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Published on: August 18, 2016
No causal association between inflammation and Chlamydia pneumoniae in patients with chronic ischemic arterial
Raúl Altman1, Jorge Rouvier, Alejandra Scazziota
1Centro de Trombosis de Buenos Aires, Argentina. draltman@arnet.com.ar
Insights
This study found no causal link between Chlamydia pneumoniae infection and arterial or valvular disease markers like C-reactive protein and fibrinogen. However, C-reactive protein and fibrinogen levels were strongly correlated in patients.
Area of Science:
- Cardiovascular disease research
- Infectious disease immunology
Background:
- Chlamydia pneumoniae is a potential etiological agent in cardiovascular diseases.
- Inflammatory markers such as C-reactive protein and fibrinogen are associated with cardiovascular risk.
Purpose of the Study:
- To investigate the association between Chlamydia pneumoniae infection and inflammatory markers in patients with arterial disease and heart valve prostheses.
Main Methods:
- Serum levels of C-reactive protein, Chlamydia-specific IgG antibody, and fibrinogen were measured.
- Patients were categorized into arterial disease and heart valve prosthesis groups.
- Statistical analysis was performed to assess correlations and differences between groups.
Main Results:
- Chlamydia pneumoniae antibodies were prevalent in both arterial (67.3%) and valvular (59.1%) groups.
- Elevated C-reactive protein and fibrinogen levels were observed in both groups, but correlations with C. pneumoniae were poor.
- Fibrinogen levels differed significantly between the arterial and valvular groups.
- A significant correlation was found between C-reactive protein and fibrinogen levels.
Conclusions:
- No causal association was found between Chlamydia pneumoniae infection and inflammation markers in the studied patient groups.
- Fibrinogen levels may help differentiate between arterial and valvular disease.
- C-reactive protein and fibrinogen are significantly correlated, indicating a shared inflammatory pathway.
Abstract:
The C-reactive protein, Chlamydia-specific IgG antibody, and fibrinogen were assayed in the serum of 159 patients with arterial disease (the arterial group) and 203 patients with heart valve prostheses (the valvular group) and no demonstrable coronary disease. In the arterial group, the Chlamydia pneumoniae antibody was > or = 1:32 for 67.3% (107/159) of the patients, the C-reactive protein was elevated in 41.5% (66/159), and the fibrinogen was elevated in 27.7% (44/159). In the valvular group, the C. pneumoniae antibody was > or = 1:32 for 59.1% (120/203) of the patients; the C-reactive protein was elevated in 34.0% (69/203), and the fibrinogen was elevated in 17.2% (35/203). Of 107 patients in the arterial group with C. pneumoniae titers > or = 1:32, only 26 (24.3%) had elevated fibrinogen (426 +/- 29 mg/dL) and 44 (41.1%) had elevated C-reactive protein (1.06 +/- 0.52 mg/dL). Similarly, of the 120 patients in the valvular group with C. pneumoniae titers > or = 1:32, 17 (14.2%) had elevated fibrinogen (409 +/- 29 mg/dL) and 34 had elevated C-reactive protein (0.99 +/- 1.1 mg/dL). Correlated poorly was C. pneumoniae with C-reactive protein and fibrinogen levels. Only the fibrinogen level could be discriminated between the arterial and the valvular group. These results suggest that no causal association exists between inflammation and C. pneumoniae. A highly significant correlation between C-reactive protein and fibrinogen levels was found.
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