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Hepatitis A IgG seropositivity and coronary atherosclerosis assessed by angiography
J Auer1, M Leitinger, R Berent
12nd Medical Department, General Hospital Wels, Grieskirchnerstrasse 42, A-4600 Wels, Austria. johann.auer@khwels.at
Insights
Hepatitis A virus (HAV) infection is not linked to coronary artery disease (CAD). However, a higher overall infectious burden from multiple pathogens is associated with increased CAD risk.
Area of Science:
- Cardiology
- Infectious Diseases
- Atherogenesis
Background:
- Infectious agents, especially persistent intracellular pathogens, may contribute to atherogenesis.
- The study investigated a potential link between Hepatitis A Virus (HAV) and coronary artery disease (CAD).
Purpose of the Study:
- To determine if Hepatitis A Virus (HAV) seropositivity is associated with significant coronary artery disease (CAD).
Main Methods:
- Examined the association between HAV infection and angiographically proven CAD.
- Tested serum IgG antibodies to HAV in 218 patients undergoing coronary angiography.
Main Results:
- 81.7% of patients had anti-HAV IgG antibodies.
- CAD prevalence was similar in HAV seropositive (66.3%) and seronegative (57.5%) patients (P=0.385).
- A higher number of infectious pathogens (4 or more of 6 tested) correlated with CAD (48.8% vs 31.2%, P=0.02).
Conclusions:
- HAV seropositivity does not predict CAD risk.
- HAV infection appears not to be associated with CAD.
- Increased 'infectious burden' from multiple pathogens correlates with CAD.
Background:
Infectious agents, in particular intracellular pathogens that can establish long-term, persistent infection, may play an important role in atherogenesis. We tested the hypothesis that hepatitis A virus (HAV) could be associated with significant coronary artery disease.
Methods:
The possible association between HAV infection and angiographically proven coronary artery disease (CAD) was studied. Blood from 218 patients undergoing coronary angiography was tested for serum IgG antibodies to HAV.
Results:
Of the 218 patients, 178 (81.7%) had anti-HAV IgG antibodies. CAD prevalence was 66.3% in HAV seropositive and 57.5% in HAV seronegative patients (P=0.385). In contrast, the number of infectious pathogens to which an individual has been exposed correlates with CAD. Four or more of the six seromarkers tested for particular infections (HAV, Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, influenza type A and type B) were positive in 48.8% of patients with CAD and in 31.2% of patients in patients without CAD (P=0.02).
Conclusions:
This analysis demonstrated that HAV seropositivity is not a predictor of risk for CAD. HAV infection, therefore, seems not to be associated with CAD. The number of infectious agents to which an individual has been exposed ('infectious burden') correlates with CAD.