New vascular biomarkers related to ABPM phenotypes in untreated patients

Abstract

Ambulatory blood pressure monitoring (ABPM) constitutes the most complete form to determine the blood pressure (BP) levels of a given patient. It shows the best correlation with cardiovascular (CV) events and death and allows the classification of patients into different phenotypes of great interest to evaluate the real risk accompanying BP.1 Recent guidelines2, 3 coming from United States and Europe have recognized the need of using ABPM mainly with two purposes: (a) classification of patients as real hypertensives, and (b) the analysis of the effect of drugs along the 24 hours.

The main phenotypes described by ABPM are white coat hypertension (WCH) and masked hypertension (MH) in untreated patients and white uncontrolled hypertension (WUCH), masked uncontrolled hypertension (MUCH) in treated patients and sustained hypertension (SUCH) in treated or untreated hypertensives.4 These phenotypes are characterized by different levels of risk of mortality with the highest accompanying MH followed by MUCH, SUCH, WCH and WUCH.1 Initially, WCH was considered as a phenotype with little risk for presenting CV and renal events but recent data have indicated that this could not be the case.5 In fact, in our data recently published the hazard ratio for mortality in WCH was 1.79 while in WUCH was only 1.06.1 The frank elevation observed in WCH could be due to the possibility that patients did not receive antihypertensive therapy for years of follow‐up during which it is known that WCH turns into SUCH.6 On the other hand, the classification of a given patient as presenting WCH must include the white coat effect during 24 hours daytime and nighttime.7 Besides allowing an adequate classification, this methodology will diminish significantly the prevalence of WCH.7

As a consequence of what we have described until here clarifying the real degree of arterial involvement in WCH and MH is of great interest to evaluate the prognosis of the patients and the adequacy and promptness of treatment of the elevated BP. In this issue of the journal Sanidas et al8 have described that the adipokines, apelin, and relaxin could be adequate markers for this purpose. Apelin is considered as a cardioprotective parameter opposing the effects of the renin‐angiotensin‐aldosteron system (RAAS) and its low levels are related to the degree of hypertension.9, 10 Relaxin is able to regulate BP levels, fibrosis, inflammation, and angiogenesis through positive effects on endothelial dysfunction in hypertension.11 Sanidas et al8 describe the finding that both adipokines exhibit diminish levels in MH compared to WCH. This finding could indicate that MH is characterized by the presence of the arterial damage accompanying SUCH while WCH, probably in its initial stages, does not present arterial alterations.

These data require confirmation due to small sample size presented in this article. However, we cannot deny the possibility that the measurement of these adipokines could help to define the presence or absence of vascular damage in WCH. Nevertheless, it has to be considered that beyond the levels of these adipokines, the balance with other vasoactive substances could modulate the situation in the presence of WCH.

In summary, the article to which this editorial is dedicated opens a new line of investigation to characterize two of the most important phenotypes that can be identified when an ABPM is performed.