Carotid-femoral pulse wave velocity (PWV), a marker of arterial stiffness, is an established independent cardiovascular (CV) risk factor. Little information is available on the pattern and determinants of the longitudinal change in PWV with aging. Such information is crucial to elucidating mechanisms underlying arterial stiffness and the design of interventions to retard it. Between 1988 and 2013, we collected 2 to 9 serial measures of PWV in 354 men and 423 women of the Baltimore Longitudinal Study of Aging, who were 21 to 94 years of age and free of clinically significant CV disease. Rates of PWV increase accelerated with advancing age in men more than women, leading to gender differences in PWV after the age of 50. In both sexes, not only systolic blood pressure (SBP) ≥140mmHg, but also SBP of 120–139mmHg was associated with steeper rates of PWV increase compared to SBP<120mmHg. Furthermore, there was a dose-dependent effect SBP in men with marked acceleration in PWV rate of increase with age at SBP ≥140mmHg compared to SBP of 120–139mmHg. Except for waist circumference in women, no other traditional CV risk factors predicted longitudinal PWV increase. In conclusion, the steeper longitudinal increase of PWV in men than women led to gender difference that expanded with advancing age. Age and systolic blood pressure are the main longitudinal determinants of pulse wave velocity and the effect of systolic blood pressure on PWV trajectories exists even in the pre-hypertensive range.

8. Wirtz H, Hasenclever D, Schwabe K, et al. ACE inhibitor for lung protection during mechanical ventilation for acute lung injury-results of the double-blind, placebo controlled, randomised ACEmeVENT pilot study.

Over the past three decades, considerable effort has been dedicated to quantifying the pace of ageing yet identifying the most essential metrics of ageing remains challenging due to lack of comprehensive measurements and heterogeneity of the ageing processes. Most of the previously proposed metrics of ageing have been emerged from cross‐sectional associations with chronological age and predictive accuracy of mortality, thus lacking a conceptual model of functional or phenotypic domains. Further, such models may be biased by selective attrition and are unable to address underlying biological constructs contributing to functional markers of age‐related decline. Using longitudinal data from the Baltimore Longitudinal Study of Aging (BLSA), we propose a conceptual framework to identify metrics of ageing that may capture the hierarchical and temporal relationships between functional ageing, phenotypic ageing and biological ageing based on four hypothesized domains: body composition, energy regulation, homeostatic mechanisms and neurodegeneration/neuroplasticity. We explored the longitudinal trajectories of key variables within these phenotypes using linear mixed‐effects models and more than 10 years of data. Understanding the longitudinal trajectories across these domains in the BLSA provides a reference for researchers, informs future refinement of the phenotypic ageing framework and establishes a solid foundation for future models of biological ageing.