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Relation between hyperinsulinemia and nonculprit plaque characteristics in nondiabetic patients with acute coronary
Takayuki Mitsuhashi1, Kiyoshi Hibi, Masami Kosuge
1Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan.
Objectives:
We sought to assess whether hyperinsulinemia is associated with percentage lipid and coronary plaque burden in nondiabetic patients with acute coronary syndromes (ACS).
Background:
Hyperinsulinemia carries an increased risk of cardiovascular disease even in pre-diabetic patients, but the precise mechanisms of its effects remain unclear.
Methods:
Nonculprit coronary lesions associated with mild-to-moderate stenosis in 82 nondiabetic patients with ACS were examined by integrated backscatter intravascular ultrasound (IB-IVUS), using a 40-MHz intravascular catheter. Conventional IVUS and IB-IVUS measurements from the worst 10-mm segment (1-mm intervals) were calculated. All patients underwent a 75-g oral glucose tolerance test (OGTT) to calculate the area under the insulin concentration-time curve (AUC insulin) from 0 to 120 min.
Results:
Patients in the high tertile of AUC insulin had a significantly greater percentage lipid area and absolute lipid volume than did patients in the intermediate and low tertiles (tertile 3 vs. tertile 2 vs. tertile 1; 37.6 ± 16.6% vs. 25.8 ± 11.9% vs. 27.5 ± 14.7%, p < 0.01 by analysis of variance [ANOVA], and 29.9 ± 22.6 mm(3) vs. 15.3 ± 12.6 mm(3) vs. 17.7 ± 12.7 mm(3), p < 0.01 by ANOVA, respectively) and a smaller percentage fibrosis area (55.0 ± 11.5% vs. 61.7 ± 9.4% vs. 60.7 ± 9.4%, p = 0.03 by ANOVA). Multiple regression analysis showed that the high tertile of AUC insulin was independently associated with an increased percentage lipid area (p < 0.05). On conventional IVUS analysis, external elastic membrane cross-sectional area was significantly increased with greater plaque volume in patients in the high tertile of AUC insulin (both p < 0.05 by ANOVA).
Conclusions:
Hyperinsulinemia is associated with an increased lipid content and a greater plaque volume of nonculprit intermediate lesions in nondiabetic patients with ACS, suggesting that plaque vulnerability is increased in this subgroup of patients.
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