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.
