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CLINICAL STUDIES

Serum insulin-like growth factor-I level is independently associated with coronary artery disease progression in young male survivors of myocardial infarction: beneficial effects of bezafibrate treatment

Giacomo Ruotolo, MD, PhD^*, Peter Båvenholm, MD, PhD, Kerstin Brismar, MD, PhD, Suad Eféndic, MD, PhD, Carl-G.öran Ericsson, MD, PhD, Ulf de Faire, MD, PhD, Jan Nilsson, MD, PhD^* and Anders Hamsten, MD, PhD^*

^* Atherosclerosis Research Unit, King Gustaf V Research Institute, Stockholm, Sweden
Department of Emergency and Cardiovascular Medicine, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden
Department of Endocrinology and Diabetology, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden
Department of Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden

Manuscript received March 29, 1999; revised manuscript received September 20, 1999, accepted November 3, 1999.

Reprint requests and correspondence: Dr. Anders Hamsten, King Gustaf V Research Institute, Karolinska Hospital, S-171 76, Stockholm, Sweden
HAMSTEN{at}instmed.ks.se

OBJECTIVES

We investigated whether the effect of bezafibrate on progression of coronary atherosclerosis in the BEzafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) was related to insulin-like growth factor (IGF)-I and glucose-insulin homeostasis.

BACKGROUND

BECAIT, the first double-blind, placebo-controlled, randomized, serial angiographic trial of a fibrate compound, demonstrated that progression of focal coronary atherosclerosis in young patients after infarction could be retarded by bezafibrate treatment.

METHODS

The treatment effects on serum concentrations of IGF-I and insulin-like growth factor binding protein (IGFBP)-1, as well as on basal and postload glucose and insulin levels, were examined, and on-trial determinations were related to the angiographic outcome measurements.

RESULTS

Bezafibrate treatment resulted in a significant reduction of serum IGF-I levels, both at two and five years, and on-trial serum IGF-I levels were directly related to changes in both minimal lumen diameter (r = 0.25, p < 0.05) and mean segment diameter (r = 0.29, p < 0.05). In contrast, none of the available indexes of insulin resistance (homeostasis model assessment estimate, basal and postload plasma insulin concentrations and serum IGFBP-1 levels) were related to the angiographic changes, nor were they significantly affected by bezafibrate treatment. Multiple stepwise regression analysis showed that the relation between on-trial serum IGF-I level and coronary artery disease (CAD) progression was independent of baseline angiographic score, age, body mass index, serum lipoprotein and plasma fibrinogen concentrations and measures of glucose–insulin homeostasis.

CONCLUSIONS

IGF-I could be implicated in the progression of premature CAD, and a reduction of serum IGF-I concentration could account partly for the effect of bezafibrate on progression of focal coronary atherosclerosis.

Abbreviations and Acronyms   BECAIT = BEzafibrate Coronary Atherosclerosis Intervention Trial   HDL = high density lipoprotein   HOMA = homeostasis model assessment   IGF = insulin-like growth factor   IGFBP = insulin-like growth factor binding protein   LDL = low density lipoprotein   Lp(a) = lipoprotein (a)   MLD = minimal lumen diameter   MSD = mean segment diameter   VLDL = very low density lipoprotein

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