Promoting healthy cardiovascular aging: emerging topics

Abstract

The development of age-related cardiovascular (CV) dysfunction increases the risk of CV disease as well as other chronic age-associated disorders, including chronic kidney disease, and Alzheimer’s disease and related dementias. Major manifestations of age-associated CV dysfunction that increase disease risk are vascular dysfunction, primarily vascular endothelial dysfunction and arterial stiffening, and elevated systolic blood pressure. Declines in nitric oxide bioavailability secondary to increased oxidative stress and inflammation are established mechanisms of CV dysfunction with aging. Moreover, fundamental mechanisms of aging, termed the “hallmarks of aging” extend to the CV system and, as such, may be considered “hallmarks of CV aging”. These mechanisms represent viable therapeutic targets for treating CV dysfunction with aging. Healthy lifestyle behaviors, such as regular aerobic exercise and certain dietary patterns, are considered “first-line” strategies to prevent and/or treat age-associated CV dysfunction. Despite the well-established benefits of these strategies, many older adults do not meet the recommended guidelines for exercise or consume a healthy diet. Therefore, it is important to establish alternative and/or complementary evidence-based approaches to prevent or reverse age-related CV dysfunction. Targeting fundamental mechanisms of CV aging with interventions such as time-efficient exercise training, food-derived molecules, termed nutraceuticals, or select synthetic pharmacological agents represents a promising approach. In the present review, we will highlight emerging topics in the field of healthy CV aging with a specific focus on how exercise, nutrition/dietary patterns, nutraceuticals and select synthetic pharmacological compounds may promote healthy CV aging, in part, by targeting the hallmarks of CV aging.

Peripheral vascular dysfunction and the aging brain

“…Elastin degradation consequently results in deposition of collagen in the arterial wall (i.e., fibrosis), ultimately creating a stiffer extracellular matrix [ 34 ]. The most well-established cellular/molecular mechanisms mediating adverse arterial wall remodeling is excessive production of ROS (relative to endogenous antioxidant defenses) and chronic low-grade inflammation [ 35 ].…”

“…Aortic PWV, measured as carotid artery to femoral artery (carotid-femoral) PWV is the reference standard non-invasive in vivo assessment of aortic stiffness in humans [ 36 ]. In rodents, aortic PWV is measured as the PWV between the aortic arch and the abdominal aorta [ 35 ]. The local distensibility of the carotid artery can also be determined in humans by assessing carotid artery compliance (change in artery diameter for a given change in arterial pressure) [ 37 ].…”

“…Endothelium-derived NO subsequently diffuses to vascular smooth muscle cells, where it activates an intracellular signaling cascade leading to vascular smooth muscle relaxation and vasodilation (endothelium-dependent dilation [EDD]) [ 38 ]. Like mechanisms mediating age-related large elastic artery stiffening, the underpinnings of reduced NO bioavailability and endothelial dysfunction with aging are primarily explained by excessive ROS-related oxidative stress and inflammation [ 35 ]. Moreover, NO-mediated endothelial dysfunction can promote large elastic artery stiffening by inducing a relative state of vasoconstriction in vascular smooth muscle cells [ 35 ].…”

“…Like mechanisms mediating age-related large elastic artery stiffening, the underpinnings of reduced NO bioavailability and endothelial dysfunction with aging are primarily explained by excessive ROS-related oxidative stress and inflammation [ 35 ]. Moreover, NO-mediated endothelial dysfunction can promote large elastic artery stiffening by inducing a relative state of vasoconstriction in vascular smooth muscle cells [ 35 ]. In addition to reducing NO bioavailability, excessive ROS production and inflammation can increase the expression of endothelin-1 (ET-1) [ 39 ].…”

Demographic and Socioeconomic Factors Associated to Fruits and Vegetables Consumption in Elderly Europeans: A Systematic Review

“…Several epidemiological studies stress the importance of decreasing the consumption of simple carbohydrates and increasing high-fiber intake, as well as maintaining frequent physical activity, to prevent chronic diseases and improve human health [ 4 , 5 ]. Dietary patterns with high fruits and vegetables consumption, such as the Mediterranean diet, are associated with a decreased incidence of cardiovascular and endocrine diseases [ 6 , 7 ].…”