Association of ischemia-modified albumin and melatonin in patients with ST-elevation myocardial infarction

Alberto Dominguez-Rodrigueza, , , Pedro Abreu-Gonzalezb, Martín J. Garcia-Gonzaleza, Sima Samimi-Farda, Russel J. Reiterc and Juan Carlos Kaskid
a) Department of Cardiology (Coronary Care Unit), University Hospital of Canarias, Ofra s/n La Cuesta E-38320, Tenerife, Spain
b) Department of Physiology, University of La Laguna, School of Medicine, Tenerife, Spain
c) Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, TX, USA
d) Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom
Received 6 August 2007; revised 23 October 2007; accepted 24 October 2007. Available online 4 December 2007.


It has been proposed that reactive oxygen species (ROS) generated during myocardial ischemia–reperfusion modify the N-terminus of serum albumin resulting in ischemia-modified albumin (IMA) formation. Likewise, several recent publications provide evidence that melatonin, a circadian endogenously produced indolamine, is a direct scavenger of ROS. We sought to investigate the relationship between IMA and melatonin in ST- elevation myocardial infarction (STEMI).


We compared IMA and melatonin levels in 27 patients with STEMI undergoing primary angioplasty and 20 age- and gender-matched healthy normal subjects. Blood samples were drawn at 02:00 h (night period) and 09:00 h (day period) while patients were resting, to assess IMA and melatonin.


In both groups, melatonin concentrations maintained a diurnal variation, but the difference between nocturnal and diurnal levels was less in the STEMI-patients than in the control group (p < 0.001). In contrast to findings about melatonin, IMA levels showed no diurnal variations in control subjects. However, the STEMI group showed a diurnal fluctuation with significantly higher levels at 02:00 h (p < 0.01). The association between IMA and melatonin remained statistically significant after adjustment for cardiovascular risk factors. An inverse correlation between IMA and melatonin at 02:00 h and at 09:00 h was observed, with respective r-values of −0.42 (p < 0.03) and −0.57 (p < 0.002).


Circulating IMA is negatively correlated to melatonin in STEMI-patients. Our results suggest that melatonin might exert a beneficial effect as a radical scavenger in a human model of myocardial ischemia–reperfusion.

Key Melatonin