An unusual treatment of coronary injury following radiofrequency ablation in a 5‐year‐old child: Systemic steroid usage

Radiofrequency catheter ablation (RFCA) procedure is performed for many tachyarrhythmias. We performed successful RFCA in a 5‐year‐old child for supraventricular tachyarrhythmia and Wolff‐Parkinson‐White syndrome. Acute circumflex artery (CxA) occlusion occurred due to RFCA. After percutaneous balloon angioplasty was performed into the CxA, the patient was treated with systemic steroid to resolve myocardial edema. To the best of our knowledge, systemic steroid was used first time for acute coronary artery injury related myocardial ischemia.

Keywords: acute coronary artery injury; percutaneous coronary intervention; radiofrequency catheter ablation; systemic steroid

Radiofrequency catheter ablation (RFCA) procedure is accepted as a safe and effective treatment modality for many tachyarrhythmias.1 Although there is an increase in the performance of RFCA procedure and success rates in recent years, it has still several acute and chronic complications. Acute coronary injury is a quite rare complication of RFCA with an incidence of approximately 0.2% from a large retrospective study.2 The close proximity of coronary arteries to common sites of ablation can result in acute coronary injury after performing RFCA due to some different mechanisms such as coronary spasm, thromboembolism, direct vessel trauma, or spontaneous plaque rupture. Acute coronary occlusion is also potentially a life‐threatening complication of the procedure.3 We herein present a case of systemic steroid usage for acute circumflex artery (CxA) occlusion due to RFCA in a 5‐year‐old child.

A 5‐year‐old boy (23 kg) was referred to our institution for RFCA of medication‐resistant supraventricular tachyarrhythmia and Wolff‐Parkinson‐White syndrome. His electrocardiography revealed short PR interval and preexcitation with delta wave in precordial leads (Figure 1A). His echocardiography demonstrated normal left ventricle function and bicuspid aortic valve with mild aortic regurgitation. Electrophysiological study (EPS) using Ensite Precision 3D electro‐anatomic mapping was performed under general anesthesia. Diagnostic catheters were positioned to the high right atrium, coronary sinus (CS), and right ventricle. For the risk stratification of accessory pathway effective refractory pathway (APERP), APERP was 270 ms and the fastest preexcitation conduction was 275 ms during atrial fibrillation. Orthodromic supraventricular tachycardia (SVT) with cycles length of 300 ms was stimulated by programmed stimulations (Figure 1B). Ventriculo atrial (VA) conduction was eccentric into the CS catheter and the earliest VA interval was nearest to the distal CS (Figure 1B). The earliest atrioventricular stimulation was on CS 3‐4 level while delta wave was also present during sinus rhythm. Thus, the left‐sided AP was demonstrated, and then, transseptal puncture was performed to reach to left atrium. Active clotting time was >250 s by administrating intravenous heparin. The location of AP was on left lateral side by using electro‐anatomic mapping during SVT. AP was disappeared in fourth attempt by RF lesion with 35 W, 48‐50°C, and 103 Ω via 7F‐4 mm RFCA catheter (Figure 1C,D). Preexcitation was disappeared after RFCA was repeated two times for 30 seconds (Figure 1E). However, hypotension (60/30 mm Hg) and acute ST segment elevation in inferior leads were screened 2 minutes later after the RFCA (Figure 1F) while arterial blood gas analysis was normal. While pericardial effusion was excluded by transthoracic echocardiographic evaluation, mild mitral regurgitation was monitored. Thus, acute coronary event was thought. Then, coronary angiography was performed immediately via right femoral artery with 6F arterial sheat. The right coronary artery was patent. The left main coronary artery ostium was selectively cannulated with a Judkins Left 3.5F guiding catheter and, total occlusion of the posterolateral branch of the CxA was demonstrated (Figure 2A). Acetylsalicylic acid 300 mg and clopidogrel 150 mg were given immediately via nasogastric tube. Intravenous 2000 IU heparin bolus was given during the percutaneous intervention. Then, additional heparin treatment was given when required to achieve an activated clotting time of 250‐350 seconds. After heparin treatment, the total occluded segment was passed through by 0.014′ floppy guidewire. After that, it was dilated with 1.2 × 8 mm, 1.5 × 15 mm, and 2 × 20 mm semi‐compliant coronary balloons, respectively (Figures 2B‐D). Then, the CxA was observed as patent (Figure 2E). After performing balloon angioplasty, regression of the ST segment elevation was observed (Figure 2F) and hemodynamic status of the patient was normal with the blood pressure of 100 of 70 mmHg. After the procedure, the patient was treated with intravenous dexamethasone 4 × 0.15 mg/kg during 1 week to remove the edematous affect of RFCA on ventricular myocardium. Oral 100 mg acetylsalicylic acid, 20 mg clopidogrel and 3 × 15 mg diltiazem treatment were also added to therapy. The patient was discharged from the hospital 1 week later after the percutaneous intervention without any symptom. One month later after the intervention, control coronary angiography revealed that the CxA was patent (Figure 2G), and the patient was still asymptomatic. We planned to continue the oral therapy during 6 months.

