期刊
HYPERTENSION
卷 73, 期 5, 页码 1018-1024出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.118.12402
关键词
aorta; arterial pressure; hypertension; cardiovascular disease; stroke volume
资金
- British Heart Foundation - Wellcome EPSRC Centre for Medical Engineering at King's College London [SP/12/4/29573, PG/17/50/32903, WT 203148/Z/16/Z]
- Medical Research Council
- British Heart Foundation
- Wellcome Trust
- European Union
- National Institute for Health Research (NIHR)
- King's College London
- NIHR Cardiovascular MedTech Co-operative at Guy's and St Thomas' NHS Foundation Trust
- MRC [MR/M016560/1] Funding Source: UKRI
We examined the influence of arterial stiffening and ventricular ejection dynamics on the age-related increase in central pulse pressure. A total of 2033 women aged 18 to 91 years from the Twins UK cohort were studied. Aortic flow and central blood pressure were measured by Doppler sonography and carotid tonometry, respectively. Measured values of central pulse pressure were compared with values predicted from aortic pulse wave velocity and ventricular ejection characteristics. Central pulse pressure at the first shoulder (P1) increased with age from 29.2 +/- 8.0 in those <40 years to 44.2 +/- 13.8 mm Hg in those >70 years (means +/- SD; P<0.001), an increase explained almost entirely by the concomitant increase in aortic pulse wave velocity. Pulse pressure, at the second pressure peak (P2, usually equal to peak central pulse pressure) increased to a greater extent with age: from 29.1 +/- 7.8 mm Hg for those <40 years to 60.2 +/- 20.5 mm Hg for those >70 years (P<0.001). The ratio of P2/P1 closely mirrored the ratio of ejection volume to ejection velocity at corresponding time points, and the proportionately greater increase in P2 compared with P1 was explained by increased ventricular ejection up to the time of P2. This increased from 52.5 +/- 13.1 to 59.3 +/- 17.8 mL (P<0.001) in parallel with an age-related increase in stroke volume and body mass index. These results suggest that the age-related change in central pulse wave morphology is driven mainly by an increase in arterial stiffening and altered pattern of ventricular ejection.
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