Leukocyte telomere length (LTL) has been regarded as a potential marker of biologic aging because it usually shortens in a predictable way with age. Recently, a growing interest in cardiovascular aging has led to a number of new epidemiologic studies investigating LTL in various disease conditions. Some methodological problems exist because there are different methods available to determine LTL, and standardization is much needed. For example, in the majority of studies, patients with early-onset coronary heart disease have been shown to have shorter LTL. In addition, patients with diabetes mellitus complications tend to have shorter LTL than control subjects. On the other hand, increased left ventricular hypertrophy or mass is associated with longer LTL, and studies investigating hypertension have reported both shorter and longer LTL than found in normotensive control subjects. There is, therefore, a need for longitudinal studies to elucidate these complicated relationships further, to provide estimations of telomere attrition rates, and to overcome analytical problems when only cross-sectional studies are used. The understanding of cardiovascular aging and telomere biology may open up new avenues for interventions, such as stem cell therapy or agents that could retard this aging process over and beyond conventional risk factor control.
Keywords: CAD; CHD; CVD; EF; FH; HR; IHD; LTL; LVH; LVMI; MI; RTL; TBP; cardiovascular disease; coronary artery disease; coronary heart disease; ejection fraction; familiar hypercholesterolemia; hazard ratio; ischemic heart disease; left ventricular hypertrophy; left ventricular mass index; leukocyte telomere length; myocardial infarction; q-PCR; quantitative polymerase chain reaction; relative telomere length; telomere binding protein.
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