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Coron Artery Dis. 2008 Sep;19(6):375-82. doi: 10.1097/MCA.0b013e3282fc617c.

Plasma levels of TNF-alpha, IL-6, and IL-10 and their relationship with left ventricular diastolic function in patients with stable angina pectoris and preserved left ventricular systolic performance.

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Department of Cardiology, Medical University, Wroclaw, Poland.



The role of inflammation--a key factor underlying coronary artery disease (CAD) and systolic heart failure--in promotion of left ventricular (LV) diastolic dysfunction has not been investigated extensively so far. The aim of this study was: (i) to evaluate plasma levels of TNF-alpha, IL-6, and IL-10 in patients with stable CAD and preserved LV systolic function and (ii) to assess their relationships with LV diastolic function.


The study population consisted of 126 patients with single vessel and 58 patients with multivessel stable CAD and LV ejection fraction >50%, and 39 healthy controls. Each participant underwent echocardiographic study including estimation of LV diastolic function indices: peak velocities of early (E) and late (A) transmitral flows, deceleration time of E wave, isovolumic relaxation time, E wave (ETT) and A wave (ATT) transit time to the LV outflow tract, and flow propagation velocity of E wave (Ep). Plasma TNF-alpha, IL-6, and IL-10 levels were evaluated by radioimmunometric method.


Patients with CAD presented higher TNF-alpha and IL-6 levels and higher values of IL-6/IL-10 and TNF-alpha/IL-10 ratio than the controls. IL-6 levels were higher in patients with multivessel disease than in those with single vessel disease. Significant correlations (all P<0.001) were found for TNF-alpha and Ep (r=-0.41), E/Ep (r=0.45), and ETT (r=0.38). IL-6 correlated with Ep (r=-0.39) and E/A (r=-0.33), whereas IL-10 with ETT (r=0.37), Ep (r=-0.44), and E/Ep (r=0.46).


In patients with stable CAD and preserved LV systolic performance, plasma levels of TNF-alpha and IL-6 are elevated and there is association between immunoinflammatory activation reflected by plasma levels of cytokines and LV diastolic dysfunction.

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