Unmasking Masked Hypertension

Masked hypertension remains the least understood of the 3 phenotypes of hypertension. For both sustained and white‐coat hypertension, the clinician has a major indicator regarding the diagnosis––the finding of an elevated office blood pressure (BP). Such an easily observed and routinely obtained clue does not exist for masked hypertension. In an attempt to reduce the need to obtain 24‐hour ambulatory BP measurement (ABPM) in every patient, some researchers have suggested that a hypertensive or hyperdynamic response to an exercise stress test may offer a clue to the underlying presence of masked hypertension.

In this issue of The Journal of Clinical Hypertension, Grossman and colleagues1 have provided some convincing evidence that dispels this myth, at least in patients with high normal BP. This well‐done retrospective study incorporates both 24‐hour ABPM and repeat stress tests to determine whether an exaggerated BP response to exercise was associated with masked hypertension. The authors incorporated some notable features in their study. They limited their analysis to patients with documented high normal office BP who had also undergone a 24‐hour ABPM and underwent at least two exercise stress tests. Their definition of exaggerated response to exercise was the reasonable finding of a rise in systolic BP ≥200 mm Hg with exercise. The reproducibility of this exaggerated response has been questioned.2 The authors confirmed this finding when they found a reproducibility of only 41% in patients in at least 50% of tests and only 21% in all their stress tests.

Additionally, when evaluating 24‐hour ABPM in patients with confirmed masked hypertension (50 patients), not only were the average BP levels, but also the rates of masked hypertension, similar in patients with reproducible exaggerated BP response (at least twice) and those with normal response to exercise as well.

When the authors sought to identify clues as to possible demographic differences between patients identified with masked hypertension and those without, they found similar CV risk factors, with the exception of higher fasting blood glucose levels in those with an exaggerated BP response than those with a normal response, but the incidence of diabetes was identical in both populations. However, this rigidly controlled study included only a relatively small number of patients; therefore, the inability to find differences between these populations is not unexpected.

This returns us to the challenge of unmasking the masked hypertensive in clinical practice. The cardiovascular risks associated with masked hypertension approach that of sustained hypertension and exceed that associated with white‐coat hypertension.3 Its incidence in some studies mirrors that of white‐coat hypertension.4 Yet, masked hypertension remains obscure, if not unknown, to many practitioners as well as patients. There needs to be a greater awareness of this condition to allow for greater opportunity for diagnosis and treatment.

Beyond the challenge of extending the knowledge of this condition, there exists additional challenges as well, including the most fundamental––the definition of the condition itself.

When the term masked hypertension was first proposed, it was used to describe patients previously described as having reverse white‐coat hypertension, gray coat, and a host of other colorful descriptions.5 Yet, when coining this term, the authors referred to those treatment‐naive patients who demonstrated a normal office BP yet elevated BPs in the out‐of‐office environment. Patients with sustained hypertension, but perhaps with a pattern of lower readings in the office than in the out‐of office environment, were not incorporated into this definition. Patients under treatment who demonstrated control in the office but not at home were also not included in this definition. Yet, many authors have included both of these phenotypes in their masked hypertensive populations in their studies and discussions. It remains unknown whether all 3 of these populations are identical. The categorization of all of them as having masked hypertension does a disservice to both patients and clinicians. Blending these phenotypes may make the determinations of risk in this population more difficult to discern, the diagnosis more uncertain, and the outcomes more obscure.

At least one universal observation is apparent: the necessity of out‐of‐office recording of BP to diagnosis this condition. However, controversy exists even here as to which method of assessment is best used to make and confirm a diagnosis of masked hypertension. Some studies have suggested that ABPM and home monitoring are not equivalent, with an association that renders home monitoring less reliable than ABPM.6 Others suggest that either metric may be used to diagnosis the presence of masked hypertension.7 Even regarding reproducibility, the association between a first and second ABPM is only noted to be 72% for masked hypertension.8 That still leaves a significant percentage of patients either misdiagnosed or undiagnosed and leaves both clinician and patient with an unanswered question as to what strategy is best utilized to make and confirm the diagnosis of masked hypertension.

Accordingly, in what patient types should we suspect possible masked hypertension? Clearly, in those patients with evidence of target organ damage yet normal office BP, the diagnosis needs to not only be considered but also excluded. Patients in whom it may be reasonable to consider will be those with high‐normal office BPs and the presence of diabetes mellitus, especially if home readings are equivalent or higher than those in the office.

In those patients, should we utilize 24‐hour ABPM or is home monitoring sufficient? Availability may be a reasonable discernment tool. If 24‐hour ABPM is available it is the best metric to establish the diagnosis. Home monitoring represents a good second option. It may also be useful to perform home monitoring in those patients who underwent 24‐hour ABPM to establish the utility of home monitoring during the treatment phase of the condition.

Masked hypertension only strengthens the argument that the use of traditional brachial artery measurement in the office needs major revision. Simply relying upon office BP readings for both diagnosis and treatment may be little better than flipping a coin. It has become increasingly apparent that the proper diagnosis and management of BP demands that readings be obtained in the out‐of‐office setting. These readings must be performed dutifully and properly, utilizing good technique and validated instruments, and completely recorded to make the diagnosis of hypertension and then manage it well.

For most patients, recording of home BP will suffice, but, for some, they will require the next step––24‐hour ABPM. Even then the utilization of this strategy will leave some patients exposed to risk, from either overdiagnosis or underdiagnosis and treatment. All suspect patients should have careful observation and systematic screening for target organ damage.

With our current metric we may need to admit that not all hypertensive patients may be easily identified, especially some with masked hypertension and their unmasking may need to await their development of either target organ damage or newer improved methods of BP measurement.