Decreased nocturnal melatonin levels during acute myocardial infarction
Article first published online: 17 OCT 2002
Journal of Pineal Research
Volume 33, Issue 4, pages 248–252, November 2002
How to Cite
Domínguez-Rodríguez, A., Abreu-González, P., García, M. J., Sanchez, J., Marrero, F. and Armas-Trujillo, D. d. (2002), Decreased nocturnal melatonin levels during acute myocardial infarction. Journal of Pineal Research, 33: 248–252. doi: 10.1034/j.1600-079X.2002.02938.x
- Issue published online: 17 OCT 2002
- Article first published online: 17 OCT 2002
- Received June 3, 2002; accepted July 22, 2002.
- free radicals;
- myocardial infarction
Abstract: Acute myocardial infarction is accompanied by an increase in cellular oxidative stress in the pericardial coverings of the heart. Melatonin is a highly potent and efficient radical scavenger. Little research has been carried out concerning the relationship between this antioxidant and acute myocardial infarction in humans. In this work, serum levels of melatonin and parameters of oxidative stress, such as glutathione peroxidase and lipid peroxidation levels were examined in light/dark periods in patients with acute myocardial infarction. Twenty-five patients diagnosed with acute myocardial infarction were studied and 25 patients with no evidence of coronary artery disease served as controls. Venous blood samples were obtained from the patients and control subjects to determine melatonin, glutathione peroxidase and lipid peroxidation; the samples were collected at 10:00 hr (light period) and 03:00 hr (dark period) in the first 24 hr after admission to the coronary care unit. Our results demonstrate the existence of differences between changes in melatonin levels in control subjects and acute myocardial infarction patients, revealing a reduced nocturnal elevation in the acute myocardial infarction group. Glutathione peroxidase levels were lower after acute myocardial infarction and did not show diurnal variations. In the control group, lipid peroxidation levels presented a light/dark pattern but in the acute myocardial infarction group diurnal variations of this parameter were lost. Our data show that acute myocardial infarction is associated with a nocturnal serum melatonin deficit as well as increased oxidative stress, suggesting that melatonin is, at least in part, depleted during the dark phase to reduce the free radicals formed in acute myocardial infarction.