Endothelial cell activation in patients with decompensated heart failure

Paolo C. Colombo, Javier E. Banchs, Sulejman Celaj, Ashok Talreja, Justine Lachmann, Shailesh Malla, Nicholas B. DuBois, Anthony W. Ashton, Farhana Latif, Ulrich P. Jorde, J. Anthony Ware, Thierry H. LeJemtel

Research output: Contribution to journalArticle

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Abstract

Background - Vascular endothelial functions, other than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients with chronic heart failure (CHF). Veins and arteries are exposed to the same circulating proinflammatory mediators in patients with CHF. The present study tested whether endothelial cell activation occurs in veins of patients with decompensated CHF and whether activation, if present, subsides with return to a clinically compensated state. Methods and Results - Fifteen patients with decompensated CHF requiring transient inotropic support and 6 age-matched, healthy controls were studied. Endothelial cells and blood were collected from a forearm vein, and brachial artery flow-mediated dilation (FMD) was measured before and 24 hours after discontinuation of short-term inotropic therapy, when patients had returned to a steady compensated state. Nitrotyrosine immunoreactivity (an intracellular marker of oxidative stress), cyclooxygenase-2 (COX-2), and inducible NO synthase (iNOS) expression were significantly higher in venous endothelial cells of patients in clinical decompensation when compared with healthy subjects. Return to a compensated state resulted in a significant reduction in nitrotyrosine immunoreactivity, COX-2, and iNOS expression. Concomitantly, a significant increase in FMD and a decline in plasma total 8-isoprostane and bicycloprostaglandin E2 levels were observed. Venous endothelial NOS expression was unaffected by clinical decompensation. Conclusions - Clinical decompensation in CHF is associated with activation of the venous endothelium. Return to a compensated state after short-term inotropic therapy results in a significant reduction in endothelial nitrotyrosine formation, COX-2, and iNOS expression.

Original languageEnglish (US)
Pages (from-to)58-62
Number of pages5
JournalCirculation
Volume111
Issue number1
DOIs
StatePublished - Jan 4 2005
Externally publishedYes

Fingerprint

Endothelial Cells
Heart Failure
Cyclooxygenase 2
Veins
8-epi-prostaglandin F2alpha
Nitric Oxide Synthase
Dilatation
Brachial Artery
Nitric Oxide Synthase Type II
Forearm
Endothelium
Blood Vessels
Healthy Volunteers
Nitric Oxide
Oxidative Stress
Arteries
Therapeutics
3-nitrotyrosine

Keywords

  • Endothelium
  • Heart failure
  • Inflammation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Colombo, P. C., Banchs, J. E., Celaj, S., Talreja, A., Lachmann, J., Malla, S., ... LeJemtel, T. H. (2005). Endothelial cell activation in patients with decompensated heart failure. Circulation, 111(1), 58-62. https://doi.org/10.1161/01.CIR.0000151611.89232.3B

Endothelial cell activation in patients with decompensated heart failure. / Colombo, Paolo C.; Banchs, Javier E.; Celaj, Sulejman; Talreja, Ashok; Lachmann, Justine; Malla, Shailesh; DuBois, Nicholas B.; Ashton, Anthony W.; Latif, Farhana; Jorde, Ulrich P.; Ware, J. Anthony; LeJemtel, Thierry H.

In: Circulation, Vol. 111, No. 1, 04.01.2005, p. 58-62.

Research output: Contribution to journalArticle

Colombo, PC, Banchs, JE, Celaj, S, Talreja, A, Lachmann, J, Malla, S, DuBois, NB, Ashton, AW, Latif, F, Jorde, UP, Ware, JA & LeJemtel, TH 2005, 'Endothelial cell activation in patients with decompensated heart failure', Circulation, vol. 111, no. 1, pp. 58-62. https://doi.org/10.1161/01.CIR.0000151611.89232.3B
Colombo PC, Banchs JE, Celaj S, Talreja A, Lachmann J, Malla S et al. Endothelial cell activation in patients with decompensated heart failure. Circulation. 2005 Jan 4;111(1):58-62. https://doi.org/10.1161/01.CIR.0000151611.89232.3B
Colombo, Paolo C. ; Banchs, Javier E. ; Celaj, Sulejman ; Talreja, Ashok ; Lachmann, Justine ; Malla, Shailesh ; DuBois, Nicholas B. ; Ashton, Anthony W. ; Latif, Farhana ; Jorde, Ulrich P. ; Ware, J. Anthony ; LeJemtel, Thierry H. / Endothelial cell activation in patients with decompensated heart failure. In: Circulation. 2005 ; Vol. 111, No. 1. pp. 58-62.
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T1 - Endothelial cell activation in patients with decompensated heart failure

