C.R. Balistreri, C. Caruso, C. Pisano, G. Bianco, K. Fattouch, M. Caruso, E. Maresi, G. Ruvolo, G. Candore

The prevalence of cardiovascular diseases (CVD) rises with ageing and is one of the main causes of mortality in Western countries. In view of the progressive population ageing, there is an urge for a better understanding of age-associated diseases, such as sporadic thoracic aortic aneurysm (S-TAA), and their underlying molecular mechanisms. Several cardiovascular risk factors (i.e. hypertension, oxidative stress, smoking, etc.) seem to explain most of risk of S-TAA in general population. However, little is known about its precise cellular, molecular mechanisms and genetic determinants. In particular, at an individual level there is wide variation in both its occurrence and complications (i.e. dissection and rupture) and age and gender manifestation, even in individuals with the same risk factor profiles. The reasons for this wide inter-individual variation in susceptibility are poorly understood. However, it is currently emerging the speculation of inter-individual variation in risk of CVDs, such as S-TAA, as result of variation in the rate of biological ageing. In particular, recent studies report blood leukocyte telomere-TTAGGG DNA repeats at the ends of chromosomes-length as potential better predictor for onset of CVDs than chronological age. In the light of this evidence, we are determining whether the mean of blood leukocyte telomere length might be a predictor for S-TAA. To this aim, peripheral blood samples were collected from 161 S-TAA patients and 128 age- and gender matched controls. Genomic DNA was extracted from leukocytes and telomere lengths determined using a chemioluminescence technique. The preliminary results, showing shorter telomeres in patients than in controls, seem to be promising confirming our hypothesis. Thus, telomere assay could contribute to identify individuals at risk for S-TAA.

Keywords (Optional): 
biological ageing
mean blood leukocyte telomere length