P3995
Advanced glycation end-products and telomere shortening contribute to cardiac aging: the relationship with myocardial strain

Extract

Introduction: There are a number of structural and functional changes in the heart with aging and each of them can have significant implications for manifestation of cardiovascular disease (CVD). Assessment of myocardial strain by using the new techniques such as speckle-tracking echocardiography (STE) could become a more sensitive analysis of the cardiac aging. One possible mechanism of the aging heart can be associated with formation glucose-dependent cross-links of collagen, termed advanced glycation end products (AGEs). AGEs accumulate with age, and can increased myocardial stiffness and changes in the biomechanics of contraction. These age-related changes can be associated with shortening of telomeres – a marker of replicative senescence. The purpose of this study was to examine the left ventricular (LV) myocardial strain in relation with glycation and telomere shortening.

Methods: 2-D speckle tracking analysis was performed on 151 healthy non-obese volunteers aged 60 to 87 years without history of CVD, diabetes and significant deviations by 12-lead electrocardiogram. LV myocardial deformations were obtained using off-line analysis program QLAB.Global longitudinal LV strain (GLS), LV systolic twist, circumferential and radial strains were measured. Methylglyoxal (MG) is a byproduct of glucose metabolism and an inducer of AGEs. Concentration of MG in serum was determined using HPLC with UV detector. Telomere length was measured in leukocyte (LTL) by real-time quantitative polymerase chain reaction.