AU - Colombo, Paolo C.

AU - Banchs, Javier E.

AU - Celaj, Sulejman

AU - Talreja, Ashok

AU - Lachmann, Justine

AU - Malla, Shailesh

AU - DuBois, Nicholas B.

AU - Ashton, Anthony W.

AU - Latif, Farhana

AU - Jorde, Ulrich P.

AU - Ware, J. Anthony

AU - LeJemtel, Thierry H.

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N2 - Background - Vascular endothelial functions, other than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients with chronic heart failure (CHF). Veins and arteries are exposed to the same circulating proinflammatory mediators in patients with CHF. The present study tested whether endothelial cell activation occurs in veins of patients with decompensated CHF and whether activation, if present, subsides with return to a clinically compensated state. Methods and Results - Fifteen patients with decompensated CHF requiring transient inotropic support and 6 age-matched, healthy controls were studied. Endothelial cells and blood were collected from a forearm vein, and brachial artery flow-mediated dilation (FMD) was measured before and 24 hours after discontinuation of short-term inotropic therapy, when patients had returned to a steady compensated state. Nitrotyrosine immunoreactivity (an intracellular marker of oxidative stress), cyclooxygenase-2 (COX-2), and inducible NO synthase (iNOS) expression were significantly higher in venous endothelial cells of patients in clinical decompensation when compared with healthy subjects. Return to a compensated state resulted in a significant reduction in nitrotyrosine immunoreactivity, COX-2, and iNOS expression. Concomitantly, a significant increase in FMD and a decline in plasma total 8-isoprostane and bicycloprostaglandin E2 levels were observed. Venous endothelial NOS expression was unaffected by clinical decompensation. Conclusions - Clinical decompensation in CHF is associated with activation of the venous endothelium. Return to a compensated state after short-term inotropic therapy results in a significant reduction in endothelial nitrotyrosine formation, COX-2, and iNOS expression.

AB - Background - Vascular endothelial functions, other than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients with chronic heart failure (CHF). Veins and arteries are exposed to the same circulating proinflammatory mediators in patients with CHF. The present study tested whether endothelial cell activation occurs in veins of patients with decompensated CHF and whether activation, if present, subsides with return to a clinically compensated state. Methods and Results - Fifteen patients with decompensated CHF requiring transient inotropic support and 6 age-matched, healthy controls were studied. Endothelial cells and blood were collected from a forearm vein, and brachial artery flow-mediated dilation (FMD) was measured before and 24 hours after discontinuation of short-term inotropic therapy, when patients had returned to a steady compensated state. Nitrotyrosine immunoreactivity (an intracellular marker of oxidative stress), cyclooxygenase-2 (COX-2), and inducible NO synthase (iNOS) expression were significantly higher in venous endothelial cells of patients in clinical decompensation when compared with healthy subjects. Return to a compensated state resulted in a significant reduction in nitrotyrosine immunoreactivity, COX-2, and iNOS expression. Concomitantly, a significant increase in FMD and a decline in plasma total 8-isoprostane and bicycloprostaglandin E2 levels were observed. Venous endothelial NOS expression was unaffected by clinical decompensation. Conclusions - Clinical decompensation in CHF is associated with activation of the venous endothelium. Return to a compensated state after short-term inotropic therapy results in a significant reduction in endothelial nitrotyrosine formation, COX-2, and iNOS expression.

KW - Endothelium

KW - Heart failure

KW - Inflammation

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