- Email: [email protected]
Melatonin and myocardial protection
Letters to the Editor [4] Vasan RS. Biomarkers of cardiovascular disease: molecular basis and practical considerations. Circulation 2006;113:2335–62. [5] Sebastián-Gámbaro MA, Lirón-Hernández FJ, Fuentes-Arderiu X. Intra- and interindividual biological variability data bank. Eur J Clin Chem Clin Biochem 1997;35:845–52. [6] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Inflammatory systemic biomarkers in setting acute coronary syndromes—effects of the diurnal variation. Curr Drug Targets 2009;10:1001–8. [7] Nicholls SJ, Hazen SL. Myeloperoxidase and cardiovascular disease. Arterioscler Thromb Vasc Biol 2005;25:1102–11.
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[8] Dominguez-Rodriguez A, Abreu-Gonzalez P. Current role of myeloperoxidase in routine clinical practice. Expert Rev Cardiovasc Ther 2011;9:223–30. [9] Morrow DA. Appraisal of myeloperoxidase for evaluation of patients with suspected acute coronary syndromes. J Am Coll Cardiol 2007;49:2001–2. [10] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Diurnal variation of circulating myeloperoxidase levels in patients with ST-segment elevation myocardial infarction. Int J Cardiol 2010;144:407–9. [11] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.03.019
Melatonin and myocardial protection Ronit Lavi a, Shahar Lavi b,⁎ a b
Department of anesthesia and perioperative medicine, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada Department of Medicine, Division of Cardiology, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada
a r t i c l e
i n f o
Article history: Received 21 March 2011 Accepted 25 April 2011 Available online 17 May 2011 Keywords: Ischemic conditioning Melatonin Reperfusion injury
To the Editor: In our review article, we described the mechanisms and possible clinical application of conditioning of the heart. We focused our review on different modes of applying ischemic conditioning and provided some data regarding medications that may have a similar protective effect [1]. To date, no medication was proved to be protective against ischemia–reperfusion injury. Mitochondrial permeability transition pores (MPTP) seem to be involved in the mechanism of ischemic conditioning. Therefore, any drug or substance that inhibits MPTP function may have a protective effect similar to ischemic conditioning. The most relevant medication that was studied in humans in the setting of an acute myocardial infarction is cyclosporine, a potent inhibitor of MPTP. Indeed in a pilot study, cyclosporine appeared to be beneficial [2]. Other agents that affect MPTP may have similar protective effect. As suggested by DominguezRodriguez et al. [3] melatonin may have such a potential effect. Melatonin has antioxidant and free radical scavenging properties. It is secreted by the pineal gland and its levels have diurnal ⁎ Corresponding author at: Division of Cardiology, The University of Western Ontario, 339 Winderemere Road, PO Box 5339, London, Canada ON N6A 5A5. Tel.: + 1 519 6633611; fax: + 1 519 6633117. E-mail address: [email protected] (S. Lavi).
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.04.028
variation and also fluctuate with sleep stages. They are higher during night and highest during rapid eye movement (REM) sleep [4]. The incidence of acute coronary syndrome also has a circadian variation. The incidence is highest in the early morning hours and this variation has been partially attributed to the hemodynamic and sympathetic changes during REM sleep [5]. Thus it would be difficult to delineate a potential effect of melatonin in this process. To make things more complicated, melatonin itself also has a differential effect on different vascular beds [6]. Results of animal studies suggest that administration of melatonin protects the heart from reperfusion injury [7,8]. Such data is lacking in humans and it would be interesting to see if administering melatonin to patients with acute myocardial infarction prior to primary percutaneous coronary intervention will be beneficial. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9]. References [1] Lavi S, Lavi R. Conditioning of the heart: from pharmacological interventions to local and remote protection: possible implications for clinical practice. Int J Cardiol 2011;146:311–8. [2] Piot C, Croisille P, Staat P, et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med 2008;359:473–81. [3] Dominguez-Rodriguez A, Abreu-Gonzalez P. Melatonin: still a forgotten antioxidant. Int J Cardiol 2011;149:382. [4] Luboshitzky R, Lavi S, Lavie P. The association between melatonin and sleep stages in normal adults and hypogonadal men. Sleep 1999;22:867–74. [5] Somers VK, Dyken ME, Mark AL, Abboud FM. Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med 1993;328:303–7. [6] Cook JS, Sauder CL, Ray CA. Melatonin differentially affects vascular blood flow in humans. Am J Physiol Heart Circ Physiol 2011;300:H670–4. [7] Petrosillo G, Colantuono G, Moro N, et al. Melatonin protects against heart ischemia–reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Am J Physiol Heart Circ Physiol 2009;297:H1487–93. [8] Lochner A, Genade S, Davids A, Ytrehus K, Moolman JA. Short- and long-term effects of melatonin on myocardial post-ischemic recovery. J Pineal Res 2006;40:56–63. [9] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
