TY - JOUR
T1 - Association of ischemia-modified albumin and melatonin in patients with ST-elevation myocardial infarction
AU - Dominguez-Rodriguez, Alberto
AU - Abreu-Gonzalez, Pedro
AU - Garcia-Gonzalez, Martín J.
AU - Samimi-Fard, Sima
AU - Reiter, Russel J.
AU - Kaski, Juan Carlos
PY - 2008/7
Y1 - 2008/7
N2 - Introduction: 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). Methods: 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. Results: 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). Conclusions: 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.
AB - Introduction: 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). Methods: 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. Results: 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). Conclusions: 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.
KW - Diurnal variation
KW - Ischemia-modified albumin
KW - Melatonin
KW - Reactive oxygen species
KW - ST-elevation myocardial infarction
UR - http://www.scopus.com/inward/record.url?scp=45249103302&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=45249103302&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2007.10.019
DO - 10.1016/j.atherosclerosis.2007.10.019
M3 - Article
C2 - 18054940
AN - SCOPUS:45249103302
SN - 0021-9150
VL - 199
SP - 73
EP - 78
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -