PMID- 12860222
OWN - NLM
STAT- MEDLINE
DCOM- 20030813
LR  - 20220318
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 92
IP  - 2
DP  - 2003 Jul 15
TI  - Elevated circulating levels of inflammatory cytokines and bacterial endotoxin in 
      adults with congenital heart disease.
PG  - 188-93
AB  - Chronic heart failure is a state of immune activation, and endotoxin is a 
      potential trigger for cytokine production. Our aim was to study whether immune 
      activation and endotoxemia occur in adults with congenital heart disease. We 
      prospectively measured tumor necrosis factor (TNF)-alpha, soluble TNF receptors 
      (sTNFR-1, sTNFR-2), interleukin-6, interleukin-10, endotoxin, and soluble CD14 
      levels in 52 consecutive adults with congenital heart disease (age 34 +/- 2 years 
      [mean +/- SEM]) and 18 healthy controls (age 31 +/- 1 years). A variety of 
      congenital heart lesions were studied: single ventricle physiology (n = 15), 
      systemic right ventricle (n = 7), tetralogy of Fallot (n = 20), and "other" 
      congenital heart disease (n = 10). Patients were subgrouped into asymptomatic 
      (New York Heart Association [NYHA] class I, n = 11), mild (NYHA class II, n = 
      30), and moderate/severe (NYHA class III/IV, n = 11) categories. Patients had 
      elevated TNF and interleukin-6 levels compared with controls (TNF 2.8 vs 2.1 
      pg/ml, p <0.05; interleukin-6 8.5 vs 5.7 pg/ml, p <0.001). TNF levels were higher 
      in patients with moderate/severe symptoms compared with patients who were 
      asymptomatic or had mild symptoms (p <0.05). Soluble TNFR-1 levels related 
      directly to the degree of systemic ventricular impairment (p <0.05). There were 
      no significant differences in sTNFR-1, sTNFR-2, interleukin-10, or sCD14 levels 
      between patients and controls. Endotoxin levels were greater in patients with 
      congenital heart disease versus controls (0.40 vs 0.26 endotoxin units/ml, p 
      <0.0001). Thus, adults with congenital heart disease have elevated levels of 
      inflammatory cytokines and bacterial endotoxin, which relate to functional 
      status. Congenital heart disease in adults may be amenable to novel 
      anti-inflammatory therapies in selected patients.
FAU - Sharma, Rakesh
AU  - Sharma R
AD  - Department of Clinical Cardiology, National Heart & Lung Institute, Imperial 
      College School of Medicine, London, UK. drsharmarakesh@aol.com
FAU - Bolger, Aidan P
AU  - Bolger AP
FAU - Li, Wei
AU  - Li W
FAU - Davlouros, Periklis A
AU  - Davlouros PA
FAU - Volk, Hans-Dieter
AU  - Volk HD
FAU - Poole-Wilson, Philip A
AU  - Poole-Wilson PA
FAU - Coats, Andrew J S
AU  - Coats AJ
FAU - Gatzoulis, Michael A
AU  - Gatzoulis MA
FAU - Anker, Stefan D
AU  - Anker SD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
RN  - 0 (Antigens, CD)
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Cytokines)
RN  - 0 (Endotoxins)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Adult
MH  - Antigens, CD/blood
MH  - Antineoplastic Agents/blood
MH  - Cross-Sectional Studies
MH  - Cytokines/*blood
MH  - Endotoxemia/*blood/etiology/*immunology
MH  - Endotoxins/*blood
MH  - Female
MH  - Heart Defects, Congenital/*blood/complications/*immunology
MH  - Humans
MH  - Inflammation/*blood/complications/*immunology
MH  - Interleukin-10/blood
MH  - Interleukin-6/blood
MH  - Lipopolysaccharide Receptors/blood
MH  - Male
MH  - Prospective Studies
MH  - Receptors, Tumor Necrosis Factor/blood
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Severity of Illness Index
MH  - Tumor Necrosis Factor-alpha/analysis
EDAT- 2003/07/16 05:00
MHDA- 2003/08/14 05:00
CRDT- 2003/07/16 05:00
PHST- 2003/07/16 05:00 [pubmed]
PHST- 2003/08/14 05:00 [medline]
PHST- 2003/07/16 05:00 [entrez]
AID - S0002914903005368 [pii]
AID - 10.1016/s0002-9149(03)00536-8 [doi]
PST - ppublish
SO  - Am J Cardiol. 2003 Jul 15;92(2):188-93. doi: 10.1016/s0002-9149(03)00536-8.