Europace Advance Access originally published online on April 17, 2007
Europace 2007 9(6):407-410; doi:10.1093/europace/eum046
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CRYOABLATION
ST segment elevation and chest pain during cryoablation of atrial flutter
1 Division of Cardiology, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden; 2 Clinical Experimental Research Laboratory, Sahlgrenska University Hospital/Östra, Göteborg, Sweden
Manuscript submitted 20 December 2006. Accepted after revision 3 March 2007.
* Corresponding author. Tel: +46 31 342 7552; fax: +46 31 82 32 41. E-mail address: birgitta.ingrid.johansson{at}vgregion.se
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Abstract |
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A 61-year-old male was treated with cryoablation for typical atrial flutter. Cryoablation was performed percutaneously with an 8-mm tip catheter to achieve a bidirectional conduction block of the cavo-tricuspid isthmus. When freezing at the point where bidirectional isthmus block occurred, the patient experienced chest pain and ECG showed ST segment elevations corresponding to the right coronary artery. Cryoablation may be painless per se, but patients should be told to report chest discomfort and surface ECG must be followed carefully during ablation.
Key Words: Atrial flutter, Ablation, Cryo, Chest pain
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Introduction |
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Catheter ablation of typical atrial flutter can be performed with a high procedural success, both acute and long-term.1
Radiofrequency (RF) energy, although effective, frequently causes some degree of pain or discomfort during ablation between the tricuspid valve and the inferior vena cava. Cryoenergy is an exciting alternative energy source that has long been used in open heart arrhythmia surgery.2 In percutaneous catheter ablation, cryoenergy has proven useful in ablation of different supraventricular tachycardias, including isthmus ablation of right-sided typical atrial flutter and pulmonary vein isolation of atrial fibrillation.3 Cryoenergy has the advantage of being painless and is supposed to be less harmful than RF energy to adjacent structures in the isthmus area, such as the right coronary artery (RCA).3–5 |
Case report |
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A 61-year-old man, with an intolerance to gluten but otherwise previously healthy, had frequent documented episodes of typical atrial flutter for a period of 6 years and, on one occasion only, atrial fibrillation. Echocardiography showed a normal ejection fraction, enlarged left atrium, 25 cm2, and normal right atrium, 17 cm2. He had tested treatment with sotalol, but immediately before the ablation he was on flecainide together with a betablocker and warfarin. It was evident that his symptoms were explained by 2:1 blocked atrial flutter, which was therefore the target of the ablation procedure. The patient was given a slight sedation before the procedure. His systolic blood pressure was 90 mm Hg and he was in sinus rhythm 43 bpm. Under local anaesthesia a quadripolar steerable catheter (BARD 6F, Dynamic XT, Bard Electrophysiology Div., USA) was inserted into the coronary sinus (CS) via the left femoral vein. A duodecapolar halo catheter (Halo XP, 7F, Biosense Webster, CA, USA) was introduced via the right femoral vein to a position along the lateral atrial wall down to the isthmus region. Finally, a 9 French quadripolar cryoablation catheter with an 8-mm tip (Freezor max, Cryocath Technologies Inc., Canada) was placed across the isthmus rather septally by means of frontal as well as left oblique views to a position where a large ventricular signal and small atrial signal were obtained. The cryoablation catheter was then connected to a cryo console filled with nitrous oxide (Cryocath Technologies Inc., Canada). Cryoablation was started in a point by point fashion during coronary sinus stimulation at a 500 ms stimulation interval with 40 s of freezing to a maximum of –80°C in each point. After successive withdrawal, a bidirectional block resulted at 29 s of ablation 6, which was then extended to 6 min (Figure 1). After completed ablation, partial reconduction appeared and ablation proceeded to the next point, where again a bidirectional block quickly occurred (Figure 2). Ablation was carried out for 4 min, and the block persisted. A decision was made to give an extra 2 min of ablation in the same point. At the very end of that additional freezing period, the patient felt a slight oppression which he did not report until questioned later.
