An interaction between glucagon-like peptide-1 and adenosine contributes to cardioprotection of a dipeptidyl peptidase 4 inhibitor from myocardial ischemia-reperfusion injury.

Dipeptidyl peptidase 4 (DPP4) inhibitors suppress the metabolism of the potent antihyperglycemic hormone glucagon-like peptide-1 (GLP-1). DPP4 was recently shown to provide cardioprotection through a reduction of infarct size, but the mechanism for this remains elusive. Known interactions between DPP4 and adenosine deaminase (ADA) suggest an involvement of adenosine signaling in DPP4 inhibitor-mediated cardioprotection.

Quantitative assessment of microcollateral recruitment during coronary occlusion using real-time intravenous myocardial contrast echocardiography.

Background: Residual collateral-derived myocardial blood flow (MBF) (A x beta) is important to protect against myocardial ischemia after acute coronary occlusion.

Methods: Recruitment of microcollateral was assessed in 22 dogs with left circumflex coronary artery occlusion by analysis of MBF and regional wall thickening (WT) using real-time myocardial contrast echocardiography.

Results: Video intensity and WT at the center of risk area were significantly lower than those at the border of risk area.