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Kort telomerlängd markör för tidigt vaskulärt åldrande

Nilsson, Peter LU and Fyhrquist, Frej (2007) In Läkartidningen 104(39). p.2801-2805
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Läkartidningen
volume
104
issue
39
pages
2801 - 2805
publisher
Sveriges Läkarförbund
external identifiers
  • pmid:17958006
  • scopus:35548994615
ISSN
0023-7205
language
Swedish
LU publication?
yes
id
c44e847c-9020-4443-9173-1bfae02bf2a0 (old id 1139694)
alternative location
http://ltarkiv.lakartidningen.se/2007/temp/pda33977.pdf
http://ltarkiv.lakartidningen.se/artNo33977
date added to LUP
2008-08-19 16:20:11
date last changed
2017-01-01 07:45:22
@article{c44e847c-9020-4443-9173-1bfae02bf2a0,
  abstract     = {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.},
  author       = {Nilsson, Peter and Fyhrquist, Frej},
  issn         = {0023-7205},
  language     = {swe},
  number       = {39},
  pages        = {2801--2805},
  publisher    = {Sveriges Läkarförbund},
  series       = {Läkartidningen},
  title        = {Kort telomerlängd markör för tidigt vaskulärt åldrande},
  volume       = {104},
  year         = {2007},
}