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Purpose of Review: The population of older adults 60-79 years globally is projected to double from 800 million to 1.6 billion between 2015 and 2050, while adults ≥ 80 years were forecast to more than triple from 125 to 430 million. The risk for cardiovascular events doubles with each decade of aging and each 20 mmHg increase of systolic blood pressure. Thus, successful management of hypertension in older adults is critical in mitigating the projected global health and economic burden of cardiovascular disease., Recent Findings: Women live longer than men, yet with aging systolic blood pressure and prevalent hypertension increase more, and hypertension control decreases more than in men, i.e., hypertension in older adults is disproportionately a women's health issue. Among older adults who are healthy to mildly frail, the absolute benefit of hypertension control, including more intensive control, on cardiovascular events is greater in adults ≥ 80 than 60-79 years old. The absolute rate of serious adverse events during antihypertensive therapy is greater in adults ≥ 80 years older than 60-79 years, yet the excess adverse event rate with intensive versus standard care is only moderately increased. Among adults ≥ 80 years, benefits of more intensive therapy appear non-existent to reversed with moderate to marked frailty and when cognitive function is less than roughly the twenty-fifth percentile. Accordingly, assessment of functional and cognitive status is important in setting blood pressure targets in older adults. Given substantial absolute cardiovascular benefits of more intensive antihypertensive therapy in independent-living older adults, this group merits shared-decision making for hypertension targets., (© 2023. The Author(s).)

Pre-hypertension, defined as blood pressure 120-139/80-89 mmHg, affects ~70 million people in the US. Blood pressures in the upper half of the pre-hypertensive range are linked with roughly threefold greater risk of incident hypertension than normal blood pressure <120/<80 mmHg, with an incidence rate of 8-20 % annually. Blood pressures in the upper half of the pre-hypertensive range also roughly double risk for cardiovascular events, even in the absence of progression to hypertension. Despite excess risk, guidelines recommend lifestyle interventions only for people with pre-hypertension in the absence of diabetes mellitus or clinical cardiovascular or chronic kidney disease. While efficacious, lifestyle changes have limited population effectiveness as Americans are heavier and their nutritional patterns less DASH-like than before DASH was published. Prevalent hypertension is higher in African Americans than Caucasians, but prevalent pre-hypertension is similar. African Americans experience a more rapid transition from pre-hypertension to hypertension than Caucasians with pre-hypertension. Interventions that normalize racial differences in incident hypertension could, over time, improve racial equity in prevalent hypertension and related clinical complications. Individuals with pre-hypertension can be safely treated with antihypertensive medications to significantly reduce incident hypertension. Given the evidence, practical clinical trials in African Americans with pre-hypertension to reduce and eliminate racial disparities in incident hypertension have merit. The results of these trials could provide the foundation for clinical guidelines to reduce racial disparities in prevalent hypertension and associated clinical cardiovascular and renal diseases.

Approximately 37% of US adults are prehypertensive; about 31 million have blood pressures in the range of 130-139/85-89 mm Hg. These stage 2 prehypertensives have threefold greater risk for developing hypertension and twofold higher risk for cardiovascular events than normotensives. Lifestyle changes only are recommended for most prehypertensives, but evidence for community-wide effectiveness is limited. Projected numbers needed to treat to prevent a cardiovascular event are similar for stage 2 prehypertension and stage 1 hypertension when both groups are matched for concomitant risk factors. However, no clinical trials document that pharmacotherapy reduces cardiovascular events in stage 2 prehypertension. The Trial of Preventing Hypertension demonstrated that angiotensin receptor blockade safely lowers blood pressure and prevents or delays progression to hypertension in stage 2 prehypertensives. We believe it is reasonable for clinicians to identify stage 2 prehypertensives at high absolute risk for progression to hypertension and cardiovascular events, and to treat them with a renin-angiotensin system blocker when lifestyle changes alone are ineffective.

Dietary salt has long been recognized as a major factor affecting blood pressure such that sodium intake is a component of lifestyle modification guidelines for control of high blood pressure. These recommendations are based on results from epidemiologic observational studies and clinical trials of various sodium diets among normotensives and hypertensives. Nonetheless, results from the different studies vary such that specific recommendations regarding sodium intake are difficult to interpret. The results from several recent major trials indicated greater associations of blood pressure and sodium intake than earlier studies as well as meta-analyses of numerous clinical trials. The studies of sodium intake and blood pressures are complicated by measurements of intake, salt sensitivity, hypertension treatment, effects of sodium independent of blood pressure, and length of interventions. Limitations in the methodology of different studies have reduced the value of the results to provide specific and reliable sodium intake levels essential for clinical and lifestyle guidelines.

The obesity epidemic is driving metabolic (insulin resistance) syndrome-related health problems including an approximately threefold increased coronary heart disease risk. Sympathetic hyperfunction may participate in the pathogenesis and complications of the metabolic syndrome including higher blood pressure, a more active renin-angiotensin system, insulin resistance, faster heart rates, and excess cardiovascular disease including sudden death. Possible factors augmenting sympathetic activation in the metabolic syndrome include alterations of insulin, leptin, nonesterified fatty acids (NEFAs), cytokines, tri-iodothyronine, eicosanoids, sleep apnea, nitric oxide, endorphins, and neuropeptide Y. Of note, high plasma NEFAs are a risk factor for hypertension and sudden death. In short-term human studies, NEFAs can raise blood pressure, heart rate, and a(1)-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance. Efforts to further identify the mechanisms and consequences of sympathetic dysfunction in the metabolic syndrome may provide insights for therapeutic advances to ameliorate the excess cardiovascular risk and adverse outcomes.

The fact that cardiovascular risk factors cluster among individuals with the insulin resistance syndrome strongly suggests a common pathogenetic denominator. For many years, abnormalities of nonesterified fatty acid metabolism have been implicated in the disturbances of carbohydrate and lipid metabolism that characterize the cluster. However, until more recently, evidence implicating fatty acids in the hemodynamic and vascular abnormalities that affect patients with this syndrome was lacking. Observations from epidemiological, clinical, and basic science suggest that fatty acids can raise blood pressure and contribute to the development of hypertension. The effects of fatty acids on blood pressure may be mediated in part by inhibition of endothelial nitric oxide synthase activity and endothelium-dependent vasodilation. Fatty acids can also increase alpha1-adrenoceptor-mediated vascular reactivity and induce vascular smooth muscle migration and proliferation. The adverse effects of fatty acids appear to be mediated in part through induction of oxidative stress. Fatty acids interact with other components of the risk factor cluster, including increased angiotensin II, to synergistically augment oxidative stress in cultured vascular smooth muscle cells. Oxidative stress is implicated in the pathogenesis of insulin resistance, hypertension, vascular remodeling, and vascular complications. A clearer definition of the specific reactive oxygen signaling pathways involved and interventions aimed at altering these pathways could lead to more rationale antioxidant therapy and improved outcomes.