[Inflammation and infection in stable coronary disease and acute coronary syndrome]
J Bermejo García1, P Martínez Martínez, J F Martín Rodríguez
1Departamentos de Cardiología, ICICOR de la Universidad, Valladolid. jbgarcia@scisquemica.org
Insights
Inflammation is present in acute coronary syndromes, but serological tests do not link infection to coronary artery disease. Further research is needed to understand the causes of this inflammatory response.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- Coronary artery disease (CAD) is a leading cause of mortality worldwide.
- The role of inflammation and infection in the development of CAD remains an area of active research.
- Previous studies have suggested potential links between specific pathogens and CAD, but findings have been inconsistent.
Purpose of the Study:
- To investigate the relationship between inflammation and infection in patients with acute and stable coronary artery disease.
- To assess the prevalence of IgG and IgM antibodies against Chlamydia pneumoniae, Cytomegalovirus, and Helicobacter pylori in CAD patients and controls.
- To evaluate C-reactive protein levels as a marker of inflammation in different CAD subgroups.
Main Methods:
- A case-control study was conducted with 60 patients with acute coronary syndrome, 40 with stable CAD, and 40 healthy controls.
- Serum samples were analyzed for IgG and IgM antibodies against C. pneumoniae, Cytomegalovirus, and H. pylori.
- C-reactive protein (CRP) levels were measured in all participants, with serial CRP measurements in the acute coronary syndrome group.
Main Results:
- No significant differences in IgG seropositivity for C. pneumoniae, Cytomegalovirus, or H. pylori were found among the acute, stable, and control groups.
- A high prevalence of C-reactive protein positivity was observed in the acute coronary syndrome group (80%) compared to the stable CAD group (25%) and controls (0%).
- CRP levels were significantly higher in Q-wave myocardial infarction than in unstable angina/non-Q-wave myocardial infarction and decreased one month after the acute event.
Conclusions:
- Inflammation, as indicated by C-reactive protein, is significantly elevated in acute coronary syndromes and to a lesser extent in stable CAD.
- Serological evidence does not support a direct link between C. pneumoniae, Cytomegalovirus, or H. pylori infection and the development of coronary syndromes.
- The inflammatory response in CAD may be driven by mechanisms other than the infections assessed, suggesting serological methods may be inadequate for establishing such relationships.
Objective:
To study whether inflammation and infection are related to coronary artery disease.
Design:
Sixty patients (44 males, mean age 62 +/- 13 years) with acute coronary syndrome and 40 with stable coronary artery disease (31 males, age 64 +/- 10 years) and a control group of 40 individuals (34 males, 53 +/- 5 years) were analyzed. IgG against Chlamydia pneumoniae, Cytomegalovirus and Helicobacter pylori plus C-reactive protein were assessed in all serum samples. In addition, IgM against C. pneumoniae and Cytomegalovirus on admission and C-reactive protein one month later were measured in acute patients.
Results:
No IgM seropositivity was observed. A high prevalence of IgG seropositivity with no significant differences among the groups was found: C. pneumoniae: acute group 44 (73%), stable group 29 (73%) and control group 25 (63%); Cytomegalovirus: 55 (92%), 37 (92%) and 38 (95%), respectively; and H. pylori, 43 (72%), 32 (80%) and 34 (85%) respectively. There was a high rate of positive C-reactive protein in the acute group: 48 (80%) vs 10 (25%) the stable group and 0% the control group (p < 0.001). C-reactive protein levels were higher in Q-wave infarction than in unstable angina/ non-Q-wave infarction (median 22.65 vs 7.69, p < 0.001). One month later, C-reactive protein levels decreased (median 22.65 vs 3.38, p < 0.001), but were still positive in 40%.
Conclusions:
These data suggest that inflammation is detected by the commonly used methods in clinic practice in acute coronary syndromes and to a lesser extent in stable coronary artery disease. It seems that different mechanisms other than infection account for this inflammatory response, at least this being so when infection is assessed by serology. Serology does not appear to be an adequate method to determine the possible relationship among coronary syndromes, infection and inflammation.
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