Key result
Type 2 diabetes did not alter myocardial glucose uptake in nonstenotic (0.38 vs 0.36 micromol/g.min; P=NS) or stenotic regions in CAD patients with preserved LVEF.
Why the study?
Does type 2 diabetes induce myocardial insulin resistance, and does acute hyperinsulinemia alter myocardial perfusion in patients with coronary artery disease and preserved LVEF?
Population
27 patients with coronary artery disease and preserved LVEF, comprising 12 with type 2 diabetes mellitus and…
Comparison
Acute hyperinsulinemia vs Without acute hyperinsulinemia (rest)
Design
Cross-sectional
Authors
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Myocardial glucose uptake appears preserved regardless of T2DM in CAD with preserved LVEF; leaves open whether resistance emerges in reduced LVEF or other phenotypes.
Cross-Sectional (n=27)
Does type 2 diabetes induce myocardial insulin resistance, and does acute hyperinsulinemia alter myocardial perfusion in patients with coronary artery disease and preserved LVEF?
Absolute Event Rate: 0.38% vs 0.36%
p-value: p=NS
Myocardial insulin resistance to glucose uptake is not an inherent feature in T2DM patients with preserved LVEF, and acute insulin exposure does not cause coronary vasodilation in CAD patients regardless of T2DM status.
Søndergaard et al. (2006) conducted a cross-sectional in Coronary artery disease (n=27). Type 2 diabetes mellitus vs. No type 2 diabetes was evaluated on Myocardial glucose uptake in nonstenotic regions (micromol/g.min) (p=NS). Type 2 diabetes did not alter myocardial glucose uptake in nonstenotic (0.38 vs 0.36 micromol/g.min; P=NS) or stenotic regions in CAD patients with preserved LVEF.
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