WCH in untreated hypertensives is important for several reasons [16]: First, the labeling of the patient as being false hypertensive is in itself of some gravity; second, insurability and cost; and third, the skewing of results of clinical trials that could include a significant number of WCH. This would translate into a lower than expected risk in the population studied. In fact, the most recent guidelines from the UK suggest that all new hypertensive patients undergo either ABPM or HBPM [17]. It has been calculated that identification of WCH in England could represent savings in the order of 10.5 million pounds in 5 years [18] based on the fact that identification of WCH provides the opportunity to avoid unnecessary treatment and medical visits.

Organ damage is less prevalent in WCH than in sustained hypertension and prospective studies have consistently shown this to be the case also for CV events and death [4, 19–21]. However, recent data indicate that the white-coat effect is strongly associated with increased arterial stiffness [22, 23], a strong predictor of CV events [2], is associated with carotid atherosclerosis in the general population [24], includes subjects with a widely different long-term risk of a CV event [25], and is accompanied by increased central aortic pressure levels [26]. These data enhance the possibility that in untreated hypertensives, WCH is accompanied by an increased global CV risk and the fact that patients with WCH frequently receive pharmacological therapy could contribute to explain a lower number of CV events [19]. It is also important to note that patients with this condition are prone to develop sustained hypertension over time; it is therefore advisable to monitor these individuals regularly so that antihypertensive therapy can be initiated when appropriate [27].

In contrast to WCH, in untreated people, MH is particularly prevalent in those presenting high–normal BP values in the office. Data from the Spanish ABPM Registry describe that 38 % of untreated hypertensives presenting BP levels within the high–normal range (130–139/85–89 mmHg) in the office are masked hypertensives [3].

As described previously, the prevalence of WCH in treated hypertensives is elevated. The relevance of this finding consists principally on the fact that patients with normal BP levels in ABPM or HBPM do not require further antihypertensive pharmacological therapy because goal BP is already attained. It has been considered that either ABPM or HBPM are required in treated hypertensives in order to have a better idea of the real BP of the patients so as to avoid an inadequate further drop in BP that could provoke unwanted CV and/or renal damage [28, 29]. Nevertheless, data from theHypertension in the Very Elderly Trial (HYVET) have shown positive data for the outcome of elderly hypertensive patients, albeit an estimate of 50 % of them presented WCH in the study [30]. The finding of any form of target organ damage in patients with WCH promotes the need to consider pharmacological therapy [2].

The presence of episodic hypertension in treated hypertensives represents an enhanced risk for them [31]. These episodes could be related to the presence of sporadic episodes of WCH and deserve further investigation.

As previously commented, the prevalence of MH is high in untreated and treated hypertensives [3]. Several factors contribute to an increase of out-of-office BP such as younger age, male gender, smoking, alcohol consumption, physical activity, anxiety, obesity, diabetes, CKD, family history of hypertension, and office BP values in the high–normal range [32]. The incidence of CV events in untreated MH is similar to that in sustained hypertension [19, 32].

It is well established that CKD is accompanied by a particularly high prevalence of arterial hypertension and also by a very significant increase of CV risk [33] . The most adequate goal BP in CKD has been considered in previous guidelines to be below 130/80 mmHg or even lower if proteinuria was present [34]. Actually, the goal considered is less than 140/90 mmHg [2] due to the fact that BP control in CKD must contemplate the very frequent simultaneous presence of CV events for which evidences of lower BP goals are absent [35]. In fact, an estimated glomerular filtration rate (eGFR) value below 60 ml/min/1.73 m² has to be considered among the five most relevant precipitators for the development of acute coronary syndrome [36] and the same could be said for stroke [37].