Systemic Inflammation and Endothelial Dysfunction in Dogs with Congestive Heart Failure

Regardless of the great progress in studying the heart failure (HF) pathophysiology, the question about involvement of immune cells activation, systemic inflammation, inflammatory cytokine dysregulation and endothelial dysfunction in maladaptive left ventricular (LV) remodeling in ischemic and nonischemic HF patients is still open to discussion. The aim was to study the characteristics of immunopathological reactions (immunoinflammatory and autoimmune), endothelial dysfunction and pathologic angiogenesis in maladaptive LV remodeling in ischemic and nonischemic HF patients. Materials and methods. A total of 20 healthy volunteers, 31 ischemic HF patients (group 1) and 43 nonischemic HF patients (group 2) were enrolled in the study. All the patients underwent coronarography, ventriculography, echocardigraphic examination. The main lymphocyte subset counts (flow cytometry), serum concentration of C-reactive protein (CRP), vascular endothelial growth factor A (VEGF), TNFα, endothelin-1 (enzyme-linked immunosorbent assay (ELISA)), autoantibodies to myocardium and vessels were detected. Results. Regardless of the HF etiology, all the examined patients demonstrated echocardiographic features of maladaptive LV remodeling and severe intracardiac hemodynamic disorders that was associated with immune system activation, namely increased total and subset lymphocyte counts, chronic systemic inflammation (CRP), autoimmune process with an increase in autoantibodies to myocardium and vessels, and endothelial dysfunction (increased endothelin-1 and VEGF). Under-expression of TNF-α combined with over-expression of VEGF seemed to indicate pathological angiogenesis in ischemic and nonischemic HF patients Conclusions. Significantly increased VEGF levels in heart failure patients can be considered as additional integral key marker of immune inflammation, endothelial dysfunction and pathological angiogenesis and may indicate maladaptive cardiac remodeling in severe heart failure.

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451 The glial fibrillary acidic protein (GFAP) as a predictor of development of endothelial dysfunction in elderly patients with congestive heart failure and preserved left ventricular ejection fraction

European Journal of Heart Failure Supplements ◽

10.1016/s1567-4215(05)80292-9 ◽

2005 ◽

Vol 4 (1) ◽

pp. 106-106

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Endothelial Dysfunction ◽

Left Ventricular Ejection Fraction ◽

Ejection Fraction ◽

Glial Fibrillary Acidic Protein ◽

Elderly Patients ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction

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Increased systemic inflammation and oxidative stress in patients with worsening congestive heart failure: improvement after short-term inotropic support

Clinical Science ◽

10.1042/cs20050317 ◽

2006 ◽

Vol 110 (4) ◽

pp. 483-489 ◽

Cited By ~ 69

Author(s):

Michel White ◽

Anique Ducharme ◽

Reda Ibrahim ◽

Lucette Whittom ◽

Joel Lavoie ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Congestive Heart Failure ◽

Systemic Inflammation ◽

Plasma Levels ◽

Inotropic Support ◽

Left Ventricular Ejection ◽

Short Term ◽

Hs Crp ◽

And Oxidative Stress

In the present study, we evaluated circulating pro-inflammatory mediators and markers of oxidative stress in patients with decompensated CHF (congestive heart failure) and assessed whether clinical recompensation by short-term inotropic therapy influences these parameters. Patients with worsening CHF (n=29, aged 61.9±2.7 years), NYHA (New York Heart Association) class III–IV, and left ventricular ejection fraction of 23.7±1.8% were studied. Controls comprised age-matched healthy volunteers (n=15; 54.1±3.2 years). Plasma levels of cytokines [IL (interleukin)-6 and IL-18], chemokines [MCP-1 (monocyte chemotactic protein-1)], adhesion molecules [sICAM (soluble intercellular adhesion molecule), sE-selectin (soluble E-selectin)], systemic markers of oxidation [TBARS (thiobarbituric acid-reactive substances), 8-isoprostaglandin F2α and nitrotyrosine] and hs-CRP (high-sensitivity C-reactive protein) were measured by ELISA and colorimetric assays at admission and 30 days following 72-h milrinone (n=15) or dobutamine (n=14) infusion. Plasma IL-6, IL-18, sICAM, E-selectin, hs-CRP and oxidative markers were significantly higher in patients on admission before inotropic treatment compared with controls (P<0.05). Short-term inotropic support improved clinical status as assessed by NYHA classification and by the 6-min walk test and significantly decreased plasma levels of IL-6, IL-18, sICAM, hs-CRP and markers of oxidation (P<0.05) at 30 days. The effects of milrinone and dobutamine were similar. In conclusion, our results demonstrate that patients with decompensated CHF have marked systemic inflammation and increased production of oxygen free radicals. Short-term inotropic support improves functional status and reduces indices of inflammation and oxidative stress in patients with decompensated CHF.

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