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A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
09:33

A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology

Published on: February 7, 2015

Infectious burden and carotid plaque thickness: the northern Manhattan study

Mitchell S V Elkind1, Jorge M Luna, Yeseon Park Moon

  • 1Neurological Institute, 710 West 168th Street, Box 182, New York, NY 10032, USA. mse13@columbia.edu

Stroke
|January 16, 2010
PubMed
Abstract

Insights

Past infections, including Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses, are linked to increased carotid plaque thickness. This suggests infections may contribute to atherosclerosis and stroke risk.

Area of Science:

  • Cardiovascular Disease Epidemiology
  • Infectious Disease Research
  • Atherosclerosis Pathogenesis

Background:

  • Prior infections are implicated in atherosclerosis and stroke risk.
  • The cumulative burden of common infections may influence vascular health.

Purpose of the Study:

  • To investigate the association between serological evidence of common infections and carotid plaque thickness.
  • To determine if a weighted index of infectious burden correlates with atherosclerosis markers.

Main Methods:

  • Antibody titers to five common pathogens (Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, herpesvirus 1 and 2) were measured.
  • A weighted infectious burden index was calculated using Cox models for stroke risk.
  • Carotid plaque thickness was assessed using high-resolution carotid duplex Doppler studies.

Main Results:

  • 861 participants had available serological and plaque thickness data.
  • Infectious burden index was significantly associated with increased maximum carotid plaque thickness (0.09 mm per SD increase).
  • 52% of participants exhibited carotid plaque.

Conclusions:

  • A quantitative index of infectious burden is associated with carotid plaque thickness in a multiethnic cohort.
  • These findings support the hypothesis that common infections contribute to atherosclerosis, potentially via inflammation.
  • Further research is needed to confirm these results and define infectious burden as a vascular risk factor.

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