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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Infectious atherosclerosis: is the hypothesis still alive? A clinically based approach to the dilemma
Carlos L Alviar1, Juan G Echeverri, Nicolas I Jaramillo
1St Luke's-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY, USA. ca2369@columbia.edu
Abstract:
Among the multiple factors involved in the pathophysiology of heart disease, infections have been proposed to play a role in atherosclerosis with most of the available evidence implicating Chlamydia pneumonia, influenza virus and Mycoplasma pneumoniae. Based on a model case presentation, we speculate that in the absence of traditional risk factors and in the context of an ongoing respiratory infection caused by a pro-inflammatory pathogen (M. pneumoniae) along with a past positive serologic history for potentially proven atherogenic microorganism (C. pneumoniae) and infection may elicit potentially pathogenic events on vascular wall cells and leukocytes of atheromatous lesions, supporting the hypothesis that such infections may potentiate atherosclerotic cardiovascular disease (CVD).
Insights
Infections like Mycoplasma pneumoniae and Chlamydia pneumoniae may contribute to atherosclerosis and cardiovascular disease (CVD) development, even without traditional risk factors. This suggests infections can trigger harmful events in blood vessels, worsening heart disease.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Pathophysiology
Background:
- Infections are increasingly recognized as potential contributors to cardiovascular disease (CVD).
- Evidence suggests a role for pathogens such as Chlamydia pneumoniae, influenza virus, and Mycoplasma pneumoniae in atherosclerosis.
- The precise mechanisms by which infections influence vascular health require further elucidation.
Observation:
- A case presentation highlighted a patient with no traditional risk factors for heart disease.
- The patient had an ongoing respiratory infection with Mycoplasma pneumoniae.
- A history of Chlamydia pneumoniae infection was also noted.
Findings:
- The co-occurrence of these infections may trigger pathogenic events in vascular cells and leukocytes within atheromatous lesions.
- This scenario supports the hypothesis that specific infections can potentiate the development or progression of atherosclerotic cardiovascular disease (CVD).
- Pro-inflammatory pathogens like Mycoplasma pneumoniae, combined with prior exposure to atherogenic microorganisms like Chlamydia pneumoniae, appear significant.
Implications:
- This research underscores the importance of considering infectious agents in the etiology of CVD, particularly in atypical cases.
- Further investigation into the mechanisms by which infections influence vascular health is warranted.
- Identifying and targeting infectious triggers could offer novel therapeutic avenues for preventing and managing atherosclerotic cardiovascular disease.
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