Introduction: Telomere length (TL), a marker of cellular aging, has been linked to cardiovascular disease (CVD). Recent studies suggest that obesity (as defined by body-mass index (BMI) may induce premature cardiovascular (CV) aging in association with telomere shortening via oxidative stress mechanisms. However, sarcopenia and accumulation of body fat with aging may confound the use of BMI as a metric of obesity evaluation among aged adults. We hypothesize that body fat mass (BFM), and not BMI, is associated with shorter TL, which in turn is associated impairments in diastolic function in these aged adults.
Methods: We studied community based participants without known CVD. Eligible participants underwent detailed body composition analyzer that measures BFM. They underwent tissue Doppler echocardiography for assessment of myocardial diastolic function. Lymphocytes were isolated from the blood samples using Ficoll-Paque. TL was measured in isolated lymphocytes at G1, using the flow cytometric method.
Results: The present analysis included 251 participants (mean age 72.5±4.4 years; 113 (45%) females, mean BMI 23.6 ±3.6 kg/m2; 152 (61%) had risk factors of hypertension, 132 (53%) dyslipidemia, 55 (22%) diabetes mellitus. Both BFM (r=-0.15, p=0.018) and BMI (r=-0.15, p=0.015) correlated with TL. However, upon adjustments for age and risk factors, BFM was independently associated with TL (β=-0.033, p=0.032) while BMI was not independently associated with TL (β=-0.056, p=0.07). Among those with high BFM, short TL was associated with worse lateral mitral annular peak velocity of atrial filling (lateral A) (0.08±0.02 vs 0.07±0.01, p=0.028) but not among participants with low BFM. Among those with high BFM, TL was independently associated with lateral A (β=-0.004, p=0.04), after adjustments for age and risk factors. Among those with low BFM, TL was not associated with cardiac function.
Conclusions: Our results show that direct measure of body fat is associated with telomere length, rather than BMI. Shorter TL is associated with diastolic dysfunction in subjects with high but not low BFM. These results suggest that accumulation of body fat is both an important mediator of cellular aging and a modulator of the latter’s impact on heart function.