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Troponin rise in patients with atrial fibrillation: A marker of adverse prognosis and increased thromboembolic risk
Letters to the Editor
4889
Troponin rise in patients with atrial fibrillation: A marker of adverse prognosis and increased thromboembolic risk Rui Providência a,⁎, Luís Paiva b, Sérgio Barra c, Ana Faustino b a b c
Faculty of Medicine, University of Coimbra, Coimbra, Portugal Cardiology Department, Coimbra's Hospital Centre and University, Coimbra, Portugal Cardiology Department, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom
a r t i c l e
i n f o
Article history: Received 17 June 2013 Accepted 3 July 2013 Available online 22 July 2013 Keywords: Atrial fibrillation Troponin Prognosis Risk stratification Coronary artery disease Myocardial infarction
We have read with interest the article by Parwani and colleagues addressing the role of atrial fibrillation (AF) in induction of troponin release in patients presenting to the Emergency Department with AF and clinical symptoms suggestive of myocardial ischemia [1]. In face of their findings in 100 patients undergoing coronary angiography, of whom 23 had an elevated cardiac troponin I (N0.09 μg/L), the authors have suggested that troponin rise may be “falsely elevated” in this setting, since the prevalence of significant stenosis was similar irrespective of troponin rise: 26% in patients with positive troponin vs. 33% in patients with normal troponin (p = ns). However, we feel that, contrary to the author's opinion, troponin rise in this setting must be addressed with care in face of the recent evidence that we will shortly present. Conti and colleagues have recently shown that elevated cardiac troponin I is a predictor of poor outcome (a composite of stroke, acute coronary syndrome, revascularization, and global death) in patients presenting to the Emergency Department with AF lasting for less than 12 h [2]. The association of minor troponin elevations with an adverse prognosis in patients with AF has also been previously addressed by Van den Bos et al. in a prospective cohort study of 407 consecutive patients with AF admitted to the cardiology ward or intensive coronary unit (patients with ST elevation myocardial infarction were excluded) [3]. These authors have found that minor rises (N0.015 ng/ mL) were present in 20% of patients and associated with death, fatal myocardial infarction and major cardiovascular events (all-cause mortality, myocardial infarction and revascularization). ⁎ Corresponding author at: Serviço de Cardiologia do Hospital Geral, Centro Hospitalar e Universitário de Coimbra, Quinta dos Vales, S. Martinho do Bispo, 3041-801 Coimbra, Portugal. Fax: +351 239445737. E-mail address: [email protected] (R. Providência).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.026
As far as risk stratification of AF is concerned, minor rises in troponin seem also to have a major role in the prediction of thromboembolic events and may improve the discriminative capability of current risk classification schemes (CHADS2 and CHA2DS2-VASc), according to data from the “Randomised Evaluation of Long Term Anticoagulant Therapy” (RE-LY) trial biomarkers substudy [4]. Based on data from patients with AF undergoing transesophageal echocardiogram, this may be explained by the increased prevalence of markers of left atrial stasis (i.e., left atrial and left atrial appendage thrombi, dense spontaneous echocardiographic contrast and low flow velocities in the left atrial appendage), which are known to very strongly associate with embolism, and to increase in prevalence as troponin levels rise [5]. Therefore, we feel that minor elevations of troponin in patients with AF should be handled with care and not promptly assumed as false positives. In a first instance, ongoing myocardial ischemia should be ruled out if the clinical context is suggestive and the pretest probability is moderate or elevated. Then, even if the results are negative or the context is not suggestive of myocardial ischemia, an adequate prevention of thromboembolism should be considered, preferentially with anticoagulants, according to data of the RE-LY Biomarkers sub-analysis, if the bleeding risk of each particular patient is not prohibitive. The authors of this manuscript have verified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology and complies with the Statement on Matching Language to the Type of Evidence Used in Describing Outcomes Data [6]. References [1] Parwani AS, Boldt LH, Huemer M, et al. Atrial fibrillation-induced cardiac troponin I release. pii: S0167-5273(13)00518-4Int J Cardiol Apr 23 2013, http://dx.doi.org/ 10.1016/j.ijcard.2013.03.087. [2] Conti A, Mariannini Y, Viviani G, et al. Abnormal troponin level as short-term predictor of poor outcome in acute atrial fibrillation. Am J Emerg Med 2013;31(4):699–704. [3] van den Bos EJ, Constantinescu AA, van Domburg RT, Akin S, Jordaens LJ, Kofflard MJ. Minor elevations in troponin I are associated with mortality and adverse cardiac events in patients with atrial fibrillation. Eur Heart J 2011;32(5):611–7. [4] Hijazi Z, Oldgren J, Andersson U, et al. Cardiac biomarkers are associated with an increased risk of stroke and death in patients with atrial fibrillation: a Randomized Evaluation of Long-term Anticoagulation Therapy (RE-LY) substudy. Circulation 2012;125(13):1605–16. [5] Providência R, Paiva L, Faustino A, et al. Cardiac troponin I: prothrombotic risk marker in non-valvular atrial fibrillation. Int J Cardiol 2013 Aug 10;167(3):877–82. [6] Editors of the Heart Group Journals. Statement on matching language to the type of evidence used in describing outcomes data. Int J Cardiol 2013;66(1):1.
