Microvascular Dysfunction after Coronary Stenting in the Ossabaw Swine Model of the Metabolic Syndrome

Ossabaw miniature swine show major components of the metabolic syndrome. We tested the hypothesis that coronary stenting would elicit microvascular dysfunction. The circumflex artery of males was stented after 40 weeks on control (n=5) or 2% cholesterol/high fat diet (H; hypercholesterolemic, n=5). Microvascular dilation was assessed 3 wk post stenting in response to intracoronary adenosine (0.167–3 μg/kg, endothelium‐independent) and bradykinin (1–4 ng/kg, endothelium‐dependent). Blood flow velocity was measured with a Doppler Flo‐wire and artery cross sectional area with intravascular ultrasound to calculate coronary blood flow (CBF) and flow reserve (CFR). Baseline CBF was similar between groups (45 ± 1 vs. 41 ± 1 mL/min). At all doses, adenosine‐induced CFR was impaired in H (e.g. 1.9 ± 0.1 vs. 2.6 ± 0.2 at 3 μg/kg, p < 0.05). Bradykinin‐induced CFR was also impaired in H vs. control (p=0.058). Histology of in‐stent sections showed no difference in intima:media ratio between groups. Conclusion coronary stenting and the metabolic syndrome elicit microvascular dysfunction. Restenosis within the stent was unaffected by hypercholesterolemia, likely due to use of a safe (1.0 x lumen diameter) stent deployment. Support: NIH RR13223, T32 RR07004, T32 HL07094, T32 AR48523, ADA.