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Assessment of systemic inflammation and infective pathogen burden in patients with cardiac syndrome X
Gaetano Antonio Lanza1, Alfonso Sestito, Giovanni Cammarota
1Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Rome, Italy. g.a.lanza@inwind.it
Insights
This study found that patients with Syndrome X (SX) exhibit low-grade systemic inflammation, distinct from Coronary Artery Disease (CAD) patients. This inflammation is not linked to common infections, suggesting other underlying causes for SX.
Area of Science:
- Cardiology
- Immunology
- Infectious Diseases
Background:
- Inflammation is a known factor in Coronary Artery Disease (CAD).
- The role of systemic inflammation in the pathogenesis of Syndrome X (SX) remains unclear.
- Potential links between SX, inflammation, and specific infections (H. pylori, C. pneumoniae, CMV, EBV) were investigated.
Purpose of the Study:
- To assess systemic inflammation markers in patients with Syndrome X (SX).
- To explore the relationship between inflammation and infections (H. pylori, C. pneumoniae, CMV, EBV) in SX patients.
- To compare inflammation levels in SX patients, CAD patients, and healthy controls.
Main Methods:
- Studied 55 SX patients, 49 CAD patients, and 60 healthy controls.
- Measured plasma levels of high-sensitivity C-reactive protein (hs-CRP) and interleukin-1 receptor antagonist (IL-1Ra).
- Assessed infections from H. pylori, C. pneumoniae, cytomegalovirus (CMV), and Epstein-Barr virus (EBV) in a subset of participants.
Main Results:
- SX patients showed higher hs-CRP levels than controls but lower levels than CAD patients.
- Both SX and CAD patients had significantly higher IL-1Ra levels than controls, with no significant difference between SX and CAD groups.
- No significant differences in the prevalence of the studied infections were found across the groups.
Conclusions:
- Evidence suggests increased low-grade systemic inflammation in patients with cardiac Syndrome X (SX).
- This inflammation in SX is not associated with an increased burden of H. pylori, C. pneumoniae, CMV, or EBV infections.
- The findings indicate that systemic inflammation in SX is independent of these specific infectious agents.
Abstract:
Inflammation plays a key role in coronary artery disease (CAD), but whether it is involved in the pathogenesis of syndrome X (SX) is not known. Thus, we assessed the presence of systemic inflammation in patients with SX and its possible relation to infections from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus. We studied 55 patients with SX (57 +/- 8 years old; 27 women), 49 with stable angina and obstructive CAD (56 +/- 8 years old; 24 women), and 60 healthy controls (57 +/- 11 years old; 24 women). Plasma levels of high-sensitivity C-reactive protein and interleukin-1 receptor antagonist were measured in all patients. Infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus was assessed in 43 patients with SX, 40 patients with CAD, and in 39 controls. Patients with SX had lower serum levels of C-reactive protein than did patients with CAD (4.06 +/- 6.8 vs 5.99 +/- 7.8 mg/L, p = 0.013) but higher levels of C-reactive protein than did controls (1.75 +/- 1.98 mg/L; p = 0.008). Plasma levels of interleukin-1 receptor antagonist were higher in patients with CAD (570 +/- 738 pg/ml) and patients with SX (494 +/- 677 pg/ml) than in controls (254 +/- 174, pg/ml; p = 0.0003 vs CAD and p = 0.013 vs SX) but did not differ significantly between patients with CAD or SX (p = 0.20). There were no differences across groups in the prevalence of infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus and in the prevalence of 1, 2, 3, and 4 infections (p = 0.99). Among patients with SX, no correlation was found between markers of inflammation and indexes of disease activity (angina episodes, exercise test results). Our data show evidence of increased low-grade systemic inflammation in patients with cardiac SX, which was unrelated to an increased infectious pathogen burden.
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