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The bidirectional block persisted after ablation was completed. When coronary sinus stimulation was stopped, pronounced ECG changes with ST segment elevations in leads II, aVF, III, V4–V6, and reciprocal ST depressions in V1–V3 and aVL, I and -aVR were observed (Figure 3). The patient felt moderate chest pain with radiation to the left arm. The systolic blood pressure was 95 mm Hg. During the next few minutes no or just slight regression of the ST changes was seen. Morphine 2.5 mg was given intravenously, nitroglycerine 0.5 mg sublingually and, because of short self-terminating ventricular tachycardias, lidocaine 50 mg was also given intravenously.
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A decision was made to perform an acute coronary angiography. All three catheters were removed and the patient was transferred to an adjacent angiography laboratory. Telemetry revealed that the ECG normalized just before the patient was moved. The chest and arm pain had disappeared and the patient was haemodynamically stable. Acute echocardiography showed inferolateral hypokinesia but no pericardial effusion.
Coronary angiography (Figure 4) was performed in normal sinus rhythm, while the surface ECG was normal. This showed no pathological changes in the coronary arteries. A couple of ecstasies were noted in the RCA, one in the position where it would most likely be closest to the closest position of the ablation catheter. Coronary flow was uninhibited but there was a slight attenuation of the shadow of about 1 cm of the artery. Two experienced angiographists found nothing definitely abnormal but, as a thrombus formation could not be excluded, the patient was subsequently treated with a combination of enoxaparin and aspirin 320 mg daily for 2 days. The subsequent course was uneventful.
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Discussion |
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A spasm of the RCA occurring during cryoablation of the isthmus area was described by Rodriguez et al.3
The onset was rapid in our patient, as was resolution, and there were no sequelae. There was a release of cardiac enzymes with CK-MB max 42 µg/L (N 
5 µg/L) and troponine T 0.62 µg/L (N 0,03 µg/L) on the day of ablation, and CK-MB was 17 µg/L and troponine T 0.55 µg/L the following morning. As the enzyme release occurred during normal haemodynamic conditions, a temporary occlusion or severely impaired coronary flow seems to be the explanation. Symptoms were present for about 1 min before the ECG abnormalities were detected and the patient complained of pain radiating to the left arm and hand. The whole sequence from the start to the disappearance of symptoms took 13 min.
During ablation, the surface ECG leads V2 and V4, CS 3,4, the ablation signal and halo signals H1,2–H19,20 were displayed. The ECG abnormalities were seen to start about 54 s into the last 2-min ablation. One immediate conclusion was that the ablation channel must be removed from the screen during each freezing in subsequent procedures in order not to obscure the interpretation of the surface ECG leads.
During freezing, a ball of ice forms around the catheter tip and underlying tissue. The size of the cryoablation lesion depends on four factors: the temperature of the cryoprobe, the diameter of the cryoprobe head, the exposure time, and the myocardial temperature.2,6 The advantages of cryo over RF are preservation of tissue architecture, minimal thrombus formation, non-arrythmogenic lesions, and lack of pain during energy delivery.2,6,7 Cryolesions created at –75°C are as deep as RF lesions but are more focused.4
The exact reason for the event is unknown. Air embolism is not likely, since we did not use sheaths where air could have leaked into the system. The ablation catheter was removed before the angiography and might have given an idea of where the ablation was made in relation to the RCA. We believe that there was a close relation because the situation quickly resolved without angiographically visible sequelae and that the time it took corresponds to the time it would take for the ball of ice around the catheter electrode to thaw. It is likely that the last 4 + 2 min of freezing took part in the same point, but, since 62 s passed before the last 2 min, it cannot be excluded that the catheter moved slightly.
