Magnetic Resonance Imaging Measurement of Transmission of Arterial Pulsation to the Brain on Propranolol Versus Amlodipine

Abstract

Background and purpose: Cerebral arterial pulsatility is associated with leukoaraiosis and depends on central arterial pulsatility and arterial stiffness. The effect of antihypertensive drugs on transmission of central arterial pulsatility to the cerebral circulation is unknown, partly because of limited methods of assessment.

Methods: In a technique-development pilot study, 10 healthy volunteers were randomized to crossover treatment with amlodipine and propranolol. At baseline and on each drug, we assessed aortic (Sphygmocor) and middle cerebral artery pulsatility (TCDtranscranial ultrasound). We also performed whole-brain, 3-tesla multiband blood-oxygen level dependent magnetic resonance imaging (multiband factor 6, repetition time=0.43s), concurrent with a novel method of continuous noninvasive blood pressure monitoring. Drug effects on relationships between cardiac cycle variation in blood pressure and blood-oxygen level dependent imaging were determined (fMRI Expert Analysis Tool, fMRIB Software Library [FEAT-FSL]).

Results: Aortic pulsatility was similar on amlodipine (27.3 mm Hg) and propranolol (27.9 mm Hg, P diff=0.33), while MCA pulsatility increased nonsignificantly more from baseline on propranolol (+6%; P=0.09) than amlodipine (+1.5%; P=0.58). On magnetic resonance imaging, cardiac frequency blood pressure variations were found to be significantly more strongly associated with blood-oxygen level dependent imaging on propranolol than amlodipine.

Conclusions: We piloted a novel method of assessment of arterial pulsatility with concurrent high-frequency blood-oxygen level dependent magnetic resonance imaging and noninvasive blood pressure monitoring. This method was able to identify greater transmission of aortic pulsation on propranolol than amlodipine, which warrants further investigation.

Keywords: MRI; amlodipine; blood pressure; central arterial pulsatility; stroke.

Figure 1. Methodology.

A) Brachial BP cuffs on each arm are sequentially inflated to ~10mmHg above DBP (balancing comfort and optimisation of the waveform) via semi-rigid plastic tubing. The two transduced waveforms are high-pass filtered (>0.04Hz), calibrated to contralateral oscillometric BPs in the non-monitored arm, weighted with a triangular-window during overlaps and summed. B) Examples of BP and BOLD voxel time series, showing arterial pulsations in ventricles and grey matter.

Figure 2. Associations between multiband BOLD signal and peripheral arterial pulsation.

A) Coherence map and cardiac cycle-averaged BOLD responses. B-D) Z-statistics from general linear modelling are shown for Amlodipine, Propranolol and for voxels with stronger associations (corrected cluster p<0.05) on propranolol versus amlodipine respectively.