Abstract 12468: Increased Level of Plasma Glucagon-Like Peptide-1 in Patients with Left Ventricular Dysfunction may Serve as a Copensatory Mechanism for Cardiac Function
Background: Anti-diabetic drug Glucagon-Like Peptide-1 (GLP-1) agonists and Dipeptidyl Peptidase-4 (DPP IV) inhibitors which stimulate GLP-1 receptors have been reported to improve left ventricular (LV) dysfunction. However, it remains unknown whether endogenous GLP-1 is involved in LV dysfunction.
Objectives: To test the hypothesis that GLP-1 is an endogenous cardioprotective agent in the heart with impaired LV dysfunction, we examined plasma GLP-1 levels and cardiac GLP-1 and GLP-1 receptors in patients with LV dysfunction.
Methods: We measured the plasma GLP-1 level, plasma Brain Natriuretic Peptide (BNP) level and the other parameters (HbA1c, immunoreactive insulin, serum creatinine and C-reactive protein) in 90 patients with coronary artery disease, cardiomyopathy and valvular heart disease undergoing cardiac catheterization, and examined their relationships with LV function. The expression of GLP-1 and GLP-1 receptor proteins were examined in endomyocardial biopsies obtained from patients with preserved and impaired LV function.
Results: The plasma GLP-1 level was significantly increased in patients with impaired LV function as compared to those with preserved LV function (5.5±2.0 (ejection fraction (EF)<55%) versus 2.7±1.6 (EF>=55%) ; P<0.001). The plasma BNP level was also significantly increased in patients with impaired LV function (508±537 (EF<55%) versus 111±177 (EF>=55%) ; P<0.001). Plasma GLP-1 and Plasma BNP level were inversely correlated with the LV EF by a multivariable regression analysis (R=0.75,P<0.01). Intensity of immunostaining for GLP-1 receptor protein was significantly enhanced in myocardial biopsies from impaired LV function compared with those from preserved LV function, while there was no difference in the intensity of immunostaining for GLP-1 protein from myocardial biopsies between preserved and impaired LV function.
Conclusion: The plasma GLP-1 level was increased in patients with impaired LV function. Plasma GLP-1 level was inversely correlated with the LV EF. The expression of cardiac GLP-1 receptors was enhanced in patients with impaired LV function. These results may indicate that endogenous plasma GLP-1 and cardiac GLP-1 receptors serve as a compensatory mechanism for LV dysfunction.
- © 2012 by American Heart Association, Inc.