Kort telomerlängd markör för tidigt vaskulärt åldrande

Age is the most important risk factor known for cardiovascular disease manifestations. However, the biological ageing of an individual may be substantially different from the chronological age in what has been called “differential ageing”. This process can be evaluated by arterial stiffness (pulse wave velocity), and the marker of telomere length and by levels of telomerase enzymatic activity. Several studies have now documented that telomeres are shorter, versus telomere length in healthy controls, in subjects with atheroscleroris, coronary heart disease, insulin resistance, congestive heart failure, elevated pulse pressure, type-1 as well as type-2 diabetes, and in many other conditions. This could be interpreted as a marker of the Early Vascular Ageing (EVA) syndrome in subjects susceptible to premature cardiovascular disease at a relatively early age. Risk factors such as smoking and obesity, but also chronic psychosocial stress, are associated with telomere attrition. A new analysis of pravastatin treatment in the WOSCOP intervention trial of middle-aged men has shown that this treatment reduced the strength of prediction of coronary events related to shorter telomere length. In summary, risk factor control and statin treatment seem to reduce the progress of EVA and its clinical consequences. This could be a useful methodological construct to evaluate the treatment of other preventive drugs and interventions. There is still, however, a lack of studies with repeated measurements of telomere length in the same individual, as well as changes in telomerase activity over time. It is still premature to use telomere length as a screening tool in clinical practice, but arterial stiffness is crudely possible to evaluate by simple (mean) pulse pressure determination.