Pulse wave velocity in white coat and masked hypertension

1. INTRODUCTION

Out‐of‐office blood pressure (BP) measurement has given the opportunity to detect various hypertension phenotypes. Among them, white coat hypertension (WCH), ie, high clinic and normal out‐of‐office BP and masked hypertension (MH), that is, normal clinic and high out‐of‐office BP have been extensively studied in the past years. Their prognostic relevance ¹ , ² , ³ and target organ involvement, ⁴ , ⁵ , ⁶ which is frequently an intermediate stage toward cardiovascular events, have been assessed. Concerning the prognostic impact, it appears still debated in WCH, ¹ , ² whereas there seems to be unanimous consensus about the adverse prognostic value of MH. ¹ , ³ In the same way, cardiac and vascular involvement look controversial in WCH, ⁴ , ⁵ while there is substantial evidence of target organ damage in MH. ⁶

A meta‐analysis in this issue of the Journal of Clinical Hypertension adds to the current knowledge by evaluating pulse wave velocity (PWV), an index of arterial stiffness, in WCH and MH in comparison with normotension and sustained hypertension. ⁷ Seven studies including 2352 subjects were assessed. Subjects with MH and WCH had significantly higher PWV than normotensive ones (d = 0.96 m/s, 95% CI: 0.49‐1.42 for MH and d = 0.85 m/s, 95% CI: 0.48‐1.22 for WCH). Moreover, subjects with MH and WCH had lower PWV than sustained hypertensive ones (d = −0.70 m/s, 95% CI: −0.87 to −0.54 for MH and d = −0.75 m/s, 95% CI: −1.52 to 0.02 for WCH). No significant difference between MH and WCH was observed (d = 0.06 m/s, 95% CI −1.04 to 1.15). Thus, the authors concluded that WCH and MH are not clinically innocent. Looking at BP values of selected studies, in comparison with normotensive subjects, clinic BP and 24‐hour BP were higher, respectively, by 23/11 mm Hg and 4/2 mm Hg in subjects with WCH and, respectively, by 8/2 mm Hg and 16/10 mm Hg in those with MH.

Measurement of PWV is a simple and noninvasive way to assess arterial stiffness, a manifestation of vascular damage associated with hypertension and aging. ⁸ Various studies have shown that arterial stiffness independently predicts cardiovascular events and it is now accepted as an intermediate end point. ⁸ The mechanisms underlying arterial stiffening are not yet completely clear. In the context of long‐standing hypertension, it has been suggested that endothelial damage, smooth muscle tone, inflammation, oxidative stress, renin‐angiotensin system activity, and extracellular matrix turnover and integrity might be involved in this process. ⁸ However, beyond the impact of vascular structural changes on PWV, this parameter may also by influenced by intercurrent BP modifications. ⁹ Indeed, a powerful confounder of PWV interpretation may be BP. Increased BP augments the arterial wall tension and adds functional arterial stiffness, that is, vessels become stiffer at higher pressures. ⁹ Therefore, the effect of BP increase should be taken into account during PWV analysis. Subjects with WCH have substantial clinic BP increase, at variance with those with normotension or MH, while measuring PWV. Thus, it cannot be totally excluded that higher PWV in subjects with WCH could be at least in part due to intercurrent functional increase of arterial stiffness. On the other hand, looking at the BP values of selected studies, it could hypothesized that long‐standing high out‐of‐office BP in MH could be associated with more advanced vascular damage and structural increase of arterial stiffness. Future studies are needed to evaluate whether and to what extent increased PWV in WCH and MH are related to intercurrent functional and/or persistent structural arterial stiffening and whether antihypertensive therapy ¹⁰ might reduce vascular stiffness in these and other hypertensive contexts.

CONFLICT OF INTEREST

None.

AUTHOR CONTRIBUTIONS

Sante D. Pierdomenico wrote the paper, revised the manuscript critically for important intellectual content and gave final approval of the version to be submitted and of the revised version. Francesca Coccina and Rosalinda Madonna revised the manuscript critically for important intellectual content and gave final approval of the version to be submitted and of the revised version.