Letters to the Editor |
Departments of Epidemiology (N.P., S.W.) and Cardiology (S.W.), Johns Hopkins Bloomberg School of Public Health,, Baltimore, MD
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
We read with great interest the recent report by Brouilette et al1 on white cell telomere length and risk of premature myocardial infarction. We agree with the authors that the findings have the potential to be of great importance in understanding the etiology of coronary heart disease and in distinguishing biological from chronological aging. We were, however, concerned about two points in the analysis.
First, in Table 2, the effect of CHD risk factors on telomere length is displayed with adjustment for case status. Each of these variables differs between cases and controls, as does telomere length. The analysis controls for case status, and the results are presented as evidence for lack of a significant relationship between each of these factors and telomere length. We are concerned that, because the CHD risk factors are so different between cases and controls, adjusting for case status may artificially attenuate the effect of the risk factor on telomere length. We would like the authors to present a stratified analysis so that the effect of CHD risk factors on telomere length can be assessed in cases and controls separately.
Second, Figure 2 and the corresponding analysis are presented without apparent adjustment for age, sex, and the other CHD risk factors. While we are confident that the relationship will remain the same, we feel that it is necessary to present the adjusted analysis to fully support the authors claim of the independence of effects of telomere length and age.
We look forward
Division of Cardiology (N.J.S.), Department of Medicine, Department of Epidemiology and Public Health (J.R.T.), University of Leicester, Leicester, United Kingdom
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