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Normal cerebral vascular pulsations in humans: changes with age and implications for microvascular disease
Mi O Kim1, Yan Li, Fangfei Wei
1aDepartment of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales, Australia bCenter for Epidemiological Studies and Clinical Trials, Shanghai Key Laboratory of Hypertension, The Shanghai Institute of Hypertension, Department of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China cSt. Vincent's Clinic dUniversity of New South Wales/VCCRI eAustralian Institute of Health Innovation, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales, Australia.
Background:
Cerebral syndromes in older humans, secondary stroke in younger persons following trauma, and sickle cell anaemia in children, are linked by unexplained microvascular damage and high cerebral pressure or flow pulsations. The aim of this study was to characterize age-related pressure and flow waveforms patterns entering the brain, to explain these in terms of disturbed physiological function, and to consider clinical implications.
Method:
Blood flow velocity waves were measured in four cerebral vascular territories by transcranial Doppler of 1020 apparently normal patients (497 men, 21-78 years). Central pressure waveforms were generated from radial artery applanation tonometry with SphygmoCor. Relationships were described in time and frequency domains.
Results And Conclusion:
Flow waveforms entering the brain showed similar pattern to central aortic pressure waveforms, and similar changes with age. Augmentation index of flow and of pressure had high correlation at different ages, and in men and women (r = 0.58, P < 0.01). Calculated cerebral vascular impedance was similar in both sexes, and at different ages, with low modulus and phase, indicating a dilated, passive cerebral vascular bed. This vascular bed is subject to pressure and flow fluctuations generated directly by the heart and boosted by strong wave reflections from the lower body.
Conclusion:
Cerebral microvascular damage in older patients is attributable to high pulsatile pressure tearing the delicate media, causing haemorrhage, and high pulsatile flow dislodging endothelial cells, causing thrombosis and microinfarcts. High pulsations in older patients are caused by early wave reflection from the lower body. Reduction of or delay in wave reflection is a logical strategy for aortic stiffening in older humans.
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