Markedly reduced insulin-like growth factor-1 in the acute phase of myocardial infarction

OBJECTIVES We investigated whether insulin-like growth factor-1 (IGF-1) is reduced in the early phase of acute myocardial infarction (AMI) and whether such a decrease might influence prognosis. BACKGROUND Insulin-like growth factor-1 protects against insulin resistance and apoptosis. Although insulin resistance has been reported in AMI, IGF-1 levels have not been investigated. METHODS We measured serum IGF-1 in 23 patients with AMI within 24 h of symptom onset and in 11 matched controls. In the first 12 patients and controls, we also measured fasting insulin, diurnal growth hormone (GH) and insulin sensitivity (assessed as glucose disappearance or T/2 after an insulin bolus), and repeated IGF-1, insulin and GH after one year. In all patients, 90-day cardiovascular death, recurrent ischemia, reinfarction, revascularization and late malignant arrhythmias were assessed. RESULTS The AMI patients versus controls showed markedly reduced IGF-1 (115 +/- 112 vs. 615 +/- 300 ng/ml, p < 0.0001) and slower T/2 (-0.98 +/- 1.5 vs. -2.57 +/- 1.0 mg/dl/min, p = 0.01). Low IGF-1 often preceded the rise of myocardial necrosis markers. Patients with 90-day events (n = 12) versus those without had lower IGF-1 (47 +/- 54 vs. 189 +/- 110 ng/ml, p < 0.0001). Acute phase GH and insulin concentrations did not differ significantly from controls. After one year, the patients' IGF-1 values had risen to 460 +/- 242 ng/ml (p = 0.1 vs. controls, p < 0.0005 vs. acute phase), whereas GH levels were lower (0.2 +/- 0.2 vs. 2.5 +/- 2.3 ng/ml, p = 0.01) and insulin levels higher (12.5 +/- 0.2 vs. 3.9 +/- 2.6 <mu>U/ml, p < 0.0001) compared with controls. CONCLUSIONS In the early phase of AMI, serum IGF-1 levels are markedly reduced and may contribute to adverse outcomes. Reduced IGF-1 preceding the rise of myocardial necrosis markers suggests a possible pathogenetic role. A compensatory increase in IGF-1 appears to occur by one year. CT Am Coil Cardiol 2001;38:26-32) (C) 2001 by the American College of Cardiology.