Scatter plots showing the linear relationships between age and leukocyte telomere length, indices of LV diastolic function and leukocyte telomere length.

<p>(A) Linear regressions between E/A ratio and leukocyte telomere length. (B) Linear regressions between Em/Am ratio and leukocyte telomere length.</p

Age-Related Left Ventricular Changes and Their Association with Leukocyte Telomere Length in Healthy People

<div><p>Introduction</p><p>With advancing age the left ventricle (LV) undergoes structural and functional changes, thereby creating the substrate for the development of diseases. One possible mechanism of the ageing heart is a cellular senescence. Leukocyte telomere length (LTL) is a marker of replicative ageing. The purpose of this study was to evaluate the structure and function of the LV in people of different ages free of cardiovascular diseases (CVD) and regular drug medication and to assess their relationship with LTL. We hypothesized that age-related changes in LV myocardium are associated with telomere length.</p><p>Methods</p><p>The study population consisted of 150 healthy, non-obese volunteers aged 28 to 78 years without history of CVD, significant deviations by 12-lead electrocardiogram and negative exercise test (treadmill stress test). All the participants underwent standardized transthoracic echocardiography using an available system (iE33; Philips). The LTL was measured by real-time quantitative polymerase chain reaction. We determined the relative ratio of telomere repeat copy number (T) to single-copy gene copy number (S).</p><p>Results</p><p>In the older people there was a higher wall thickness than in the younger (1.03±0.09 vs. 0.88±0.10, p<0.01), whereas LV mass index was comparable between them (85.8±15.40 vs. 83.1±11.8, p = 0.20). There was a decrease in LV dimensions with advancing age (p<0.001). Older subjects had impairment in LV relaxation. LTL was associated with decreased E/A, Em/Am ratio (β = -0.323, p = 0.0001) after adjusting for age, sex and risk factors. There is no relation between the LTL and the structure of LV.</p><p>Conclusions</p><p>Our data suggest that the ageing process leads to changes in LV structure and diastolic function and is linked with a phenotype of concentric LV remodeling. Telomere attrition is associated with age-related LV diastolic dysfunction. Telomere length appears to be a biomarker of myocardial ageing.</p></div

Comparison of the main clinical, echocardiographic characteristics and leukocyte telomere length between younger and older individuals.

<p>Measurements are shown as means ± SD. <i>LVDD</i>, LV diameter at the end of diastole; <i>LVDS</i>, LV diameter at the end of systole; <i>LVDV</i>, LV end-diastolic volume; <i>LVSV</i>, end-systolic volume; <i>LVMI</i>, LV mass index; <i>EF</i>, ejection fraction; <i>SWT</i>, septal wall thickness; <i>PWT</i>, posterior wall thickness; <i>E</i>, peak early phase filling velocity; <i>A</i>, peak atrial phase filling velocity; <i>DTE</i>, E wave deceleration time; <i>IVR</i>T, isovolumic relaxation time; <i>Em</i>, peak early diastolic mitral annular velocity; <i>Am</i>, peak diastolic mitral annular velocity; <i>S</i>, peak systolic velocity of pulmonary venous flow; <i>D</i>, peak anterograde diastolic velocity of pulmonary venous flow; <i>PV Ar</i>, peak retrograde velocity in late diastole of pulmonary venous flow.</p><p>Comparison of the main clinical, echocardiographic characteristics and leukocyte telomere length between younger and older individuals.</p