Asymptomatic Acute Inferior ST Elevation Myocardial Infarction from Thermal Injury Complicating Radiofrequency Ablation for Atri

Catheter-based radiofrequency ablation (RFA) is an increasingly utilized modality for the treatment of symptomatic tachyarrhythmias. It is both safe and effective, but complications do infrequently occur. We present a case of asymptomatic acute inferior ST elevation myocardial infarction from thermal injury following radiofrequency modification of the “slow pathway” for the treatment of atrioventricular nodal re-entrant tachycardia (AVNRT). Case Report. A 34-year-old female with a history of tobacco use, paroxysmal supraventricular tachycardia (SVT) and normal left ventricular function was referred for elective mapping and possible ablation for recurrent SVT. There was no antecedent history of coronary artery disease or stress testing. Typical AVNRT was induced using programmed atrial stimulation. AV nodal “slow pathway” modification was successful after targeting the superior portion of the coronary sinus os. Power and temperature settings were 50 watts and 60 °C, respectively, except for the lesion delivered at the coronary sinus os, which was 50°C. Three hours after the procedure, the patient developed asymptomatic non-sustained polymorphic ventricular tachycardia captured on telemetry as well as inferior ST elevation that was not electrocardiographically present at admission (Figure 1). Blood pressure was 113/72 mmHg, with a regular pulse of 80 beats per minute and an unremarkable physical examination. Laboratory studies revealed normal hematological indices, renal function and electrolytes. Creatine kinase (CK) was 542 U/L with an MB fraction of 29 ng/ml and troponin T of 1.07 ng/ml. Ultra-sensitive C-reactive protein was 1.6 mg/L. The patient was transferred to the coronary intensive care unit where bedside echocardiography revealed preserved left ventricular function and no significant valvular abnormalities or pericardial effusion but severe infero-posterior hypokinesis. The patient continued to remain asymptomatic despite persistent inferior ST elevation electrocardiographically. Urgent coronary angiography was performed which demonstrated an acute occlusion of a large posterior ventricular branch of the right coronary artery (RCA) (Figure 2). Note the proximity of the coronary sinus to the site of coronary occlusion (Figure 3). The patient underwent successful balloon angioplasty and deployment of a 2.5 x 18 mm Bx Velocity Hepacoat™ stent (Cordis Corporation, Miami, Florida) without complication (Figure 4). The peak CK was 1,136 U/L with an MB of 71 ng/mL. Discussion. One of the more common regular supraventricular tachyarrhythmias encountered in clinical practice is AVNRT. The mechanism of AVNRT in more than 90% of cases involves antegrade conduction down the “slow pathway” and retrograde conduction up the “fast pathway.” Radiofrequency modification of the slow pathway has evolved into the preferred treatment strategy. The AV nodal slow pathway is usually found on a 5–10 mm band of tissue known as the cavo-tricuspid isthmus located anterior to the coronary sinus os and posterior to the tricuspid annulus (Figure 5). Radiofrequency current is delivered to this site for 1–2 minutes with a target temperature of 60°C. Complications from AV nodal ablation can include bleeding at the site of venous access, infection, pneumothorax, AV block, thromboembolic complications, valvular damage and cardiac perforation with or without tamponade.1 Serious complications such as stroke, myocardial infarction and death occur in less than 3% of patients at 30 days according to a series of 1,050 patients who underwent RFA for accessory pathways, AVNRT and the AV node.2 The NASPE Prospective Voluntary Registry3 of 3,357 patients who underwent catheter ablation of all types suggests that the incidence of myocardial infarction as a complication is less than 0.1%. Myocardial necrosis at the site of RFA often leads to a rise in cardiac biomarkers that is commonly seen post-procedure, peaking at 8 hours, with troponin being a more sensitive biomarker than creatine kinase.4 A series of 23 patients undergoing linear RFA and 16 undergoing focal RFA demonstrated that linear ablations were more prone to myocardial injury than focal ablations as estimated by CK release (CK range, 45–1,583 U/L for linear ablations and 29–212 U/L for focal ablations).5 It is not known whether some of these patients actually had silent myocardial infarctions. Given the proximity of the coronary os ablation site, our patient was thought to have sustained thermal injury with subsequent inflammation and thrombosis of the posterior ventricular branch of the RCA secondary to the radiofrequency current. Further credence to this idea is given by the absence of coronary atherosclerosis elsewhere in the coronary tree. Experimental evidence in a porcine model of 16 pigs that underwent RFA of the cavo-tricuspid isthmus supports this.6 None had clinical evidence of myocardial ischemia electrocardiographically, but 14 had microscopic evidence of focal RCA inflammation within the adventitia and 2 within the vascular smooth muscle. The striking feature of this case was the complete absence of symptoms. It is possible that thermal injury also causes focal denervation potentially leading to silent myocardial infarction. This case illustrates an unusual mechanism leading to acute myocardial infarction as a complication of a commonly performed electrophysiology procedure that should be recognized by both interventionalists and electrophysiologists and treated aggressively with percutaneous revascularization.

1. Wellens HJJ. Catheter ablation of cardiac arrhythmias: Usually cure but complications may occur. Circulation 1999;99:195–197. 2. Calkins H, et al., for the ATAKR Multicenter Investigators. Catheter ablation for accessory pathways, atrioventricular nodal reentrant tachycardia and the atrioventricular junction: Final results of the multicenter clinical trial. Circulation 1998;98:262–270. 3. Scheinman MM, Huang S. The 1998 NASPE prospective catheter ablation registry. Pacing Clin Electrophysiol 2000;23:1020–1028. 4. Madrid AH, et al. Biochemical markers and C-troponin I release after radiofrequency catheter ablation: Approach to the size of the necrosis. In: Farre J, Moro C (eds). Ten Years of Radiofrequency Catheter Ablation. Armonk, New York: Futura Publishing Co., 1998:pp31–40. 5. Carlsson J, et al. Myocardial injury during radiofrequency catheter ablation: Comparison of focal and linear lesions. Pacing Clin Electrophysiol 2001;24:962–968. 6. Madrid AH, et al. Macroscopic and microscopic study of the right coronary artery after radiofrequency catheter ablation of the cavo-tricuspid isthmus in an experimental model. Rev Esp Cardiol 2001;54:693–702.