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In this chapter, we will refer to the “elderly” as those individuals aged 65 years or older, as this is the definition used by the United Nations in its reports on aging. This rapidly growing segment of the population accounts for 9% of individuals globally and 16.5% in the United States and is expected to reach 22% by 2050.
Hypertension prevalence increases with age, with a sharp rise in people older than age 55 years. In the elderly, hypertension is the rule, afflicting more than two-thirds of individuals. Data from the National Health and Nutrition Examination Surveys (NHANES) show that 64% of men and 69% of women between ages 64 and 74 years have hypertension, which is defined as blood pressure (BP) of 140/90 mm Hg or higher or antihypertensive therapy. Hypertension affects 67% of men and 79% of women aged 75 years or older.
In 2017 the American College of Cardiology and the American Heart Association (ACC/AHA) updated their hypertension guidelines and redefined hypertension as BP of 130/80 mm Hg or higher. Using these new thresholds, the estimated prevalence of hypertension increased to 77% among patients aged 65 years or older.
In recent years, the rate of BP control to levels under 140/90 mm Hg has increased among the elderly. Current NHANES estimates indicate that approximately 49% of elderly hypertensives have controlled BP with similar numbers among men and women.
BP Measurement – Evaluation of Both Arms. Significant inter-arm BP differences (>10 mm Hg) are observed in ∼11% of all hypertensive patients. Inter-arm differences are associated with underlying peripheral arterial disease and are more common among older men than other groups. Because of the impact such differences can have on treatment decisions, it is recommended that all patients be screened by simultaneous BP measurements (or in rapid sequence). If a disparity is noted, the higher level is always used. Even though not formally recommended by guidelines, it is reasonable to rescreen elderly patients for inter-arm differences periodically.
BP Measurement – Pseudohypertension. Older patients often have arterial calcification that may lead to limited compressibility of the brachial artery resulting in falsely high BP readings. This should be considered in patients with very high BP levels and no evidence of target organ damage or in those with hypotensive symptoms despite high measured BP. In the past, the Osler sign (the brachial and radial artery remain palpable distal to a maximally inflated BP cuff) was thought to be diagnostic, but it has limited diagnostic reliability. Therefore if pseudohypertension is suspected, intra arterial measurements are necessary to settle the issue.
BP Measurement – Orthostatic Vital Signs. Orthostatic hypotension, often asymptomatic, occurs in up to a third of older patients with hypertension. It is defined as a BP fall greater than 20/10 mm Hg with standing. Some guidelines have recommended checking orthostatic vital signs in the elderly as well as in patients with chronic kidney disease and diabetes. Although it is best to perform orthostatic testing after at least 5 minutes of supine rest followed by 3 minutes of standing, we recognize the difficulties of doing this in a busy clinical practice. A reasonable compromise is to measure BP in the seated position followed by BP after 1 minute standing. Because this technique is less sensitive, the proposed threshold to diagnose orthostatic hypotension using this abbreviated method is a BP drop greater than 15/7 mm Hg with standing.
Out-of-Office BP Assessment. Out-of-office BP monitoring with 24-hour ambulatory BP or home BP monitoring is now uniformly recommended for the diagnosis of hypertension, and the 2017 ACC/AHA guidelines also endorse its use to guide therapy. Despite these recommendations, the uptake by physicians at large is still suboptimal. This is problematic in the elderly because both white coat hypertension (elevated office BP with normal ambulatory BP) and masked hypertension (normal office BP with high ambulatory BP) are more common with aging, thus demanding the use of out-of-office BP monitoring to avoid both over- and undertreatment. White coat hypertension was observed in 3.2% of those younger than age 60 years and 29% of those 60 years or older. Likewise, NHANES estimated the prevalence of masked hypertension to increase significantly with aging, from 8% in adults younger than 44 years, to 17% in those 45 to 64 years, to 28% in those 65 years or older. These data support a recommendation for routine out-of-office BP measurement for evaluation and management of elderly hypertensive patients.
Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) increase with age up to the sixth decade of life. After that, DBP starts to decline, resulting in increased pulse pressure (PP). Consequently, isolated diastolic and systo-diastolic hypertension are the predominant subtypes in younger patients. In the elderly, data from NHANES indicate that isolated systolic hypertension (ISH, defined as SBP ≥140 mm Hg with DBP <90 mm Hg) is the predominant subtype, representing 80% to 90% of cases.
The major pathogenic factor in ISH is increased arterial stiffness. Aging results in elastin fragmentation and degradation followed by collagen deposition in place of elastin fibers in the large elastic arteries, rendering them stiffer. Multiple mechanisms underlie this process including excessive activity of several matrix metalloproteinases, collagen cross-linking by advanced glycation end-products, vascular smooth cell proliferation and stiffening, calcification of the vascular media, endothelial dysfunction, and vascular wall inflammation and fibrosis. Other common prohypertensive factors are often increased in elderly patients such as salt sensitivity, increased sympathetic tone, and relative increase in activity of the renin-angiotensin system. Finally, arterial stiffening is accelerated by many common age-associated disorders such as atherosclerosis, diabetes mellitus, the metabolic syndrome, chronic kidney disease, and hypertension itself (i.e., high BP is both result and cause of arterial injury and stiffening).
Under normal conditions, an incident pulse wave generated during systole travels to the periphery and is reflected back, returning to the aortic root in diastole and augmenting diastolic pressure. Arterial stiffening, however, increases pulse wave velocity, thus making the incident forward wave travel faster to the periphery and the reflected wave return faster to the central circulation. Because of faster travel, the reflected wave reaches the aortic root while systole is still occurring. This results in increased SBP and greater decay of the DBP curve (thus lower diastolic DBP), resulting in widening of the PP. Although arterial stiffness can be measured using a variety of clinical tools, high brachial SBP with low DBP and increased PP are the “poor man’s” clinical hallmarks of arterial stiffness.
Increased left ventricular pressure during systole results in pressure-induced left ventricular hypertrophy. Systolic stress also leads to increased cardiomyocyte energy consumption leading to relative ischemia, particularly given the associated impairment in diastolic coronary perfusion produced by the decrease in DBP. These mechanisms are important mediators of the increased incidence of cardiovascular events and death in patients with ISH.
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