Researchers explain the existence of pathophysiological links between longevity and cardiovascular aging.

Cardiovascular aging is defined as structural and functional changes in older individuals that can lead to cardiovascular diseases [1]. The changes that most commonly occur during cardiovascular aging include decreases in systolic and diastolic function, left ventricular hypertrophy and myocardial remodeling.

Previous research has indicated a progressive rise in the proportion of older individuals throughout the world. The population of people aged 65 years and above has increased to 28.4% in Japan and 11.9% in China. However, aging is reported to be associated with several age-associated diseases, especially cardiovascular disease (CVD). CVD is reported to be a significant cause of death globally as well as the largest independent risk factor for cardiovascular aging [2].

Longevity.Technology: Several studies have identified an association between longevity and cardiovascular aging through various pathophysiological mechanisms. Many factors that cause cardiovascular diseases have also been found to be associated with aging processes and vice versa. Studies have reported that many cardio-metabolic disorders including dyslipidemia, insulin resistance, arterial hypertension and hyperglycemia share similar pathophysiological mechanisms with longevity and aging.

Additionally, several genetic modulators of longevity have also been observed to have an impact on cardiovascular aging. Knowledge regarding these aging mechanisms can thus help to develop interventions to delay cardiovascular aging and thereby improve the longevity of individuals.

Five places in the world have been identified to have the highest percentage of centenarians – these are also termed “Blue Zones”. This study was carried out on the residents of Ikaria island in Greece which is one such Blue Zone. The most important pathophysiological links that have been found to exist between longevity and cardiovascular aging include oxidative stress, inflammatory activation, metabolic disorders, arterial stiffness, hypertension, genetic factors, lifestyle changes and environmental factors [3].

An increase in oxidative stress can cause an imbalance between the production of reactive oxygen species (ROS) production and antioxidant defenses. This can cause mitochondrial DNA mutations and damage to other mitochondrial constituents. Several studies have reported that increased activity of antioxidants and resistance to oxidative stress can prolong the lifespan and thereby provide protection against cardiovascular diseases (CVD).

Several studies have shown low-grade inflammation to be a significant risk factor for many age-related pathologies, including CVD. An increase in pro-inflammatory molecules has been observed in the elderly population as well as certain age-related diseases. Moreover, cellular senescence has been found to promote the secretion of these molecules that can negatively impact the longevity of individuals and increase the risk of CVD.

Furthermore, metabolic disorders such as hyperglycemia, insulin resistance and dyslipidemia have also been observed to accelerate cardiovascular aging. Hyperglycemia leads to the downregulation of proteins that promote longevity. Many studies have highlighted that an increase in low-density lipoprotein cholesterol is associated with an increased risk of developing CVD and reduced longevity. Additionally, an increase in arterial stiffness and hypertension has been found to negatively impacts longevity thereby increasing the risk of CVD.

Among genetic factors, telomere length and epigenetic clocks are most commonly associated with longevity and CVD. Short telomere length has been found to increase the risk of CVD and reduce the longevity of individuals. On the other hand, epigenetic clocks can serve as an important biomarker for CVD. Another phenomenon, clonal hematopoiesis of indeterminate potential (CHIP), which is the mutation of hematopoietic stem cells can also determine the risk of CVD. Mutations of the hemopoietic stem cells most commonly lead to cell death; however, some mutated cells survive and undergo clonal expansion. If the mutations related to CHIP are located in the DNMT3A, JAK2, ASXL1 and TET2 genes, it is suggestive of CVD [3].

Furthermore, a few common lifestyle changes that have been found to improve longevity include intake of healthy food, an increase in physical activity and exercise and cessation of smoking. Environmental factors that have been observed to impact longevity and cardiovascular aging include climate, air pollution and gamma radiation.

Therefore, these findings and observations are important for the development of treatment and prevention methods for cardiovascular aging. They can also prevent age-related diseases, improve longevity, as well as reduce the burden of CVD among elderly individuals.

[1] https://www.frontiersin.org/articles/10.3389/fcvm.2021.728228/full
[2] https://www.hindawi.com/journals/omcl/2021/9570325/
[3] https://www.sciencedirect.com/science/article/pii/S0735109720378682