The event occurred while freezing in the exact spot at which the bidirectional block was obtained. We have never observed the same phenomenon with RF energy, neither in effective nor ineffective sites. One total thrombotic occlusion of the posterior left ventricular branch of the RCA has been reported.8 In that patient, an 8-mm tip ablation catheter, capable of deep lesion formation, together with a high-wattage output from the RF generator (100 W), was placed to the posterior (septal) side of the cavo-tricuspid isthmus. On angiography, a > 70% stenosis was seen on the mid portion of RCA, probably impairing the cooling blood flow. In another report, histopathological findings after successful RF ablation of isthmus with an 8-mm tip catheter showed an intramural haemorrhage in the RCA adjacent to the side of the lesion.9
We used 40 s of freezing for ‘mapping’ and extended this to 4–6 min if an effect was seen. The first 4 min were uneventful and the event started during the period of additional freezing. It was necessary to stop the procedure before the traditional line had been completed. An interesting question is whether it is necessary to complete the isthmus-cava line after a stable bidirectional block has been obtained. Since no effect at all on the conduction across the isthmus during coronary sinus stimulation was obtained in the first four freezing points, and this was followed by an increase of the conduction time during ablation 5 and a complete effect during ablations 6 and 7, the critical gap in this patient was very narrow. Montenero et al. found that the critical area was often located in the inferior rim of the CS os where the final cryoablation was applied. In this way of isolating the inferior rim of the CS os from the right atrium, they achieved a bidirectional block without creating a complete isthmus line and reported an acute success rate of 92.1% in patients with common atrial flutter.4
We conclude that coronary flow was transiently severely impaired during cryoablation in the effective site, producing a bidirectional block and that no definitely abnormal findings were seen after recovery and coronary angiography 27 min later. For safety reasons, we gave enoxaparin and aspirin for 2 days. The noise during ablation should be avoided by removing the ablation signal from the screen during freezing, so that available surface ECG leads can be seen and followed well enough during ablation. The ablation may be painless per se, but patients should be told to report any discomfort, whether or not they find it endurable.
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References |
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[1] Jais P, Shah DC, Haissaguerre M, Hocini M, Garrigue S, Le Metayer P, et al. Prospective randomized comparison of irrigated-tip versus conventional-tip catheters for ablation of common flutter. Circulation (2000) 101:772–6.
[2] Lustgarten DL, Keane D, Ruskin J. Cryothermal ablation: Mechanism of tissue injury and current experience in the treatment of tachyarrhythmias. Prog Cardiovasc Dis (1999) 41:481–98.[CrossRef][Web of Science][Medline]
[3] Rodriguez LM, Geller JC, Tse HF, Timmermans C, Reek S, Lee KL, et al. Acute results of transvenous cryoablation of supraventricular tachycardia (atrial fibrillation, atrial flutter, Wolff-Parkinson-White syndrome, atrioventricular nodal reentry tachycardia). J Cardiovasc Electrophysiol (2002) 13:1082–9.[CrossRef][Web of Science][Medline]
[4] Montenero AS, Bruno N, Antonelli A, Mangiameli D, Murphy O, O'Connor S, et al. Safety and efficacy of cryoablation catheter for the treatment of atrial flutter: acute and long-term results. Ital Heart J (2004) 5((Suppl. 1)):131–7.
[5] Skanes AC, Yee R, Krahn AD, Klein GJ. Cryoablation of atrial arrhythmias. Cardiac Electrophysiol Rev (2002) 6:383–8.[CrossRef][Medline]
[6] Rodriguez LM, Leunissen J, Hoekstra A, Korteling BJ, Smeets JL, Timmermans C, et al. Transvenous cold mapping and cryoablation of the AV node in dogs: observations of chronic lesions and comparison to those obtained using radiofrequency ablation. J Cardiovasc Electrophysiol (1998) 9:1055–66.[Web of Science][Medline]
[7] van Ouveren W, Crijns HJ, Korteling BJ, Wegereef EW, Haan J, Tigchelaar I, et al. Blood damage, platelet and clotting activation during application of radiofrequency or cryoablation catheters: a comparative in vitrostudy. J Med Eng Technol (1999) 23:20–5.[CrossRef][Web of Science][Medline]
[8] Ouali S, Anselme F, Savouré A, Cribier A. Acute coronary occlusion during radiofrequency catheter ablation of typical atrial flutter. J Cardiovasc Electrophysiol (2002) 13:1047–9.[CrossRef][Web of Science][Medline]
[9] Weiss C, Becker J, Hoffmann M, Willems S. Can radiofrequency current isthmus ablation damage the right coronary artery? Pacing Clin Electrophysiol (2002) 25:860–2.[CrossRef][Medline]
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