Europace Advance Access originally published online on June 6, 2007
Europace 2007 9(9):854; doi:10.1093/europace/eum114
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LETTERS TO THE EDITOR
IMA—the role of oxidative stress
St Georges Hospital Medical School
Cranmer Terrace
London SW17 0RE
UK
St Georges Hospital Medical School
Cranmer Terrace
London SW17 0RE
UK
Tel: +44 7984443250 E-mail address: droy{at}sghms.ac.uk/ droy{at}sgul.ac.uk
In a recent paper, Sbarouni et al.1
report that unlike cardiac troponin, ischaemia modified albumin (IMA) plasma levels did not change significantly in patients undergoing radiofrequency (RF) ablation. They interpret these findings as an expression of RF induced myocardial necrosis without preceding ischaemia. Previous studies from our group have shown that IMA levels increase after RF ablation.2 The discrepancies between the two studies, which included relatively similar patients, are intriguing and deserve further explanation. In our study,2 IMA levels increased significantly after 30 min and returned to baseline at 8 h. We obtained an early (30 min) sample as previous data from our group indicated that IMA levels increase within 30 min following balloon inflation during percutaneous coronary intervention (PCI).3 Furthermore, IMA levels have been shown to be elevated 1 h after direct current cardioversion.4 In the Sbarouni et al.'s1 study, samples were taken immediately after RF ablation and 2 h later. It is therefore conceivable that because of the transient nature of IMA elevation, the optimal time frame for detecting the increase in IMA levels could have been missed in this study. Little data exist regarding the release kinetics of IMA in different clinical settings. In addition to the above, discrepancies between the two studies could also relate to the differences in sample storage temperature and handling, which may affect IMA values. Differences in patient albumin levels could have also affected IMA results. IMA measurements by the Albumin Cobalt Binding test appear also to be affected by lactate production.5
Another important consideration is that although it has been demonstrated that IMA levels increase during myocardial ischaemia triggered by a primary reduction of blood flow, as seen in patients during PCI3 and the acute coronary syndrome,6 myocardial ischaemia may not necessarily be the only trigger for IMA elevation in plasma. In our RF ablation study,2 where IMA levels increased after the procedure, we purposely excluded patients with the potential for myocardial ischaemia in any vascular territory, including peripheral vascular disease. We have suggested that IMA elevations are likely to be the result of oxidative stress.7 Thermal injury of myocardial cells that occurs during RF ablation leads to a rapid release of electrolytes and free radicals from intracellular sites.8 Direct current countershocks to the heart have also been shown to result in free radical production.9 It can therefore be speculated that the underlying mechanism of IMA formation in these settings is oxidative stress-related damage to the N-terminus of albumin associated with the release of reactive oxygen species. Indeed, results from in vitro work from our group support this hypothesis and suggest that the generation of reactive oxygen species can at least transiently modify the N-terminal region of albumin to yield increased levels of IMA.7
The effect of oxygen radical production and other substances like lactate may have implications regarding the clinical utility of this biomarker. Increased oxygen free radical production is commonly found in a wide variety of medical conditions other than myocardial ischaemia and this may partly explain IMA's baseline variability and low specificity for the detection of acute coronary syndrome.6
Further studies are required to understand the mechanisms leading to increased IMA levels during myocardial necrosis, whether preceded or not by myocardial ischaemia. Future work also needs to focus on the exact nature of albumin modification especially in the context of reactive oxygen species generation.
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[1] Sbarouni E, Geoorgiadou P, Panagiotakos D, Livanis EG, Theodorakis GN, Kremastinos DT. Ischemia modified albumin in radiofrequency catheter ablation. Europace (2007) 9:127–9.
[2] Roy D, Quiles J, Sinha M, Floros D, Gaze D, Collinson P, et al. Effect of radiofrequency catheter ablation on the biochemical marker ischemia modified albumin. Am J Cardiol (2004) 94:234–6.[CrossRef][Web of Science][Medline]
[3] Sinha MK, Gaze DC, Tippins JR, Collinson PO, Kaski JC. Ischemia modified albumin is a sensitive marker of myocardial ischemia after percutaneous coronary intervention. Circulation (2003) 107:2403–5.
[4] Roy D, Quiles J, Sinha M, Aldama G, Gaze D, Kaski JC. Effect of direct current cardioversion on ischemia modified albumin levels in patients with atrial fibrillation. Am J Cardiol (2004) 94:234–6.[CrossRef][Web of Science][Medline]
[5] Zapico-Muniz E, Santalo-Bel M, Merce-Muntanola J, Montiel JA, Martinez-Rubio A, Ordonez-Llanos J. Ischemia-modified albumin during skeletal muscle ischemia. Clin Chem (2004) 50:1063–5.
[6] Sinha MK, Roy D, Gaze D, Collinson PO, Kaski JC. Role of ischemia modified albumin: a new biochemical marker of myocardial ischaemia, in the early diagnosis of acute coronary syndromes. Emerg Med J (2004) 21:29–34.
[7] Roy D, Quiles J, Gaze D, Collinson PO, Kaski JC, Baxter GF. Role of reactive oxygen species in the formation of the novel diagnostic marker ischemia modified albumin. Heart (2006) 92:113–4.
[8] Erdogan A, Carlsson J, Grumbrecht S, Kostin S, Schulte B, Schlapp M, et al. Electrochemical potentials during radiofrequency energy delivery: a new method to control catheter ablation of arrhythmias. Europace (2001) 3:201–7.
[9] Caterine MR, Spencer KT, Pagan-Carlo LA, Smith RS, Buettner GR, Kerber RE. Direct current shocks to the heart generate free radicals: an electron paramagnetic resonance study. J Am Coll Cardial (1996) 28:1598–60.[Abstract]
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