4889
Troponin rise in patients with atrial fibrillation: A marker of adverse prognosis and increased thromboembolic risk Rui Providência a,⁎, Luís Paiva b, Sérgio Barra c, Ana Faustino b a b c
Faculty of Medicine, University of Coimbra, Coimbra, Portugal Cardiology Department, Coimbra's Hospital Centre and University, Coimbra, Portugal Cardiology Department, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom
a r t i c l e
i n f o
Article history: Received 17 June 2013 Accepted 3 July 2013 Available online 22 July 2013 Keywords: Atrial fibrillation Troponin Prognosis Risk stratification Coronary artery disease Myocardial infarction
We have read with interest the article by Parwani and colleagues addressing the role of atrial fibrillation (AF) in induction of troponin release in patients presenting to the Emergency Department with AF and clinical symptoms suggestive of myocardial ischemia [1]. In face of their findings in 100 patients undergoing coronary angiography, of whom 23 had an elevated cardiac troponin I (N0.09 μg/L), the authors have suggested that troponin rise may be “falsely elevated” in this setting, since the prevalence of significant stenosis was similar irrespective of troponin rise: 26% in patients with positive troponin vs. 33% in patients with normal troponin (p = ns). However, we feel that, contrary to the author's opinion, troponin rise in this setting must be addressed with care in face of the recent evidence that we will shortly present. Conti and colleagues have recently shown that elevated cardiac troponin I is a predictor of poor outcome (a composite of stroke, acute coronary syndrome, revascularization, and global death) in patients presenting to the Emergency Department with AF lasting for less than 12 h [2]. The association of minor troponin elevations with an adverse prognosis in patients with AF has also been previously addressed by Van den Bos et al. in a prospective cohort study of 407 consecutive patients with AF admitted to the cardiology ward or intensive coronary unit (patients with ST elevation myocardial infarction were excluded) [3]. These authors have found that minor rises (N0.015 ng/ mL) were present in 20% of patients and associated with death, fatal myocardial infarction and major cardiovascular events (all-cause mortality, myocardial infarction and revascularization). ⁎ Corresponding author at: Serviço de Cardiologia do Hospital Geral, Centro Hospitalar e Universitário de Coimbra, Quinta dos Vales, S. Martinho do Bispo, 3041-801 Coimbra, Portugal. Fax: +351 239445737. E-mail address: [email protected] (R. Providência).
0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.026
As far as risk stratification of AF is concerned, minor rises in troponin seem also to have a major role in the prediction of thromboembolic events and may improve the discriminative capability of current risk classification schemes (CHADS2 and CHA2DS2-VASc), according to data from the “Randomised Evaluation of Long Term Anticoagulant Therapy” (RE-LY) trial biomarkers substudy [4]. Based on data from patients with AF undergoing transesophageal echocardiogram, this may be explained by the increased prevalence of markers of left atrial stasis (i.e., left atrial and left atrial appendage thrombi, dense spontaneous echocardiographic contrast and low flow velocities in the left atrial appendage), which are known to very strongly associate with embolism, and to increase in prevalence as troponin levels rise [5]. Therefore, we feel that minor elevations of troponin in patients with AF should be handled with care and not promptly assumed as false positives. In a first instance, ongoing myocardial ischemia should be ruled out if the clinical context is suggestive and the pretest probability is moderate or elevated. Then, even if the results are negative or the context is not suggestive of myocardial ischemia, an adequate prevention of thromboembolism should be considered, preferentially with anticoagulants, according to data of the RE-LY Biomarkers sub-analysis, if the bleeding risk of each particular patient is not prohibitive. The authors of this manuscript have verified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology and complies with the Statement on Matching Language to the Type of Evidence Used in Describing Outcomes Data [6]. References [1] Parwani AS, Boldt LH, Huemer M, et al. Atrial fibrillation-induced cardiac troponin I release. pii: S0167-5273(13)00518-4Int J Cardiol Apr 23 2013, http://dx.doi.org/ 10.1016/j.ijcard.2013.03.087. [2] Conti A, Mariannini Y, Viviani G, et al. Abnormal troponin level as short-term predictor of poor outcome in acute atrial fibrillation. Am J Emerg Med 2013;31(4):699–704. [3] van den Bos EJ, Constantinescu AA, van Domburg RT, Akin S, Jordaens LJ, Kofflard MJ. Minor elevations in troponin I are associated with mortality and adverse cardiac events in patients with atrial fibrillation. Eur Heart J 2011;32(5):611–7. [4] Hijazi Z, Oldgren J, Andersson U, et al. Cardiac biomarkers are associated with an increased risk of stroke and death in patients with atrial fibrillation: a Randomized Evaluation of Long-term Anticoagulation Therapy (RE-LY) substudy. Circulation 2012;125(13):1605–16. [5] Providência R, Paiva L, Faustino A, et al. Cardiac troponin I: prothrombotic risk marker in non-valvular atrial fibrillation. Int J Cardiol 2013 Aug 10;167(3):877–82. [6] Editors of the Heart Group Journals. Statement on matching language to the type of evidence used in describing outcomes data. Int J Cardiol 2013;66(1):1.