OBJECTIVES: The aim of this study was to evaluate resistin levels in patients with coronary artery disease (CAD) with or without chronic heart failure, in order to define its independent predictor. METHODS: One hundred and seven outpatients with CAD were enrolled in the study and divided into three groups: CAD without left-ventricular systolic dysfunction (group 1); CAD with left-ventricular dysfunction without heart failure symptoms (group 2); CAD with overt heart failure (group 3). Plasma resistin was determined by ELISA. RESULTS: Resistin progressively increased from group 1 (10.7±5.0 ng/ml) to groups 2 (11.8±5.8 ng/ml) and 3 (17.0±6.8 ng/ml), with the difference reaching statistical significance in group 3 versus groups 1 and 2 (P=0.001). A multivariable model of analysis demonstrated that the best predictor of plasma resistin level was the estimated glomerular filtration rate (P<0.001), indicating that reduction of kidney function was the main cause of the adipokine increase observed in patients with CAD and overt heart failure. CONCLUSIONS: Our data confirm the rise of resistin plasma levels previously described in patients affected by chronic heart failure; however, in our study, this relationship seemed to be mediated mainly by the level of kidney function, and only partially by the severity of ventricular dysfunction.
OBJECTIVES: The aim of this study was to evaluate resistin levels in patients with coronary artery disease (CAD) with or without chronic heart failure, in order to define its independent predictor. METHODS: One hundred and seven outpatients with CAD were enrolled in the study and divided into three groups: CAD without left-ventricular systolic dysfunction (group 1); CAD with left-ventricular dysfunction without heart failure symptoms (group 2); CAD with overt heart failure (group 3). Plasma resistin was determined by ELISA. RESULTS:Resistin progressively increased from group 1 (10.7±5.0 ng/ml) to groups 2 (11.8±5.8 ng/ml) and 3 (17.0±6.8 ng/ml), with the difference reaching statistical significance in group 3 versus groups 1 and 2 (P=0.001). A multivariable model of analysis demonstrated that the best predictor of plasma resistin level was the estimated glomerular filtration rate (P<0.001), indicating that reduction of kidney function was the main cause of the adipokine increase observed in patients with CAD and overt heart failure. CONCLUSIONS: Our data confirm the rise of resistin plasma levels previously described in patients affected by chronic heart failure; however, in our study, this relationship seemed to be mediated mainly by the level of kidney function, and only partially by the severity of ventricular dysfunction.
Authors: Daniel R Schwartz; Erika R Briggs; Mohammed Qatanani; Heloisa Sawaya; Igal A Sebag; Michael H Picard; Marielle Scherrer-Crosbie; Mitchell A Lazar Journal: Endocrinology Date: 2013-08-27 Impact factor: 4.736