{"title":"Increasing paced heart rate reduces cerebral pulsatility.","authors":"A J S Webb, J Thomas, O Llwyd, N Herring","doi":"10.1113/EP094034","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":3.0000,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670880/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP094034","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.