leading to this RCA occlusion: 1) the thin muscle layers between the ablation site and the RCA; and 2) the use of an 8 mm tip ablation catheter. In contrast to the previous case report on this subject, we have no evidence to suggest that a previous lesion may have contributed to this process. Acute coronary occlusion is a very rare, but reported complication of radiofrequency catheter ablation. When ablating near the cavotricuspid isthmus, consideration should be given to the use of smaller tipped catheters and lower duration and power output of RF energy. Given the proximity of the ablation to the RCA, there should be a high index of suspicion for RCA occlusion when applying RF energy to the cavotricuspid isthmus. Reprinted with permission from the Journal of Invasive Cardiology 2005;17:92-93.