207
[8] Dominguez-Rodriguez A, Abreu-Gonzalez P. Current role of myeloperoxidase in routine clinical practice. Expert Rev Cardiovasc Ther 2011;9:223–30. [9] Morrow DA. Appraisal of myeloperoxidase for evaluation of patients with suspected acute coronary syndromes. J Am Coll Cardiol 2007;49:2001–2. [10] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Diurnal variation of circulating myeloperoxidase levels in patients with ST-segment elevation myocardial infarction. Int J Cardiol 2010;144:407–9. [11] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.03.019
Melatonin and myocardial protection Ronit Lavi a, Shahar Lavi b,⁎ a b
Department of anesthesia and perioperative medicine, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada Department of Medicine, Division of Cardiology, London Health Sciences Centre, The University of Western Ontario, London, Ontario, Canada
a r t i c l e
i n f o
Article history: Received 21 March 2011 Accepted 25 April 2011 Available online 17 May 2011 Keywords: Ischemic conditioning Melatonin Reperfusion injury
To the Editor: In our review article, we described the mechanisms and possible clinical application of conditioning of the heart. We focused our review on different modes of applying ischemic conditioning and provided some data regarding medications that may have a similar protective effect [1]. To date, no medication was proved to be protective against ischemia–reperfusion injury. Mitochondrial permeability transition pores (MPTP) seem to be involved in the mechanism of ischemic conditioning. Therefore, any drug or substance that inhibits MPTP function may have a protective effect similar to ischemic conditioning. The most relevant medication that was studied in humans in the setting of an acute myocardial infarction is cyclosporine, a potent inhibitor of MPTP. Indeed in a pilot study, cyclosporine appeared to be beneficial [2]. Other agents that affect MPTP may have similar protective effect. As suggested by DominguezRodriguez et al. [3] melatonin may have such a potential effect. Melatonin has antioxidant and free radical scavenging properties. It is secreted by the pineal gland and its levels have diurnal ⁎ Corresponding author at: Division of Cardiology, The University of Western Ontario, 339 Winderemere Road, PO Box 5339, London, Canada ON N6A 5A5. Tel.: + 1 519 6633611; fax: + 1 519 6633117. E-mail address: [email protected] (S. Lavi).
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.04.028
variation and also fluctuate with sleep stages. They are higher during night and highest during rapid eye movement (REM) sleep [4]. The incidence of acute coronary syndrome also has a circadian variation. The incidence is highest in the early morning hours and this variation has been partially attributed to the hemodynamic and sympathetic changes during REM sleep [5]. Thus it would be difficult to delineate a potential effect of melatonin in this process. To make things more complicated, melatonin itself also has a differential effect on different vascular beds [6]. Results of animal studies suggest that administration of melatonin protects the heart from reperfusion injury [7,8]. Such data is lacking in humans and it would be interesting to see if administering melatonin to patients with acute myocardial infarction prior to primary percutaneous coronary intervention will be beneficial. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9]. References [1] Lavi S, Lavi R. Conditioning of the heart: from pharmacological interventions to local and remote protection: possible implications for clinical practice. Int J Cardiol 2011;146:311–8. [2] Piot C, Croisille P, Staat P, et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med 2008;359:473–81. [3] Dominguez-Rodriguez A, Abreu-Gonzalez P. Melatonin: still a forgotten antioxidant. Int J Cardiol 2011;149:382. [4] Luboshitzky R, Lavi S, Lavie P. The association between melatonin and sleep stages in normal adults and hypogonadal men. Sleep 1999;22:867–74. [5] Somers VK, Dyken ME, Mark AL, Abboud FM. Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med 1993;328:303–7. [6] Cook JS, Sauder CL, Ray CA. Melatonin differentially affects vascular blood flow in humans. Am J Physiol Heart Circ Physiol 2011;300:H670–4. [7] Petrosillo G, Colantuono G, Moro N, et al. Melatonin protects against heart ischemia–reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Am J Physiol Heart Circ Physiol 2009;297:H1487–93. [8] Lochner A, Genade S, Davids A, Ytrehus K, Moolman JA. Short- and long-term effects of melatonin on myocardial post-ischemic recovery. J Pineal Res 2006;40:56–63. [9] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.