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Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
Endothelial function and proinflammatory cytokines in patients with ischemic heart disease and dilated cardiomyopathy
Costas Tentolouris1, Dimitris Tousoulis, Charalambos Antoniades
1Cardiology Units, Hippokration Hospital, Athens University Medical School, 69 S. Karagiorga, 16675 Athens, Greece.
Insights
Heart failure patients show impaired endothelial function and higher inflammation markers, with ischemic heart failure exhibiting greater dysfunction than dilated cardiomyopathy, suggesting atherosclerosis plays a role.
Area of Science:
- Cardiology
- Immunology
- Vascular Biology
Background:
- Proinflammatory cytokines like tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are key in immune responses and linked to endothelial dysfunction in coronary artery disease (CAD) and heart failure.
- Endothelial dysfunction is a critical factor in cardiovascular diseases.
Purpose of the Study:
- To compare endothelial function and levels of IL-6 and TNF-alpha in patients with ischemic heart failure, dilated cardiomyopathy, CAD, and healthy controls.
- To investigate the relationship between inflammation and endothelial dysfunction in different heart failure etiologies.
Main Methods:
- Enrolled 20 dilated cardiomyopathy, 48 ischemic cardiomyopathy, 26 CAD, and 14 healthy control participants.
- Measured forearm blood flow using venous occlusion strain gauge plethysmography.
- Assessed endothelium-dependent (reactive hyperemia) and independent (nitrate) vasodilation.
Main Results:
- Significantly higher IL-6 levels in ischemic and dilated cardiomyopathy compared to controls and CAD patients.
- Significantly higher TNF-alpha levels in both ischemic and dilated cardiomyopathy groups compared to CAD and controls.
- Lower forearm vasodilatory response (RH%) in both ischemic and dilated cardiomyopathy compared to CAD and controls, with greater impairment in ischemic heart failure.
Conclusions:
- Both ischemic and dilated cardiomyopathy demonstrate impaired endothelial function and elevated inflammatory markers.
- Ischemic heart failure exhibits more severe endothelial dysfunction than dilated cardiomyopathy.
- Underlying atherosclerosis likely contributes to the greater endothelial dysfunction observed in ischemic heart failure.
Background:
Proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are important mediators of immune response, associated with endothelial dysfunction in patients with coronary artery disease (CAD) or heart failure. We compared endothelial function and levels of IL-6 and TNF-alpha between patients with ischemic heart failure, dilated cardiomyopathy, CAD and healthy controls.
Methods:
The population consisted of 20 patients with dilated cardiomyopathy, 48 patients with ischemic cardiomyopathy, 26 patients with CAD and normal left ventricle function and 14 healthy controls. Forearm blood flow was measured using venous occlusion strain gauge plethysmography. Forearm vasodilatory response to reactive hyperemia (RH%) or to nitrate were considered as indexes of endothelium-dependent and endothelium-independent dilation, respectively.
Results:
Levels of IL-6 were significantly higher in ischemic cardiomyopathy compared to CAD patients (P<0.05) or controls (P<0.05) and in patients with dilated cardiomyopathy compared to controls (P<0.05). TNF-alpha levels were significantly higher in both groups with ischemic or dilated cardiomyopathy compared to CAD (P<0.05) or controls (P<0.05). RH% was significantly lower in ischemic and dilated cardiomyopathy compared to CAD (P<0.05) or controls (P<0.001) and higher in dilated than ischemic cardiomyopathy (P<0.05).
Conclusions:
Impaired endothelial function and increased inflammatory process were found in both types of heart failure. A greater endothelial dysfunction was observed in patients with ischemic heart failure compared to those with dilated cardiomyopathy, implying that the underlying atherosclerosis may participate in this process.
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