JL Fleg (Bethesda, MD, US) analysed the magnitude of the problem and described the decline of cardiovascular performance in the elderly. Data was derived from the Baltimore longitudinal study.
With advancing age (20-80 years), the arterial tree stiffens, causing a rise in systolic blood pressure and an increase in pulse pressure; as a result, the left ventricle (LV) thickens (concentric remodeling). This however results in a reduced rate of early diastolic filling and decreased left ventricular compliance. Increased arterial elastance leads to; increased ventricular elastance, preserved ventricular-arterial coupling and optimal energetical transfer. As a consequence, pump function and cardiac output at rest are preserved with age. Longitudinal systolic function and left ventricular twisting-untwisting are altered. Cardiovascular performance during exercise is impaired. This adaptation goes along with increased atrial pressures, increased atrial contribution to LV filling, increased LA volume and altered LA function, especially during exercise.
Other data came from the Rochester Minnesota project (M. Redfield) and indicated that these age-related changes are not at all benign and are associated with a marked increase in global mortality and morbidity. In addition, the ageing atria and their altered morphology and function become more vulnerable to exercise-facilitated atrial fibrillation. It has to be further investigated what the effect of ageing is, in contrast to the effects of traditional and recent cardiovascular risk factors.
Vascular & cardiac, morphology & function as a function of age. Data from 2524 healthy subjects, 35-55 years old (ASKLEPIOS study, BE) IMT intima-media thickness, PWV pulse wave velocity, LVMI left ventricular mass index, EF ejection fraction.
S.J. Bekaert and E.R. Rietzschel (Ghent BE) presented recent European population data (Asklepios study) on telomere biology and cardiovascular ageing. Why are individuals succesful in managing of the ageing process? Can we unravel the fountain of youth? One of the key aspects is the telomere length of the chromosomes. This is the chomosome clock.
Telomeres are the protections of the chromosome ends. With age, these telomeres shorten and this determines cell replication and survival. The telomere attrition rate is a biological measurement of ageing as opposed to calendar ageing. Women have longer telomeres than men. Differences between men and women are due to different attrition rates. In the given age range of the study (35-55), the classical risk factors were not associated with TL, in contrast to earlier reports. There was an inverse association with inflammation (hsCRP, fibrinogen and IL6), and with oxidative stress (oxidised LDL). Surprisingly TL was inversely related with a pro-ageing lifestyle (waist circumference, alcohol overconsumption, smoking duration) and directly related to fruit and vegetable intake. The influences are of limited magnitude for each individual factor, but cumulative and quite impressive when poor lifestyle is considered as a whole, presumably by the mechanism of exposing cells to increased oxidative stress.
M. Giorgio (Milan IT) focused on the mitochondrial clock and the protein p66Shc, which localises in different intracellular compartments of the cell including the mitochondria intermembrane space. The mitochondria host the electron chain transfers, the ATP production and also the generation of ROS - which promotes ageing. Reducing H2O2 produced by mitochondria promoted longevity. Indeed cells, as well as mice lacking p66Shc, developed less oxidative damage and apoptosis, and had a longer lifespan.
S. Pepe (Melbourne AU) explained how diet could modify cardiac substrate at the level of mitochondrial and other cardiac cell membranes. While the aging process results in altered membrane lipid composition in qualitative terms, lipid-protein interactions and pathological outcomes are altered due to modified production of lipid metabolites and their interactions with reactive oxygen species, which modify proteins (adducts) to diminish energy metabolism, and to trigger pathological signalling and outcomes. The major effect of ageing at the mitochondrial membrane level is deficiency in omega-3 PUFA and this can be modified by increased dietary intake of omega-3 PUFA. This could potentially prevent atrial fibrillation when the follow up data of this population will be available. This is one of the first solid reports showing that some effects of ageing can be, to a certain extent, limited.