An increased blood flow pulsatility index (PI) in large cerebral arteries is a prognostic factor in stroke and has been linked to small vessel disease (SVD) ^[1]. Along with increased PI, these patients show decreased hypercapnia induced cerebrovascular reactivity (CVR) ^[2,3]. CVR is an autoregulatory mechanism responding at a timescale of seconds to minutes, while PI reflects hemodynamic processes which manifest over the course of a single cardiac cycle. Both CVR and PI provide information on a vascular reserve capacity. CVR reflects the ability to maintain constant blood flow under changes in perfusion pressure. PI reflects the ability of the vessels to dampen the pulse pressure wave.

Decreased vascular reserve is associated with dilation of the cerebral vasculature. We hypothesize that dilated vessels lose their ability to stretch and passively dampen the pulse pressure wave. While most PI studies are performed in large vessels, it is possible to measure PI in cerebral perforating arteries using 7T phase contrast (PC) MRI ^[4]. Measuring PI changes in the perforators during a vascular challenge could shed light on how autoregulation influences the damping of the pulse pressure wave in small vessels. The aim of this ongoing study was to determine whether the blood flow velocity and pulsatility change during a hypercapnic breathing challenge.

Four healthy volunteers were scanned on a 7T MRI system (Philips Healthcare) with 32 channel receive head coil (Nova Medical) while manipulating partial pressure of end-tidal carbon dioxide (PetCO2) using a RespirAct™ device (Thornhill Research Inc.). The scan protocol consisted of two cardiac gated single slice PC-MRI acquisitions, alternated with T1-weighted (T1w) 3D TFE acquisitions for segmentation of white matter (WM) (see Table 1 for scan parameters). The PC acquisition was planned in the semi oval center (CSO) in order to measure flow velocities in WM perforators (Figure 1). The first PC image was acquired at baseline gas PetCO2. The second PC image was acquired while targeting PetCO2 at 10 mmHg above baseline (Figure 2).

Perforator identification and PI calculation was performed as previously published ^[4]. Because the signal to noise ratio (SNR) of the velocity measurement in the PC images was higher than the contrast to noise ratio in the modulus images, identification was only based on velocity and not on modulus contrast. Change in average velocity (Vmean) and PI between baseline and hypercapnia was tested using a paired two-sample t-tests, all parameters were averaged per subject before testing, so individual vessels were not regarded as independent measurements. The same tests were performed after limiting the set of arteries to those that were identified in both acquisitions. Matching of the arteries between the two acquisitions was automatically performed, by taking the closest vessel within a radius of 2 mm (to account for possible subject motion). All analyses were performed using in-house developed software in Matlab (The Mathworks Inc.).

Average baseline of PetCO2 was 35 mmHg, with an average increase of 9 mmHg during the challenges. Significantly more arteries were identified in the CSO during hypercapnia compared to baseline (40 versus 31 arteries, p = 0.024, Table 2). Although not significant, Vmean increased by 8.6% during the hypercapnia, when looking at matched vessels only. Hypercapnia caused a significant increase in the amount of detectable perforators, but no significant change in Vmean or PI. If all other factors remain constant, distal vasodilation reduces the resistance, causing blood flow velocity to increase. Cerebral blood flow and blood flow velocity of large supplying arteries of the brain can be expected to increase roughly 9% per mmHg increase PaCO2 from baseline ^[5]. This inherently increases the SNR of the velocity measurements and increases the SNR of the magnitude through the T1 inflow effect and, thus, the detectability of the vessels. Local vasodilation of the perforator itself on the other hand could also increase the SNR of blood, caused by decreasing partial volume effect with surrounding tissue, which has a lower velocity and a lower signal intensity than blood. These effects would both reduce the underestimation of velocity, which increases with partial voluming ^[4]. Significantly more vessels were found during hypercapnia, but no change in pulsatility was observed in this small group. To what extent PI is truly independent of vasodilation may depend on the condition of the vessels, and needs further research in both healthy subjects and patients with impaired vasoreactivity and/or increased vessel stiffness.