Acute myocardial infarction is associated with increased susceptibility of serum lipids to copper-induced peroxidation in vitro.

BACKGROUND: Low-density lipoprotein (LDL) oxidation in the arterial intima plays a pivotal role in atherogenesis. Under physiologic conditions, several mechanisms protect LDL against oxidation, including hydrolysis of oxidation products by high-density lipoprotein (HDL)-associated enzymes. Some of these protective mechanisms are less effective under acute phase conditions. HYPOTHESIS: Conditions of acute phase response, including acute myocardial infarction (MI), may be expected to result in increased susceptibility of serum lipids to oxidation. The present study was undertaken to test this possibility. METHODS: Using our previously developed spectroscopic method, we have monitored prospectively the kinetics of copper-induced oxidation of serum lipids obtained from 15 men during and after acute MI. This was tested within 6 h from the onset of chest pain, on Days 1, 3, and 7 of infarction and 1 year after recovery. RESULTS: The lag phase preceding oxidation of serum lipids was much shorter during the first week after MI when compared with values obtained after recovery (52-59 vs. 107 min, respectively, p <0.001). During the first week after MI, we observed no significant correlations between kinetic parameters and serum lipid composition, in contrast both to the correlations previously reported for hyperlipidemic patients and to the similar correlations observed in the present study after recovery. CONCLUSIONS: Acute MI is associated with an increased susceptibility of serum lipids to oxidation in vitro. This propensity for oxidation may reflect enhanced in vivo formation of free radicals and/or reduced efficiency of defense mechanisms. Both these possibilities may carry detrimental effects on the course, complications, and prognosis of the patients after acute MI.