Journal of hypertension · 2022
Blood pressure response to standing is a strong determinant of masked hypertension in young to middle-age individuals.
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Palatini Paolo, Mos Lucio, Rattazzi Marcello, Spinella Paolo, Ermolao Andrea, Vriz Olga, Battista Francesca, Saladini Francesca
Аннотация
OBJECTIVE: The pathophysiologic mechanisms of masked hypertension are still debated. The aim of this study was to investigate whether the blood pressure response to standing is a determinant of masked hypertension in young individuals.
DESIGN AND METHODS: We studied 1078 individuals (mean age 33.2 ± 8.5 years) with stage-1 untreated hypertension at baseline. Orthostatic response was defined as the difference between six SBP measurements in the orthostatic and supine postures. People with a response more than 6.5 mmHg (upper decile) were defined as hyperreactors. After 3 months of follow-up, 24-h ambulatory BP was measured and the participants were classified as normotensives (N = 120), white-coat hypertensive individuals (N = 168), masked hypertensive individuals (N = 166) and sustained hypertensive individuals (N = 624). In 591 participants, 24-h urinary epinephrine was also measured.
RESULTS: Orthostatic response was an independent predictor of masked hypertension after 3 months (P = 0.001). In the whole group, the odds ratio for the Hyperreactors was 2.5 [95% confidence interval (95% CI) 1.5-4.0, P < 0.001]. In the participants stratified by orthostatic response and urinary epinephrine, the odds ratio for masked hypertension was 4.2 (95% CI, 1.8-9.9, P = 0.001) in the hyperreactors with epinephrine above the median and was 2.6 (95% CI, 0.9-7.3, P = 0.069) in those with epinephrine below the median. The association between orthostatic response and masked hypertension was confirmed in the cross-sectional analysis after 3 months (P < 0.001).
CONCLUSION: The present findings indicate that hyperreactivity to standing is a significant determinant of masked hypertension. The odds ratio for masked hypertension was even quadrupled in people with an orthostatic response more than 6.5 mmHg and high urinary epinephrine suggesting a role of sympathoadrenergic activity in the pathogenesis of masked hypertension.
DESIGN AND METHODS: We studied 1078 individuals (mean age 33.2 ± 8.5 years) with stage-1 untreated hypertension at baseline. Orthostatic response was defined as the difference between six SBP measurements in the orthostatic and supine postures. People with a response more than 6.5 mmHg (upper decile) were defined as hyperreactors. After 3 months of follow-up, 24-h ambulatory BP was measured and the participants were classified as normotensives (N = 120), white-coat hypertensive individuals (N = 168), masked hypertensive individuals (N = 166) and sustained hypertensive individuals (N = 624). In 591 participants, 24-h urinary epinephrine was also measured.
RESULTS: Orthostatic response was an independent predictor of masked hypertension after 3 months (P = 0.001). In the whole group, the odds ratio for the Hyperreactors was 2.5 [95% confidence interval (95% CI) 1.5-4.0, P < 0.001]. In the participants stratified by orthostatic response and urinary epinephrine, the odds ratio for masked hypertension was 4.2 (95% CI, 1.8-9.9, P = 0.001) in the hyperreactors with epinephrine above the median and was 2.6 (95% CI, 0.9-7.3, P = 0.069) in those with epinephrine below the median. The association between orthostatic response and masked hypertension was confirmed in the cross-sectional analysis after 3 months (P < 0.001).
CONCLUSION: The present findings indicate that hyperreactivity to standing is a significant determinant of masked hypertension. The odds ratio for masked hypertension was even quadrupled in people with an orthostatic response more than 6.5 mmHg and high urinary epinephrine suggesting a role of sympathoadrenergic activity in the pathogenesis of masked hypertension.