Exercise Capacity and Mortality in Elderly Hypertensive (page 30)
Higher exercise capacity is associated with lower mortality risk in middle-aged individuals with hypertension. In this issue of Hypertension, Faselis et al reported that the fitness-related health benefits are extended to individuals with hypertension aged ≥70 years. In 2153 elderly men, increased exercise capacity (as expressed by metabolic equivalents [METs]) was associated with significantly lower all-cause mortality risk. The association was inverse, independent, and graded. Mortality risk was 11% lower for every 1-MET increase in exercise capacity. When fitness categories were considered, mortality risk was 18%, 36%, and 48% lower for the low-fit (4.1–6 METs), moderate-fit (6.1–8.0 METs), and high-fit (>8.0 METs) categories, respectively, compared with individuals in the lowest fitness category (≤4.0 METs). These findings support the concept that increased cardiorespiratory fitness is associated with lower mortality risk in men with hypertension regardless of age. The relatively low level of exercise capacity (>4.0 METs) associated with lower mortality risk is achievable by most elderly engaging in a brisk walk of 20 to 40 minutes most days of the week. Because walking requires virtually no instructions, has a relatively low cost, carries a low risk of injury, and can be easily implemented to large populations, it may constitute an effective intervention to mitigate the deleterious effects of hypertension in the elderly.
Aldosterone and Death, End-Stage Renal Disease, and Cardiovascular Events (page 103)
Chronic kidney disease affects ≈13% of the US population and is a well-recognized risk factor for adverse cardiovascular events. In chronic kidney disease, treatment with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers delays the progression of kidney disease; however, limited data suggest any reduction in cardiovascular morbidity and mortality. This recognition has resulted in investigations to assess whether aldosterone escape is a risk marker and potential therapeutic target. In this issue of Hypertension, results from the Chronic Renal Insufficiency Cohort (CRIC) study indicate that baseline concentrations of serum aldosterone were not associated with death, end-stage renal disease, or the composite atherosclerotic end point defined as incident myocardial infarction, stroke, or peripheral vascular disease. Each SD increase in aldosterone, however, was associated with a 21% increase in the incidence of heart failure. This aldosterone–heart failure association was stronger in blacks compared with whites. These results from >3800 participants with chronic kidney disease suggest that baseline aldosterone concentrations have limited prognostic value in this population. Activation of the mineralocorticoid receptor, however, may still occur through other pathways. As such, clinical trials to evaluate the use of mineralocorticoid receptor blockers in the chronic kidney disease population are strongly needed.
Angiotensin-Converting Enzyme 2 Deficiency Exacerbates Vascular Disease (page 157)
Bicuspid aortic valve is the most common congenital cardiac abnormality, occurring in 1% of the population. Bicuspid aortic valve is associated with increased risk of ascending aortic dilatation. The underlying connective tissue disorder that causes bicuspid aortic valve also affects the tissue layers that form the walls of the aorta. As the tissue layers degenerate, the aortic walls lose their strength and stretch out of their normal configuration. Eventually, this can lead to the formation of an aortic aneurysm. The resulting aortic dilatation promotes dissection and rupture, making it a potentially lethal disease. In this issue of Hypertension, Patel et al report upregulation of angiotensin-converting enzyme 2, which converts angiotensin II into angiotensin 1–7 in the aorta of patients with bicuspid aortic valve, as well as in the aorta of angiotensin II–infused mice, a widely accepted, clinically relevant preclinical model of vascular disease. Aortic dilation and adverse vascular remodeling in angiotensin II–infused angiotensin-converting enzyme 2 knockout mice were associated with increased vascular smooth muscle cell apoptosis, oxidative stress, and increased matrix metalloproteinase activity. Importantly, histopathological changes in human aortic aneurysms predominantly affect the medial layer that is dominated by elastic fibers and vascular smooth muscle cells, and the vascular smooth muscle cell phenotypic changes, including apoptosis, are associated with aortic aneurysm formation. These data provide important evidence that angiotensin-converting enzyme 2 is a key negative regulator of an activated renin–angiotensin system–driven adverse vascular remodeling, and enhancing angiotensin-converting enzyme 2 could have beneficial effects in vascular diseases.
- © 2014 American Heart Association, Inc.