Oxidative stress correlates with left ventricular volume after acute myocardial infarction.

It has been suggested that oxidative stress may play a role in the pathophysiology of heart failure. However, little is known about the clinical relationship between oxidative stress and left ventricular dilatation after acute myocardial infarction (AMI). We prospectively studied 28 consecutive patients, successfully treated with primary coronary angioplasty, after their first AMI. To evaluate oxidative stress, plasma oxidized low-density LDL levels (U/mL) were measured serially I day, 7 days, 14 days, 30 days, and 90 days after the onset of AMI using a specific sandwich enzyme-linked immunosorbent assay. Left ventriculography and coronary angiography were obtained in all patients 3 months after the AMI and infarct-related arteries were all patent. Peak plasma oxidized LDL, levels were seen 7 days after AMI (after 1 day: 14.7+/-1.5, 7 days: 21.0+/-2.8, 14 days: 20.2+/-2.8, 30 days: 18.3+/-2.5, 90 days: 16.5+/-2.3 U/mL). Plasma oxidized LDL levels 7 days after AMI were significantly correlated with left ventricular end-diastolic volume (115+/-7 mL; r=0.54, P=0.0025) and end-systolic volume (58+/-5 mL; r=0.49, P=0.008) 3 months after the AMI. Moreover, they were also correlated with end-diastolic volume index (68+/-4 mL/m(2), r=0.40, P<0.05). However, no correlation was seen between peak plasma oxidized LDL levels and ejection fraction. These findings suggest that oxidative stress may play an important role in the development and progression of left ventricular remodeling after AMI.