Experimental Physiology
Increasing paced heart rate reduces cerebral pulsatility
By Alastair J.S. Webb, J. Thomas, Osian Llwyd and 1 others.
Abstract
Abstract Cerebral pulsatility is a key index of cerebral haemodynamics, a central determinant of intravascular shear stress within intracranial vessels, and is associated with cerebral small vessel disease. It increases with a spontaneously falling heart rate, but the effect of altering heart rates on cerebral haemodynamics is unknown. We therefore tested whether increasing paced heart rate would reduce middle cerebral artery Gosling's pulsatility index (PI)on transcranial ultrasound, during emergency or elective implantation of a pacemaker for bradycardia. In 20 participants (14 males, mean age 78), paced heart rate was increased from 50 bpm or the individual's resting heart rate up to 100 bpm in 10 bpm increments. Cerebral pulsatility was strongly and inversely associated with heart rate, with an average reduction in PI of 0.07 per 10 beats per minute in unadjusted analyses, and 0.08 in mixed effects linear models adjusted for age, sex and cardiovascular risk factors ( P < 0.001). Increasing heart rate reduced peak systolic velocity by 2.51 cm/s per 10 bpm and increased end‐diastolic velocity by 1.26 cm/s per 10 bpm, which both mediated the effect on cerebral pulsatility. However, there was no effect on mean velocity. The decrease in peak systolic middle cerebral artery velocity was linear with increasing heart rate, but end‐diastolic velocity was maximal at a heart rate of 80 bpm. Overall, cerebral pulsatility was inversely and causally associated with paced heart rate. Heart rate modification could be a potential intervention to modify cerebral pulsatility, particularly in the context of bradycardia induced by heart block.



