White coat hypertension in untreated patients or white coat effect in treated patients was originally defined as an elevated office BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic with a mean awake ambulatory BP <135/85 mmHg in untreated individuals. Latest guidelines now propose this definition for patients with office BP ≥140/90 mmHg and a mean 24-h BP <130/80 mmHg to take into account nocturnal BP since it is recognized to be superior to daytime BP in predicting cardiovascular risk [28, 33]. Furthermore, the 24-h mean BP is a more reproducible value than the awake, daytime BP values [1, 28].

White coat hypertension/white coat effect is seen in 15–25 % of the elderly and is a more common syndrome in older versus younger people [51, 52]. Indeed, age is an independent factor influencing white coat hypertension [53] and even seen more frequently in centenarians [54]. Cross-sectional and prospective cohort studies have shown repeatedly that people with white coat hypertension have a better prognosis than those with sustained hypertension outside of the clinical environment [38, 39]. In some clinical outcome studies, patients with WCH may have a slightly increased, nonsignificant cardiovascular risk compared with normotensive individuals, though in most of the studies showing this effect, the ambulatory BP of the white coat hypertensive patients was higher than in normotensive individuals [55, 56]. A meta-analysis performed by the IDACO group showed that any increased risk of future cardiovascular event in a patient with white coat hypertension was very small and substantially lower than the risk seen with either persistent hypertension or masked hypertension [57].

Several guidelines recommend ABPM in patients suspected of having white coat hypertension [1, 2, 32]. In the US, this diagnosis (ICD-9-CM code 796.2, ICD-10-CM code R03.0) is a key indication for ambulatory BP monitoring recognized for coverage by the Centers for Medicare and Medicaid Services [58].

A gradual rise in systolic BP attributed to increased aortic stiffness is observed as age advances. Diastolic BP peaks and plateaus in the fifth–sixth decades of life and begins to decline thereafter [59]. The pulse wave velocity used to estimate arterial distensibility correlates well with ambulatory systolic BP and may be used as a surrogate to estimate aortic stiffness [60]. Epidemiologic studies have shown that isolated systolic hypertension is seen in more than 90 % of hypertensive patients >70 years of age with a higher prevalence in women than men [61]. The 24-h systolic BP is associated with more substantial adverse cardiovascular events and mortality than the ambulatory diastolic BP [62]. The Systolic Hypertension in the Elderly Program (SHEP) , a randomized, double-blind, placebo-controlled trial on 4736 subjects >60 years of age, demonstrated that treatment of isolated systolic hypertension in older patients reduced all strokes, both fatal and nonfatal, by 36 %; all myocardial infarctions (MIs), both fatal and nonfatal, by 27 %; all coronary heart disease by 27 %; and all cardiovascular disease by 32 %. Total mortality was reduced by 13 % [6]. Ambulatory systolic BP is a better predictor of cardiovascular risk than office systolic BP. The cardiovascular risk conferred by a conventional systolic BP of 160 mmHg in the doctor’s office is similar to that associated with a 24-h, daytime or nighttime systolic BP of 142 mmHg, 145 mmHg, or 132 mmHg, respectively [42]. In addition, the pulse pressure is an independent determinant of cardiovascular risk in older persons [63]. In the population-based Framingham Heart Study of 1924 subjects between 50 and 79 years of age, pulse pressure was superior to systolic or diastolic BP in predicting coronary artery disease risk [64]. Ambulatory pulse pressure has also been directly associated with cardiovascular risk [65].

The circadian pattern of blood pressure and heart rate observed in humans correlates with cardiovascular events, including both myocardial infarction and stroke [66]. Reduction of about 10–30 % of blood pressure is observed during sleep relative to the awake period in majority of normotensive and hypertensive people. This is followed by a rise in BP upon awakening which coincides with the transition from sleep to wakefulness [67].

A non-dipping pattern which is defined as a reduced or absent decline in sleep BP (generally less than 10 % decline) is seen in 25–35 % of hypertensive people and is more commonly seen in older people, both in men, women, and centenarian patients [68–71]. Increasing age is observed to be an independent marker of non-dipping after correction for confounding factors of diabetes, reduced glomerular filtration rate, low HDL-cholesterol, and elevated urinary albumin excretion [72]. This BP pattern is associated with increased target organ damage including left ventricular hypertrophy, albuminuria, and small vessel disease of the brain [25, 73, 74]. Cardiovascular prognosis is worse in elderly non-dippers with ISH than with dipper profiles [42]. Patients lacking a nocturnal decline in the BP are prone to developing congestive heart failure, myocardial infarction, stroke, and progression to end-stage renal failure. Increased incidence of fatal and non-fatal CV events is also observed in association with blunted decline in nocturnal BP [75–77].

Studies have shown poor reproducibility of the nocturnal dipping status [78, 79]. Absolute nocturnal BP values are more reproducible than the categories of dippers and non-dippers. The study observing reproducibility of ambulatory BP in elderly subjects by Campbell et al. found substantial variability in the dipping status over a period of 2 years [36]. Changes in hypertensive status based on absolute nocturnal systolic BP demonstrated improved reproducibility compared with categorical changes.