TY - JOUR
T1 - Inflammation, infection, and aortic valve sclerosis
T2 - Insights from the Olmsted County (Minnesota) population
AU - Agmon, Yoram
AU - Khandheria, Bijoy K.
AU - Tajik, A. Jamil
AU - Seward, James B.
AU - Sicks, Jo Rean D.
AU - Fought, Angela J.
AU - O'Fallon, W. Michael
AU - Smith, Thomas F.
AU - Wiebers, David O.
AU - Meissner, Irene
N1 - Funding Information:
Supported, in part, by research grant NS-06663 from the NINDS.
PY - 2004/6
Y1 - 2004/6
N2 - Atherosclerosis-related mechanisms, including inflammation and possibly infection, are likely to be involved in the pathogenesis of calcific aortic valve disease. The purpose of this study was to examine whether systemic inflammatory markers and Chlamydia pneumoniae seropositivity are associated with aortic valve sclerosis (AVS) in a sample of the general population. Transesophageal echocardiography was performed in 381 subjects (median age: 67 years, range: 51-101; 52% men), a sample of the adult population in Olmsted County, Minnesota. The associations between systemic inflammatory markers (blood counts, including white blood cells differential counts, fibrinogen, and high-sensitivity C-reactive protein [hs-CRP]), C. pneumoniae immunoglobulin G (IgG) antibody titers, and AVS were examined. AVS was present in 140 subjects (37% of the population). After adjustment for age, sex, and smoking status: (1) hs-CRP was associated with AVS (odds ratio: 1.20 per two-fold increase in hs-CRP; 95% confidence interval: 1.01-1.43; P=0.04), but this association was not significant after adjustment for additional risk factors for AVS, including body mass index (P=0.52). (2) Blood counts and fibrinogen were not associated with AVS (P-values >0.30). (3) C. pneumoniae IgG antibody titers (low [1:16-1:32], intermediate [1:64-1:128], or high [≥1:256] titers, compared with titers <1:16) were not associated with AVS (P=0.21). In conclusion, hs-CRP is weakly associated with AVS, an association that is not independent of other AVS risk factors. Blood counts, fibrinogen, and C. pneumoniae seropositivity are not associated with AVS. These findings suggest that other non-inflammatory non-infectious mechanisms are likely to have a role in the pathogenesis of calcific aortic valve disease.
AB - Atherosclerosis-related mechanisms, including inflammation and possibly infection, are likely to be involved in the pathogenesis of calcific aortic valve disease. The purpose of this study was to examine whether systemic inflammatory markers and Chlamydia pneumoniae seropositivity are associated with aortic valve sclerosis (AVS) in a sample of the general population. Transesophageal echocardiography was performed in 381 subjects (median age: 67 years, range: 51-101; 52% men), a sample of the adult population in Olmsted County, Minnesota. The associations between systemic inflammatory markers (blood counts, including white blood cells differential counts, fibrinogen, and high-sensitivity C-reactive protein [hs-CRP]), C. pneumoniae immunoglobulin G (IgG) antibody titers, and AVS were examined. AVS was present in 140 subjects (37% of the population). After adjustment for age, sex, and smoking status: (1) hs-CRP was associated with AVS (odds ratio: 1.20 per two-fold increase in hs-CRP; 95% confidence interval: 1.01-1.43; P=0.04), but this association was not significant after adjustment for additional risk factors for AVS, including body mass index (P=0.52). (2) Blood counts and fibrinogen were not associated with AVS (P-values >0.30). (3) C. pneumoniae IgG antibody titers (low [1:16-1:32], intermediate [1:64-1:128], or high [≥1:256] titers, compared with titers <1:16) were not associated with AVS (P=0.21). In conclusion, hs-CRP is weakly associated with AVS, an association that is not independent of other AVS risk factors. Blood counts, fibrinogen, and C. pneumoniae seropositivity are not associated with AVS. These findings suggest that other non-inflammatory non-infectious mechanisms are likely to have a role in the pathogenesis of calcific aortic valve disease.
KW - Aortic valve
KW - Echocardiography
KW - Infection
KW - Inflammation
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U2 - 10.1016/j.atherosclerosis.2004.01.028
DO - 10.1016/j.atherosclerosis.2004.01.028
M3 - Article
C2 - 15136064
AN - SCOPUS:2342582680
SN - 0021-9150
VL - 174
SP - 337
EP - 342
JO - Atherosclerosis
JF - Atherosclerosis
IS - 2
ER -