Role of Helicobacter pylori infection in pathogenesis of atherosclerosis

Rajesh Vijayvergiya1, Ramalingam Vadivelu1

  • 1Rajesh Vijayvergiya, Ramalingam Vadivelu, Department of Cardiology, Advanced Cardiac Centre, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India.

Insights

Infection may contribute to atherosclerosis, a debated topic. Research suggests links between Helicobacter pylori and vascular diseases, highlighting inflammation and genetic factors.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease Epidemiology

Background:

  • The role of infection in atherosclerosis remains a debated topic despite a century-old hypothesis.
  • Epidemiological and clinical studies suggest an association, but conflicting results stem from population and methodological heterogeneity, and confounders.

Purpose of the Study:

  • To explore the debated role of infection in the pathogenesis of atherosclerosis.
  • To review the evidence linking infectious agents, particularly Helicobacter pylori, to vascular diseases.

Main Methods:

  • Review of epidemiological and clinical studies investigating the link between infection and atherosclerosis.
  • Analysis of proposed pathogenetic mechanisms, including chronic inflammation, dyslipidemia, and genetic modulation.

Main Results:

  • Infection can trigger chronic inflammation, a key factor in atherosclerosis development.
  • Studies indicate a positive association between Cytotoxic associated gene-A positive Helicobacter pylori strains and vascular diseases like coronary artery disease and stroke.
  • Infection-mediated genetic modulation is an emerging theory in atherosclerosis pathogenesis.

Conclusions:

  • Infection is a potential contributor to atherosclerosis, acting through chronic inflammation and possibly genetic modulation.
  • Further large-scale studies are needed to clarify the multifaceted role of infection in atherosclerosis.
  • Understanding these pathogenetic mechanisms is crucial for refining knowledge on infection and atherosclerosis.

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