Objective: The clinical significance of masked hypertension (MHT) and white-coat hypertension (WCHT) remains controversial, whereas subclinical inflammation and arterial stiffness are associated with an adverse prognosis. We examined the interrelationships of MHT, WCHT, and sustained hypertension (SHT) with high-sensitivity C-reactive protein (hs-CRP) and arterial stiffness.
Methods: Our population consisted of 291 untreated nondiabetic patients with MHT [office blood pressure (BP) < 140/90 mmHg and daytime BP ≥ 135/85 mmHg; n = 32], WCHT (office BP ≥ 140/90 mmHg and daytime BP < 135/85 mmHg; n = 81), SHT (office BP ≥ 140/90 mmHg and daytime BP ≥ 135/85 mmHg; n = 178), and 44 age-matched and sex-matched control normotensives.
Results: SHT compared with WCHT, MHT, and normotension exhibited higher pulse wave velocity (PWV; 8.2 ± 1.4 vs. 7.5 ± 1.2 vs. 7.3 ± 0.9 vs. 6.8 ± 0.5 m/s, respectively; P < 0.05) and hs-CRP (2.8 ± 0.7 vs. 2.2 ± 0.6 vs. 1.9 ± 0.4 vs. 1.2 ± 0.3 mg/l, respectively; P < 0.05), independently of confounders. Of note, there was no difference between the MHT and WCHT groups with regard to hs-CRP and PWV levels (P = not significant). In hypertensives, hs-CRP was associated with 24-h systolic BP (r = 0.350, P < 0.0001) and PWV (r = 0.228, P < 0.0001), whereas PWV was associated with 24-h systolic BP (r = 0.330, P < 0.0001).
Conclusion: MHT and WCHT represent two states of equivalent subclinical vascular dysfunction reflected by hs-CRP and PWV. Moreover, MHT and WCHT are characterized by a higher degree of inflammatory activation and arterial stiffening compared with normotension and by a lesser degree compared with SHT. The association of 24-h BP with both hs-CRP and PWV underscores the dominant role of hemodynamic load on hypertensive damage progression.