Plasma GLP-1 levels were significantly elevated in patients with impaired left ventricular function (5.7±1.9 pmol/L) compared to those with preserved function (2.7±1.6 pmol/L).
Cross-Sectional (n=108)
No
Are plasma GLP-1 levels and cardiac GLP-1 receptor expression associated with left ventricular systolic dysfunction?
Elevated plasma GLP-1 levels and enhanced cardiac GLP-1 receptor expression are associated with impaired left ventricular systolic function, suggesting a potential compensatory mechanism.
Tasa de eventos absoluta: 5.7% vs 2.7%
Objective We aimed to elucidate usefulness of plasma glucagon-like peptide-1 (GLP-1) levels for the assessment of left ventricular (LV) dysfunction by examining the relationship among plasma GLP-1 levels, expression of cardiac GLP-1 receptors and LV function in patients with impaired and preserved LV function. Design Prospective study. Setting Number of participating center: 1, Gifu, Japan. Participants Number of patients enrolled: 102 patients who underwent elective cardiac catheterisation for coronary artery disease, cardiomyopathy and valvular heart disease, and 6 patients who underwent cardiac biopsy. Results The plasma GLP-1 level was significantly increased in patients with impaired LV function (5.7±1.9 pmol/L) as compared with those with preserved LV function (2.7±1.6 pmol/L). Plasma GLP-1 and plasma brain natriuretic peptide (BNP) levels were inversely correlated with the LV ejection fraction(EF), respectively. Plasma GLP-1 level positively correlated with plasma BNP level. Multivariate logistic regression analysis revealed that plasma GLP-1 level was an independent determinant of the impaired LV function, whereas plasma BNP level was not. Intensity of immunostaining for GLP-1 receptor protein was significantly enhanced in patients with impaired LV function compared with those with preserved LV function. Conclusions The plasma GLP-1 level was increased in patients with impaired systolic LV function and inversely correlated with the LVEF. The expressions of GLP-1 receptors were enhanced in hearts with impaired LV function. These may suggest that endogenous GLP-1-GLP-1 receptor system serves as a compensatory mechanism for systolic LV dysfunction. Trial registration UMIN-CTR, ID=UMIN000009361, registration number: R000011000.
Hattori et al. (Sun,) conducted a cross-sectional in Left ventricular systolic dysfunction (n=108). Impaired left ventricular function vs. Preserved left ventricular function was evaluated on Plasma GLP-1 level (pmol/L). Plasma GLP-1 levels were significantly elevated in patients with impaired left ventricular function (5.7±1.9 pmol/L) compared to those with preserved function (2.7±1.6 pmol/L).