Radiofrequency ablation is frequently used to treat several arrhythmias such as Wolff‐Parkinson‐White syndrome, atrial tachyarrhythmia, and ventricular tachyarrhythmia.1 RFCA treatment procedure generally exhibits high efficacy and safety results. However, it can be related with some complications including pericardial effusion or cardiac tamponade, peri‐procedural cerebrovascular accident, atrio‐esophageal fistula, pulmonary vein stenosis, coronary artery injury, and peripheral vascular complications such as deep vein thrombosis, pseudoaneurysm, and catheter insertion site hematoma. These complications rates vary from 1 to 5% in recent studies.4 Coronary artery injury is one of the rarest complications of RFCA. In a study by Calkins et al, 250 consecutive patients with Wolff‐Parkinson‐White syndrome or paroxysmal supraventricular tachycardia involving a concealed accessory AV connection undergoing RFCA were evaluated and coronary artery injury was demonstrated with the incidence of 0.2%.2 However, the actual incidence of coronary artery injury may be more often than reported due to the close proximity of common ablation sites to coronary arteries. Undetected or asymptomatic injury can cause this suggestion. In a prospective study by Schneider, 212 consecutive patients younger than 21 years with supraventricular tachyarrhythmia were evaluated and selective coronary angiography was performed before and 30 minutes after RFCA or cryoablation. In two of 117 patients (1.7%) who had RFCA for an accessory pathway, an acute reduction in luminal diameter of the coronary artery adjacent to the ablation site was observed.5 The most important reason of this injury is the anatomic relation of the coronary arteries and targeted ablation sites. The CxA lies in the epicardium of the atrioventricular groove. It is also in a close proximity to the CS and mitral isthmus. So, it is under a risk of damage during RFCA. Additionally, in a study, it was demonstrated that the CxA was ≤2 mm from the lateral mitral annulus in 24% of patients.6 Unsurprisingly, in our patient, left‐sided accessory pathway ablation resulted in CxA occlusion. RFCA‐depended acute coronary injury can occur due to coronary spasm, thromboembolism, or direct vessel trauma. Coronary spasm is the most common cause of RFCA‐related coronary artery injury. The underlying mechanism of the spasm is the increase in autonomic activity at nerve terminals in the densely innervated left atrium.7‐8 Although spasm can resolve with nitrates treatment, we could not give nitrates due to hypotension of the patient. Additionally, spasm is generally resistant to nitrates. However, we could not rule out coronary spasm because we did not try nitrates. Therefore, we treated our patient with diltiazem therapy for possible coronary spasm association. RFCA also causes functional and morphological damage to the coronary artery endothelium results in impairment of regulating vascular tone and coagulation results in increasing thrombosis. Furthermore, left‐sided ablation strategies can cause coronary thromboembolism. However, we did not think that the possible mechanism of coronary occlusion was thromboembolism in our patient due to recurrent occlusions despite balloon angioplasty. The other mechanism of RFCA‐related coronary artery injury is heat‐induced collagen shrinkage and subsequent vessel narrowing. It is known that heat‐induced denaturation of collagen fibers in the vessel wall causes coronary artery stenosis. The application of RFCA results in acute edema with wall thickening and luminal narrowing.9 It could be one of the most important underlying mechanisms of coronary artery occlusion in our patient. Thus, in our patient, systemic steroid treatment was given to reduce the edematous effect of RFCA on left ventricle. To the best of our knowledge, it was the first case report of successful systemic steroid usage in a patient with acute coronary injury due to RFCA. Additionally, spontaneous coronary plaque rupture can also be seen during RFCA procedure. However, young age of the patient suggests that this was unlikely. At this point, additional imaging modality may provide us useful information to detect underlying mechanism of coronary occlusion. However, we have not tried any extra imaging methods such as intravascular ultrasound (IVUS) or optical frequency‐domain imaging (OFDI) due to the technical insufficiency. In the light of foregoing data, although nitrates can resolve coronary artery occlusion, it could not be performed in the presence of serious hypotension. Percutaneous coronary interventions with or without stent implantation are the other treatment strategies. However, we could not deploy stent into the coronary artery due to the younger age of the patient and smaller vessel diameter. In some cases, spontaneous regression of coronary injury without mentioned treatment modalities was demonstrated in the literature. Some procedural characteristics can reduce coronary artery injury. Minimal radiofrequency energy delivery is protective, especially in younger patients in whom coronary arteries may have close relation to the ablation site. And it is also important in patients with known coronary artery disease. The other proposed protective strategy is intracoronary chilled saline irrigation.10 In addition to these, use of smaller tip catheters prior to RFCA and fluoroscopic catheter position confirmation are important to reduce coronary artery injury.11 It is also known that cryoenergy has a lower risk of coronary injury than radiofrequency.9

Coronary artery injury is extremely rare and can be a life‐threatening complication of RFCA. Although different underlying mechanisms are described, optimal treatment modality is still uncertain. The most important point is early diagnosis and therapy for this event. However, systemic steroid was used first time to reduce left ventricle edema linked to RFCA.

• Acute coronary artery injury during RFCA can be a life‐threatening complication even if experienced operators.
• Invasive pediatric and adult cardiologists should be able to work together in the same laboratory under the necessary conditions.
• Some equipment for percutaneous coronary intervention such as guidewire and balloon can be used in children by experienced cardiologists.
• Stent deployment should not be the first step therapy for acute coronary injury in children while the procedure can be finished with balloon angioplasty alone.
• Steroid treatment should not be ignored unlike other types of acute myocardial ischemia.

The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.