Clinical manifestations of atherosclerosis in an elderly population are related to plasma neopterin, NGAL and endothelin-1, but not to Chlamydia pneumoniae serology.
BACKGROUND
Inflammatory mediators secreted by leukocytes are implicated in atherogenesis. Chlamydia (C.) pneumoniae infection has been suggested as a trigger of this process. We investigated relationships between C. Pneumoniae serology, inflammatory mediators and symptomatic cardiovascular disease in old age.


METHODS
In a cross-sectional study at baseline with a prospective 4 year follow-up, intraplatelet cyclic 3'-5'adenosine monophosphate (cAMP) and cyclic 3'-5'guanosine monophosphate (cGMP), plasma neutrophil gelatinase associated lipocalin (NGAL), plasma soluble tumor necrosis factor receptor-1 (TNFR-1) plasma neopterin and plasma endothelin-1 (ET-1) were analysed together with IgG and IgA antibodies for C. Pneumoniae in an elderly reference population (n=140, median age 71 years, 71 females). Twenty-one subjects had clinical manifestations of cardiovascular disease at baseline and another 21 were diagnosed with cardiovascular disease during follow-up.


RESULTS
In age adjusted logistic regression, subjects with cardiovascular disease showed higher plasma levels of neopterin (p=0.02), NGAL (p=0.04), and ET-1 (p<0.01). If subjects with cardiovascular disease at baseline were excluded from the analysis, higher plasma neopterin (p=0.01) and lower serum HDL cholesterol (p=0.03) predicted cardiovascular disease during follow-up. The presence of IgG or IgA against C. pneumoniae was not associated with cardiovascular disease. Neither were there any associations between inflammatory or endothelial parameters and C. pneumoniae serology.


CONCLUSIONS
The inflammatory mediators neopterin and NGAL and endothelial derived vasoconstrictive ET-1 were increased in elderly subjects with symptomatic cardiovascular disease. Increased plasma neopterin predicted cardiovascular disease during follow-up. No relationships were found between C. Pneumoniae serology and cardiovascular disease.
Department of Vascular Diseases, University of Lund, Sweden.
J
J
Forsblad
A
A
Gottsäter
K
K
Persson
L
L
Jacobsson
F
F
Lindgärde
D000209:Acute-Phase Proteins; D000368:Aged; D001161:Arteriosclerosis / Q000097:blood* / Q000209:etiology / Q000382:microbiology*; D002352:Carrier Proteins / Q000097:blood*; D023521:Chlamydophila Infections / Q000276:immunology; D016993:Chlamydophila pneumoniae / Q000302:isolation & purification*; D003430:Cross-Sectional Studies; D000242:Cyclic AMP / Q000097:blood; D006152:Cyclic GMP / Q000097:blood; D019332:Endothelin-1 / Q000097:blood*; D005260:Female; D006801:Humans; D000071068:Lipocalin-2; D054834:Lipocalins; D016015:Logistic Models; D008297:Male; D019798:Neopterin / Q000097:blood*; D015513:Oncogene Proteins / Q000097:blood*; D011518:Proto-Oncogene Proteins
D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D019332:Endothelin-1; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D019798:Neopterin; D000242:Cyclic AMP; D006152:Cyclic GMP