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Atherosclerosis. 2010 Dec;213(2):604-10. doi: 10.1016/j.atherosclerosis.2010.09.015. Epub 2010 Sep 24.

Resistin, exercise capacity, and inducible ischemia in patients with stable coronary heart disease: data from the Heart and Soul study.

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Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.



Resistin is an adipocytokine involved in insulin resistance, inflammation, and atherosclerosis. Its role in the development and progression of coronary heart disease (CHD) is not yet well-characterized. We performed a cross-sectional study to evaluate the association between serum resistin levels, exercise capacity, and exercise-induced cardiac ischemia among patients with stable CHD.


We measured serum resistin concentrations and determined treadmill exercise capacity and inducible ischemia by stress echocardiography in 899 outpatients with documented CHD. Of these, 215 (24%) had poor exercise capacity (<5 metabolic equivalent tasks), and 217 (24%) had inducible ischemia. As compared with participants who had resistin levels in the lowest quartile, those with resistin levels in the highest quartile were more likely to have poor exercise capacity (33% versus 16%, odds ratio [OR] 2.68, P<0.0001) and inducible ischemia (30% versus 17%, OR 2.08, P=0.001). Both associations remained robust after adjusting for numerous clinical risk factors, metabolic variables, and markers of insulin resistance (poor exercise capacity adjusted OR 1.73, P=0.04; inducible ischemia adjusted OR 1.82, P=0.01). However, further adjustments for C-reactive protein, interleukin-6, and tumor necrosis factor-α eliminated the association with poor exercise capacity (adjusted OR 1.50, P=0.14) and substantially weakened the association with inducible ischemia (adjusted OR 1.72, P=0.03).


Elevated serum resistin is associated with poor exercise capacity and exercise-induced cardiac ischemia in patients with stable coronary disease. Adjustment for inflammatory markers attenuated these associations, suggesting a possible role for resistin in inflammation and CHD pathophysiology.

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