The term “masked hypertension” refers to elevated average ambulatory BP coinciding with a non-elevated office BP [1]. The definition originally applied to people with the described BP measurements who were not taking antihypertensive therapy. However, patients on antihypertensive therapy may also exhibit the same BP measurement pattern. The term “masked uncontrolled hypertension” is now suggested to describe patients on BP-lowering treatment who exhibit non-elevated office but elevated ambulatory BP [2].

For either group (masked hypertension and masked uncontrolled hypertension), non-elevated office BP is typically defined as <140/90 mmHg, usually by an average of repeated measurements [3]. The threshold for defining elevated ambulatory BP varies somewhat in the literature [4, 5], but the most widely used threshold has been a mean awake ambulatory BP ≥135/85 mmHg [6, 7]. If the 24-h BP average is used, the threshold is typically an average of ≥130/80 mmHg [3].

The nighttime BP average has also been incorporated into the definition of masked hypertension. According to the European Society of Hypertension, elevated nighttime BP is defined as ≥120/70 mmHg [2]. Thus, individuals with non-elevated office BP with elevated mean awake ambulatory BP and/or elevated mean 24-h ambulatory BP, and/or elevated mean nighttime ambulatory BP are said to exhibit masked hypertension.

Masked hypertension is present in approximately 10 % of the general adult population [4, 6, 8, 9]. Among the general adult population of those with non-elevated office BP, it is present in approximately 15–30 % [10]. The first cross-sectional study of masked hypertension in the general population was conducted in Ohasama, a small community in Japan [11]. Among 969 adults (some under treatment for hypertension), 13 % of those with normal office BPs had masked hypertension detected by ambulatory BP monitoring (ABPM). A second study conducted in Italy examined 3200 adults and found a 9 % prevalence of masked hypertension by ABPM (Sega et al. [12]). A third study (N = 1400) conducted in Spain used home BP monitoring for the out-of-office BP measurements and also found a 9 % prevalence of masked hypertension [13]. Other studies have examined the prevalence in certain subpopulations. In a worksite study of 267 men, 14 % had masked hypertension by ABPM [14]. In a study of 319 healthy adult volunteers with normal office BP, 23 % had masked hypertension detected by ABPM [15]. Among 578 Swedish men 70-years of age, 14 % had masked hypertension [8]. In national and international databases, the prevalence of masked hypertension among people with normal office BP ranges from 9 to 54.5 % [16]. The variability in prevalence estimates is due to the heterogeneous definition of masked hypertension as well as differences in the sample characteristics across studies.

Among certain clinical subgroups, masked hypertension may be even more common. Diabetics have a higher prevalence of masked hypertension [17–19]. In the International Database of Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes (IDACO) , among the 7826 participants not taking BP-lowering medications, the prevalence of masked hypertension (clinic BP < 140/90 mmHg and daytime ambulatory BP average ≥135/85 mmHg) was higher in the clinic normotensive participants with diabetes (29 %) than in those without diabetes (19 %) [17].

Masked hypertension also appears more common among patients with chronic kidney disease (CKD) . One Spanish study of 5693 hypertensive patients with CKD showed that the proportion of individuals with masked hypertension was 7 % among all the patients and 32 % among patients with clinic normotension [20]. In a cross-sectional study of 617 treated hypertensive African Americans with CKD, the prevalence of masked uncontrolled hypertension was 70 % among individuals with controlled clinic BP [21].

Obstructive sleep apnea (OSA) may also be associated with masked hypertension. In one study of 133 newly diagnosed OSA patients taking no medications, 30 % exhibited masked hypertension using mean 24-h ambulatory pressures [22]. In another study of 61 otherwise healthy men with normal clinic BP, obstructive sleep apnea was associated with masked hypertension even using mean awake ambulatory BP, suggesting that OSA adversely affects ambulatory BP beyond the sleep period [23].

