Rate of telomere shortening and cardiovascular damage: a longitudinal study in the 1946 British Birth Cohort.

AIM: Cross-sectional studies reported associations between short leucocyte telomere length (LTL) and measures of vascular and cardiac damage. However, the contribution of LTL dynamics to the age-related process of cardiovascular (CV) remodelling remains unknown. In this study, we explored whether the rate of LTL shortening can predict CV phenotypes over 10-year follow-up and the influence of established CV risk factors on this relationship. METHODS AND RESULTS: All the participants from the MRC National Survey of Health and Development (NSHD) with measures of LTL and traditional CV risk factors at 53 and 60-64 years and common carotid intima-media thickness (cIMT), cardiac mass and left ventricular function at 60-64 years were included. LTL was measured by real-time polymerase chain reaction and available at both time points in 1033 individuals. While LTL at 53 years was not linked with any CV phenotype at 60-64 years, a negative association was found between LTL and cIMT at 60-64 years (ß = -0.017, P = 0.015). However, the strongest association was found between rate of telomere shortening between 53 and 60-64 years and values of cIMT at 60-64 years (ß = -0.020, P = 0.006). This association was not affected by adjustment for traditional CV risk factors. Cardiac measurements were not associated with cross-sectional or longitudinal measures of LTL. CONCLUSION: These findings suggest that the rate of progression of cellular ageing in late midlife (reflected by the rate of LTL attrition) relates to vascular damage, independently from contribution of CV risk factor exposure.

The Year in Cardiology 2012: focus on cardiovascular disease prevention.

Current data suggest that advances in cardiovascular (CV) treatment have resulted in significant reduction in CV mortality but also in prolongation of life with disability. Focus on CV prevention is likely to reverse this unfavourable trend. In this review we provide information on the new European guidelines on CV prevention and discuss biomarkers and vascular imaging techniques which can assist in refining CV risk prediction. Finally, we provide new information on lifestyle and pharmacological advances which are likely to result in significant CV risk reduction.

Blood pressure and vascular alterations with growth in childhood.

The long preclinical phase of atherosclerosis involves the interaction of genetic and environmental factors that modulate the progression of disease from early life. A variety of noninvasive tests have been used to study the arterial phenotype of childhood, allowing identification of arterial alterations long before clinical symptoms of cardiovascular (CV) disease become apparent. These techniques have improved our understanding of the evolution of atherosclerosis, indentifying three major developmental factors which influence the future risk of CV disease in childhood: prenatal growth, early postnatal growth and childhood obesity. Specific changes in arterial properties and increased values of blood pressure are detectable in children with low birth weight, suggesting that intrauterine growth retardation could programme the future risk of CV disease. However, an accelerated growth rate in infancy and early childhood is often associated with low birth weight and with specific vascular alterations, making it difficult to distinguish the contribution of prenatal and postnatal growth patterns to later cardiovascular disease risk. Relationships between growth patterns and CV disease risk are further complicated by the link between rapid postnatal growth and later development of childhood overweight and obesity, conditions associated with early changes in vascular physiology and that potentially affect future CV outcome. This article aims to provide an overview of evidence in support of fetal programming and growth acceleration hypotheses for adult CV disease. Specific attention is given to obesity-related vascular alterations and their effects on future CV disease risk. We also summarise current non-invasive approaches to investigate the precursors and early development of CV disease, emphasising their potential applications in childhood.

Comparison of two automatic methods for the assessment of brachial artery flow-mediated dilation.

OBJECTIVES: Brachial artery flow-mediated dilation (FMD) is associated with risk factors providing information on cardiovascular prognosis. Despite the large effort to standardize the methodology, the FMD examination is still characterized by problems of reproducibility and reliability that can be partially overcome with the use of automatic systems. We developed real-time software for the assessment of brachial FMD (FMD Studio, Institute of Clinical Physiology, Pisa, Italy) from ultrasound images. The aim of this study is to compare our system with another automatic method (Brachial Analyzer, MIA LLC, IA, USA) which is currently considered as a reference method in FMD assessment. METHODS: The agreement between systems was assessed as follows. Protocol 1: Mean baseline (Basal), maximal (Max) brachial artery diameter after forearm ischemia and FMD, calculated as maximal percentage diameter increase, have been evaluated in 60 recorded FMD sequences. Protocol 2: Values of diameter and FMD have been evaluated in 618 frames extracted from 12 sequences. RESULTS: All biases are negligible and standard deviations of the differences are satisfactory (protocol 1: -0.27 ± 0.59%; protocol 2: -0.26 ± 0.61%) for FMD measurements. Analysis times were reduced (-33%) when FMD Studio is used. Rejected examinations due to the poor quality were 2% with the FMD Studio and 5% with the Brachial Analyzer. CONCLUSIONS: In conclusion, the compared systems show a optimal grade of agreement and they can be used interchangeably. Thus, the use of a system characterized by real-time functionalities could represent a referral method for assessing endothelial function in clinical trials.