Time-dependent changes in plasma osteopontin levels in patients with anterior-wall acute myocardial infarction after successful reperfusion: correlation with left-ventricular volume and function.

Osteopontin is a secreted extracellular-matrix glycoprotein that plays a role in the healing of remodeling tissue. We examined the relationship of plasma osteopontin levels with left-ventricular (LV) volume and function in 18 consecutive patients who underwent successful reperfusion after anterior-wall acute myocardial infarction (AMI). The plasma osteopontin level was within the control range at admission (mean +/- SD 420 +/- 195 ng/mL), began to increase on day 2 (935 +/- 464 ng/mL), and reached a maximum around day 3 (1139 +/- 482 ng/mL). The level remained high on days 4, 5, and 7 ( approximately 1000 ng/mL) and then decreased on day 14. Maximal plasma osteopontin levels and the difference between maximal and minimal levels were positively correlated with LV end-systolic volume index (r = .58, P < .05; and r = .65, P < .01, respectively) and negatively correlated with LV ejection fraction (r = -.52, P < .05; and r = -.60, P < .01, respectively). The area under the curve of plasma osteopontin levels for 14 days after AMI was significantly correlated with LV end-systolic volume index (r = .66, P < .01), LV end-diastolic volume index (r = .50, P < .05), and LV ejection fraction (r = -.55, P < .05). In subgroup patients with the same area of risk for myocardial infarction (ie, responsible lesions located at the same proximal left anterior descending coronary artery), essentially the same or a closer relationship between plasma osteopontin level and LV volume and function was noted. Plasma osteopontin levels were correlated substantially with plasma levels of high-sensitivity C-reactive protein (hsCRP) and weakly with serum creatine kinase release. In conclusion, the plasma level of osteopontin changes in a time-dependent fashion and is correlated with LV volumes and function and associated substantially with the extent of the inflammatory response indicated by the plasma hsCRP level and weakly with infarct size estimated on the basis of cardiac-enzyme release.