Hemodynamic variability and cerebrovascular control after transient cerebral ischemia

Abstract

We investigated if hemodynamic variability, cerebral blood flow (CBF) regulation, and their interrelationships differ between patients with transient ischemic attack (TIA) and controls. We recorded blood pressure (BP) and bilateral middle cerebral artery flow velocity (MCAv) in a cohort of TIA patients (n = 17), and age-matched controls (n = 15). Spontaneous fluctuations in BP and MCAv were characterized by spectral power analysis, and CBF regulation was assessed by wavelet phase synchronization analysis in the very low- (0.02-0.07 Hz), low- (0.07-0.20 Hz), and high-frequency (0.20-0.40 Hz) ranges. Furthermore, cerebrovascular CO2 reactivity was assessed as a second metric of CBF regulation by inducing hypercapnia with 8% CO2 inhalation followed by hyperventilation driven hypocapnia. We found that TIA was associated with higher BP power (group effect, P < 0.05), but not MCAv power (P = 0.11). CBF regulation (assessed by wavelet phase synchronization and CO2 reactivity) was intact in patients (all P ≥ 0.075) across both hemispheres (all P ≥ 0.51). Pooled data (controls and affected hemisphere of patients) showed that BP and MCAv power were positively correlated at all frequency ranges (R(2) = 0.20-0.80, all P < 0.01). Furthermore, LF phase synchronization index was a significant determinant of MCAv power (P < 0.05), while VLF and HF phase synchronization index, and TIA were not (all P ≥ 0.50). These results indicate that CBF stability and control is maintained in TIA patients, but BPV is markedly elevated. BPV attenuation may be an important therapeutic strategy for enhancing secondary stroke prevention in patients who suffer a TIA.

Keywords: Blood pressure; cerebral blood flow; cerebral hemodynamics; transient ischemic attack.

Figure 1

Comparisons for blood pressure and middle cerebral artery flow velocity spectral powers. (A) Patient versus control comparison for BP power. (B) Patient (affected and unaffected hemispheres) versus control comparisons for MCAv power. Spectral powers were log-transformed for statistical analyses, however, for ease of interpretation, they are shown here in raw units on log axes. *P < 0.05 for group and hemisphere main effect. BP, blood pressure; MCAv, middle cerebral artery flow velocity; VLF, very low-frequency; LF, low-frequency; HF, high-frequency.

Figure 2

Wavelet phase synchronization between BP and MCAv, with P_ETCO₂ as an additional input. (A) PSI against corresponding pseudo-frequencies (representing the result of wavelet scale to frequency conversion). (B) Patient (affected and unaffected hemispheres) versus control comparisons for mean PSI. BP, blood pressure; MCAv, middle cerebral artery flow velocity; P_ETCO₂, partial pressure of end-tidal CO₂; PSI, phase synchronization index; VLF, very low-frequency; LF, low-frequency; HF, high-frequency.

Figure 3

Bivariate linear correlations between BP and MCAv spectral powers. Group data are pooled (affected hemisphere in patients [n = 15] and controls [n = 15]). Results of multiple regression analysis with additional predictors are reported in text. R² values are coefficients of determination. Data has been log-transformed and plotted on linear axes. BP, blood pressure; MCAv, middle cerebral artery flow velocity; VLF, very low-frequency; LF, low-frequency; HF, high-frequency.