Adiponectin and inducible ischemia in patients with stable coronary heart disease: data from the Heart and Soul study
Received 5 July 2008; received in revised form 14 November 2008; accepted 17 November 2008. published online 29 December 2008.
Abstract
Objective
Elevated concentrations of adiponectin are associated with a favorable metabolic profile but also with adverse cardiovascular outcomes. This apparent discrepancy has raised questions about whether adiponectin is associated with an increased or decreased risk of coronary heart disease (CHD). We sought to determine whether higher adiponectin levels are associated with exercise-induced ischemia in patients with stable CHD.
Methods and results
We measured total serum adiponectin concentrations and evaluated exercise-induced ischemia by stress echocardiography in a cross-sectional study of 899 outpatients with documented stable CHD. Of these, 217 (24%) had inducible ischemia. Although adiponectin levels correlated negatively with diabetes prevalence, body mass index, serum insulin, fasting glucose, low-density lipoprotein cholesterol, and triglycerides and positively with high-density lipoprotein cholesterol (all P<0.005), elevated adiponectin concentrations were also associated with a greater risk of inducible ischemia. Each standard deviation (0.08μg/mL) increase in log adiponectin was associated with a 35% greater odds of inducible ischemia (unadjusted odds ratio 1.35; 95% confidence interval 1.15–1.57; P=0.0002). Although attenuated, this association remained present after multivariable adjustment for traditional cardiovascular risk factors and other measures of cardiac function (adjusted odds ratio 1.21; 95% confidence interval 1.02–1.43; P=0.03).
Conclusions
Elevated concentrations of adiponectin are independently associated with inducible ischemia in patients with stable CHD. These findings raise the possibility that the presence of chronic inducible ischemia may alter the cardio-protective effects afforded by adiponectin secretion in the healthy population.
bDepartment of Medicine, University of Hawaii and the Queen's Medical Center, Honolulu, HI, USA
cSection of General Internal Medicine, Veterans Affairs Medical Center, San Francisco, CA, USA
dDepartment of Medicine, University of California, San Francisco, CA, USA
eDepartment of Epidemiology and Biostatistics, University of California, San Francisco, CA, USA
Corresponding author at: University of California, San Francisco, 4150 Clement Street (111A1), San Francisco, CA 94121, USA. Tel.: +1 415 221 4810x3386; fax: +1 415 379 5573.
ABSTRACT