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[Chlamydia pneumoniae and Helicobacter pylori infections in acute myocardial infarction]
G Di Tano1, I Picerno, M L Calisto
1Divisione di Cardiologia, Azienda Ospedale Piemonte, Messina. giditano@tin.it
Insights
Infection and heart attacks share a link. This study found higher Chlamydia pneumoniae (CP) antibodies in acute myocardial infarction patients, suggesting CP may trigger heart conditions.
Area of Science:
- Cardiology
- Infectious Diseases
- Epidemiology
Background:
- Growing evidence links infections to acute coronary syndromes.
- This study investigated Chlamydia pneumoniae (CP) and Helicobacter pylori (HP) antibodies in myocardial infarction patients.
Purpose of the Study:
- To determine the frequency of CP and HP antibodies in patients with acute myocardial infarction (AMI) compared to controls.
- To explore potential links between these infections and AMI.
Main Methods:
- 206 AMI patients and 142 controls were analyzed.
- Antibodies to HP and CP were measured using ELISA and immunofluorescence.
- Patients and controls were matched for age, sex, and socio-economic status, excluding smokers, diabetics, and hypertensive individuals.
Main Results:
- No significant difference in HP antibodies between AMI patients and controls.
- Significantly higher CP antibody titers were found in 83% of AMI patients versus 57% of controls (p < 0.001).
- CP seropositivity in AMI patients correlated with increased fibrinogen levels.
Conclusions:
- Acute myocardial infarction is associated with increased CP seropositivity.
- CP antibodies were not linked to elevated C-reactive protein.
- Further controlled studies are needed to confirm CP's role in triggering acute coronary syndromes.
Background:
Increasing evidence suggests an acute or chronic linkage between infection and acute coronary syndromes. The aim of this study was to assess the frequency of Chlamydia pneumoniae (CP) and Helicobacter pylori (HP) antibodies in patients with angiographically defined acute myocardial infarction and in population controls. Case patients and controls were drawn from the same geographic area (city of Messina and its province).
Methods:
Blood samples were collected in 206 incident cases of acute myocardial infarction presenting to the Coronary Care Unit (196 men, 10 women, mean age 58+/-7 years) in the period from March 1997 to June 1999. Case patients were selected if they were non-smokers, non-diabetic and if they had no history of hypertension. The control group consisted of 142 healthy subjects, without a known history of smoking, diabetes, and hypertension. Controls were matched to acute myocardial infarction patients for age, sex and socio-economic status. Commercial ELISA assay was used to measure IgG antibody to HP (positive titer > 8 IU/ml) and indirect immunofluorescence method was used to assess IgG antibody anti-CP (IgG titer > 1:64 was considered a marker of chronic infection).
Results:
No significant difference was observed in the frequency of HP antibodies in acute myocardial infarction patients and in the control group (43.3 vs 41.5%, p = NS, odds ratio-OR 1, 95% confidence interval-CI 0.7-1.6). On the contrary, CP titers were increased in 83% of acute myocardial infarction patients, and in 57% of control subjects (p < 0.001, OR 3.6, 95% CI 2.2-5.7). In acute myocardial infarction patients seropositivity for CP was associated with increased basal fibrinogen levels (539 vs 445 mg/dl). No correlation was found between seropositivity to CP and C-reactive protein, and with total or fractionated cholesterol and triglyceride concentrations.
Conclusions:
The present data indicate that, in our sample, acute myocardial infarction was associated with an increased frequency of CP seropositivity. The presence of CP antibodies was not associated with elevated levels of C-reactive protein. Our data support the need for controlled studies to investigate the role of these infective agents as a trigger of acute coronary syndromes.