Hypertension and Cerebral Vasoreactivity

Hypertension is associated with microvascular and macrovascular brain injury but its direct influence on the cerebral circulation is not fully clear. Our objective was to investigate the association of hypertension with global and regional cerebral vasoreactivity to CO(2) using continuous arterial spin labeling MRI, independent of stroke and white matter hyperintensities. Participants (n=62; mean age: 66.7±1.0 years, 55% women, 84% white, 65% hypertension, 47% stroke) underwent arterial spin labeling perfusion MRI during normal breathing, 5% CO(2) rebreathing, and hyperventilation, as well as 24-hour ambulatory blood pressure monitoring. Vasoreactivity was the slope of the regression between cerebral perfusion and end-tidal CO(2). White matter hyperintensity volumes were quantified. Nighttime dipping was calculated as the percentage decline in nighttime/daytime blood pressure. After accounting for stroke and white matter hyperintensity volume, hypertensive participants had lower global vasoreactivity (1.11±0.13 versus 0.43±0.1 mL/100 g per minute per millimeter of mercury; P=0.0012). Regionally, this was significant in the frontal, temporal, and parietal lobes. Higher mean systolic blood pressure was associated with lower vasoreactivity (decreased by 0.11 U/10-mm Hg increase in systolic blood pressure; P=0.04), but nighttime dipping was not (P=0.2). The magnitude of decrease in vasoreactivity in hypertension without stroke was comparable to the magnitude of decrease in vasoreactivity in stroke without hypertension. Hypertension has a direct negative effect on the cerebrovascular circulation independent of white matter hyperintensities and stroke that is comparable to that seen with stroke. Because lower vasoreactivity is associated with poor outcomes, studies of the impact of antihypertensive on vasoreactivity are important.