Several studies have examined target organ damage and outcomes associated with masked hypertension, finding that the risk associated with masked hypertension approaches that of sustained hypertension. In a study published in 1999, left ventricular mass index (LVMI) and carotid plaque were measured among people with masked hypertension and compared to those with true normotension and those with sustained hypertension [24]. The LVMI was 73 g/m² in the true normotensives, 86 g/m² in the masked hypertensives, and 90 g/m² in the sustained hypertensives. Carotid plaque was present in 15 % of true normotensives and in 28 % of both the masked and sustained hypertensives. In another study, LVMI in people with masked hypertension was 91 g/m² compared to 79 g/m² in true normotensives and 94 g/m² in people with sustained hypertension [12]. The association with carotid atherosclerosis was also confirmed in a 2007 study [25]. Thus, masked hypertension is associated with target organ damage on an order of magnitude approaching that associated with sustained hypertension.

More importantly, there is also evidence of increased cardiovascular disease (CVD) events (stroke, myocardial infarction, cardiovascular mortality) occurring in people with masked hypertension. A meta-analysis of seven studies including a total of 11,502 subjects followed over a mean of 8 years showed a twofold higher incidence of CVD events (HR 2.00; 95 % CI 1.58–2.52) in people with masked hypertension compared to those with true normotension [26]. This risk approaches the risk conferred by sustained hypertension (HR 2.28; 95 % CI 1.87–2.78). Table 16.2 summarizes the target organ damage associations and cardiovascular event rates in true normotension, masked hypertension, and sustained hypertension.

In another analysis, individual-level data from the IDACO was used to examine differences in CVD risk among 7030 people comparing white coat hypertension, masked hypertension, and sustained hypertension. At a median follow-up of 9.5 years (64,958 person years), compared to people with sustained normotension, the adjusted hazard ratios for CVD events were 1.22 (95 % CI 0.96–1.53) for those with white coat hypertension, 1.62 (95 % CI 1.35–1.96) for those with masked hypertension, and 1.80 (95 % CI 1.59–2.03) for those with sustained hypertension [27]. Notably, the hazard ratios between masked hypertension and sustained hypertension were not significantly different (p = 0.14).

Missing from the current literature is any evidence that identification and treatment of masked hypertension reduces CVD events or mortality. In order to conduct such studies, a practical approach to detecting masked hypertension is needed. At the very least, identification of people with masked hypertension may allow earlier, more aggressive lifestyle modifications and closer monitoring for progression to overt (sustained) hypertension. However, there is limited evidence on how best to identify people with masked hypertension. One approach would be to perform ABPM on all adults, perhaps over a certain age, with non-elevated office BP. Given the relatively new recommendations that ABPM ought to be performed in adults before diagnosing hypertension (in order to exclude white coat hypertension) [28, 29], an approach that also uses ABPM among people with “normal” office BP would in effect mean everyone would be getting ABPM. Such an approach is not practical.

An alternative detection strategy would be to target ABPM to people who are at high risk for having masked hypertension. While some factors associated with masked hypertension have been observed, they are not consistent, and no validated risk assessment tool has yet been developed. The most reliable risk factor may simply be the office BP level. Recent evidence suggests that the BP cutoff that may have the most reasonable tradeoff between sensitivity and specificity is approximately 126 mmHg systolic [30]. Similarly, other studies have shown that office BP in the upper prehypertensive range predicts masked hypertension [31]. Another study examined the diagnostic overlap between masked hypertension and prehypertension (systolic BP 120–139 mmHg or diastolic BP 80–89 mmHg) [7]. Among 813 participants not on antihypertensive medications, 769 participants had non-elevated clinic BP. The overall prevalence of masked hypertension in the participants with non-elevated clinic BP was 15 % using a cutoff of 135/85 mmHg for mean awake ambulatory BP. The prevalence of masked hypertension was only 4 % in participants with office BP <120/80 mmHg. In the subgroup of participants with prehypertension, the prevalence of masked hypertension increased to 34 % and reached 52 % in the upper prehypertensive range (systolic BP 130–139 mmHg or diastolic BP 80–89 mmHg). Other studies have shown a similarly high prevalence of masked hypertension among patients with borderline prehypertensive office BP levels [32, 33].