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Polymorphism rs7023923 and monocyte count in blood donors and coronary artery disease patients
Jarosław Szymon Świrta, Marzena Krzemień-Grandys, Justyna Totoń-Żurańska
1Uniwersytet Jagielloński Collegium Medicum. Pawel.Wolkow@uj.edu.pl.
Insights
Genetic associations with monocytosis, like rs7023923, may not apply to coronary artery disease (CAD) patients. Environmental factors in CAD patients likely confound these genetic links, requiring cautious interpretation in clinical settings.
Area of Science:
- Cardiovascular Genetics
- Immunology
- Population Health
Background:
- Monocytes play a key role in coronary artery disease (CAD), with elevated levels linked to increased incidence.
- Both genetic and environmental factors influence monocyte counts, with specific genetic polymorphisms identified in healthy populations.
- The association between genetic polymorphisms and monocytosis may differ between healthy individuals and patient populations due to confounding environmental factors.
Purpose of the Study:
- To investigate if the genetic association of the polymorphism rs7023923 with monocytosis observed in healthy individuals is consistent in patients diagnosed with CAD.
- To assess the clinical relevance of genetic predisposition to monocytosis in the context of established coronary artery disease.
Main Methods:
- Comparison of monocyte counts and the association with rs7023923 between healthy blood donors and patients undergoing elective coronarography for CAD diagnosis.
- Statistical analysis to determine the significance of the association, adjusting for age and sex.
Main Results:
- While leucocytosis and neutrophilocytosis were higher in CAD patients, monocyte counts did not significantly differ between groups (p = 0.25).
- The association between rs7023923 and monocytosis was confirmed in healthy blood donors (p = 0.0156) but not in CAD patients (p = 0.61).
- Age and sex did not alter the observed lack of association in the patient group.
Conclusions:
- The translation of genetic association findings from healthy populations to patient cohorts, such as those with CAD, should be approached with caution.
- Environmental factors differentiating healthy individuals from CAD patients may confound the magnitude of genetic associations, complicating interpretation in clinical settings.
Background:
The importance of the role of monocytes in coronary artery disease (CAD) is well documented. An increased number of circulating monocytes is associated with higher incidence of CAD. Both environmental and genetic factors influence monocytosis. The latter have been extensively studied since the development of high-throughput genome-wide association studies. Several associations between polymorphisms and monocytosis were found among healthy individuals; the first example was rs7023923. The magnitude of the association of studied polymorphisms with the trait of interest is often confounded by environmental factors and may therefore differ between patient and healthy populations. It is very important to determine the magnitude of the association among patients to predict outcome of the disease, e.g. myocardial infarction.
Aim:
To determine whether the magnitude of association of rs7023923 with monocytosis, previously reported among healthy volunteers, is similar in patients in whom diagnosis of CAD was determined during elective coronarography.
Methods And Results:
Leucocytosis and neutrophilocytosis were higher among patients with CAD, while thrombocytosis was lower. Monocyte count did not differ among the studied groups (p = 0.25). We confirmed the association of rs7023923 with monocytosis among healthy blood donors (p = 0.0156) but not among patients admitted for elective coronarography (p = 0.61). Inclusion of the age and sex of patients in the statistical model did not modify the results.
Conclusions:
Our data suggest that translation of the results of genetic association with the studied traits from healthy to patient population should be implemented with caution. It is possible that numerous environmental factors, which discriminate healthy volunteers from CAD patients, confound the magnitude of genetic associations and make interpretation of the data in patients less clear.
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