Diabetes and Cardiovascular Disease in Older Adults
Even up to age 80, there are no substantial aging-related changes in overall resting cardiac function, but there are notable age-associated changes in specific aspects of cardiac structure and cardiovascular function (Table 2). Lifestyle-associated stressors, such as poor diet, physical inactivity, and smoking, can accelerate these changes.
Diabetes also has a major impact on the heart. Systolic and diastolic dysfunction and changes in coronary blood flow in the presence of diabetes suggest that diabetes impairs the ability of the heart to use free fatty acids as energy substrates. The impact of hyperglycemia on left ventricular function can be influenced by many factors, including sex, endothelial dysfunction, duration of diabetes, alterations in cellular metabolism, and dysfunction in the autonomic nervous system. Diabetes can worsen age-related changes in diastolic dysfunction by as much as fivefold. It is not clear if microvascular abnormalities contribute to overall cardiac dysfunction or how the presence of diabetes affects responses to cardiovascular injury or infarct with aging.
The mechanisms underlying age- and diabetes-related changes to the vasculature are not understood fully, but inflammation and oxidative stress appear to play a synergistic role. Aging arteries exhibit a chronic inflammatory profile similar to that seen with atherosclerosis, hypertension, and diabetes. Inflammation and oxidative stress together promote extracellular matrix remodeling, increased tone, and intrinsic cell stiffness in the vascular smooth muscle. Oxidative stress resulting from increased superoxide availability in the arteries, uncoupling of nitric oxide synthase, and mitochondrial dysfunction also promotes endothelial dysfunction. Angiotensin II plays a role in this synergy by mediating interactions among chronic inflammation, mitochondrial dysfunction, longevity pathways, and diabetes-related pathways. The effects of inhibiting angiotensin II signaling mimic those of caloric restriction. While there may be an important role for adult stem cells located in perivascular areas in maintaining endothelial function, this topic was not discussed at the workshop.
Acute hyperglycemia does not appear to affect endothelial function, but vessel function appears to be impaired among individuals with type 2 diabetes. Diminished sympathetic nerve activity and insulin resistance are possible factors, as insulin itself can be sympathoexcitatory. These effects might be counteracted by lifestyle changes. Sodium restriction, caloric restriction, and weight loss improve elastic artery compliance and vascular endothelial function. Aerobic exercise partially preserves vascular endothelial function and large elastic artery compliance.
Vulnerabilities of the Heart and Blood Vessels to Aging and Diabetes
Even up to age 80, there are no substantial aging-related changes in overall resting cardiac function, but there are notable age-associated changes in specific aspects of cardiac structure and cardiovascular function (Table 2). Lifestyle-associated stressors, such as poor diet, physical inactivity, and smoking, can accelerate these changes.
Diabetes also has a major impact on the heart. Systolic and diastolic dysfunction and changes in coronary blood flow in the presence of diabetes suggest that diabetes impairs the ability of the heart to use free fatty acids as energy substrates. The impact of hyperglycemia on left ventricular function can be influenced by many factors, including sex, endothelial dysfunction, duration of diabetes, alterations in cellular metabolism, and dysfunction in the autonomic nervous system. Diabetes can worsen age-related changes in diastolic dysfunction by as much as fivefold. It is not clear if microvascular abnormalities contribute to overall cardiac dysfunction or how the presence of diabetes affects responses to cardiovascular injury or infarct with aging.
The mechanisms underlying age- and diabetes-related changes to the vasculature are not understood fully, but inflammation and oxidative stress appear to play a synergistic role. Aging arteries exhibit a chronic inflammatory profile similar to that seen with atherosclerosis, hypertension, and diabetes. Inflammation and oxidative stress together promote extracellular matrix remodeling, increased tone, and intrinsic cell stiffness in the vascular smooth muscle. Oxidative stress resulting from increased superoxide availability in the arteries, uncoupling of nitric oxide synthase, and mitochondrial dysfunction also promotes endothelial dysfunction. Angiotensin II plays a role in this synergy by mediating interactions among chronic inflammation, mitochondrial dysfunction, longevity pathways, and diabetes-related pathways. The effects of inhibiting angiotensin II signaling mimic those of caloric restriction. While there may be an important role for adult stem cells located in perivascular areas in maintaining endothelial function, this topic was not discussed at the workshop.
Acute hyperglycemia does not appear to affect endothelial function, but vessel function appears to be impaired among individuals with type 2 diabetes. Diminished sympathetic nerve activity and insulin resistance are possible factors, as insulin itself can be sympathoexcitatory. These effects might be counteracted by lifestyle changes. Sodium restriction, caloric restriction, and weight loss improve elastic artery compliance and vascular endothelial function. Aerobic exercise partially preserves vascular endothelial function and large elastic artery compliance.
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