BACKGROUND AND PURPOSE: Chronic hypertension impairs cerebrovascular regulation in adults, but its effects on the pediatric population are unknown. The objective of this study was to investigate cerebrovascular abnormalities in hypertensive children and adolescents. METHODS: Sixty-four children and adolescents aged 7 to 20 years underwent transcranial Doppler examinations of the middle cerebral artery at the time of rebreathing CO2. Time-averaged maximum mean cerebral blood flow velocity and end-tidal CO2 were used to quantify cerebrovascular reactivity during hypercapnia. Patients were clinically categorized as hypertensive, prehypertensive, or white coat hypertensive based on 24-hour ambulatory blood pressure measurements. Their reactivities were compared with 9 normotensive control subjects and evaluated against baseline mean blood pressure z-scores and loads. RESULTS: Untreated hypertensive children had significantly lower hypercapnic reactivity than normotensive children (2.556 +/- 1.832 cm/s x mm Hg versus 4.256 +/- 1.334 cm/s x mm Hg, P < 0.05). Baseline mean diastolic blood pressure z-scores (r = -0.331, P = 0.037) and diastolic blood pressure loads (r = -0.351, P = 0.026) were inversely related to reactivity. CONCLUSIONS: Untreated hypertensive children and adolescents have blunted reactivity to hypercapnia, indicating deranged vasodilatory reactivity. The inverse relationship between diastolic blood pressure indices and reactivity suggests that diastolic blood pressure may be a better predictor of cerebral end organ damage than systolic blood pressure.
BACKGROUND AND PURPOSE: Chronic hypertension impairs cerebrovascular regulation in adults, but its effects on the pediatric population are unknown. The objective of this study was to investigate cerebrovascular abnormalities in hypertensivechildren and adolescents. METHODS: Sixty-four children and adolescents aged 7 to 20 years underwent transcranial Doppler examinations of the middle cerebral artery at the time of rebreathing CO2. Time-averaged maximum mean cerebral blood flow velocity and end-tidal CO2 were used to quantify cerebrovascular reactivity during hypercapnia. Patients were clinically categorized as hypertensive, prehypertensive, or white coat hypertensive based on 24-hour ambulatory blood pressure measurements. Their reactivities were compared with 9 normotensive control subjects and evaluated against baseline mean blood pressure z-scores and loads. RESULTS: Untreated hypertensivechildren had significantly lower hypercapnic reactivity than normotensive children (2.556 +/- 1.832 cm/s x mm Hg versus 4.256 +/- 1.334 cm/s x mm Hg, P < 0.05). Baseline mean diastolic blood pressure z-scores (r = -0.331, P = 0.037) and diastolic blood pressure loads (r = -0.351, P = 0.026) were inversely related to reactivity. CONCLUSIONS: Untreated hypertensivechildren and adolescents have blunted reactivity to hypercapnia, indicating deranged vasodilatory reactivity. The inverse relationship between diastolic blood pressure indices and reactivity suggests that diastolic blood pressure may be a better predictor of cerebral end organ damage than systolic blood pressure.
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