title: Increased stroke volume and aortic stiffness contribute to isolated systolic hypertension in young adults.
abstract: Isolated systolic hypertension is a common condition in individuals aged older than 60 years. However, isolated systolic hypertension has also been described in young individuals, although the mechanisms are poorly understood. We hypothesized that in young adults, isolated systolic hypertension and essential hypertension have different hemodynamic mechanisms and the aim of this study was to test this hypothesis in a cohort of subjects from The ENIGMA Study. Peripheral and central blood pressure, aortic pulse wave velocity, cardiac output, stroke volume, and peripheral vascular resistance were determined in 1008 subjects, aged 17 to 27 years. Compared with normotensive subjects, those with isolated systolic hypertension had significantly higher peripheral, central, and mean blood pressure, aortic pulse wave velocity, cardiac output, and stroke volume (P<0.001 for all comparisons). However, there were no differences in pulse pressure amplification, heart rate, or peripheral vascular resistance between the two groups. Compared with subjects with essential hypertension, mean pressure, heart rate, and peripheral vascular resistance were all significantly lower in isolated systolic hypertensive subjects, but pulse pressure amplification, aortic pulse wave velocity, cardiac output, and stroke volume were higher (P<0.001 for all comparisons). We have demonstrated that in young adults, isolated systolic hypertension and essential hypertension arise from different hemodynamic mechanisms. Isolated systolic hypertension appears to result from an increased stroke volume and/or aortic stiffness, whereas the major hemodynamic abnormality underlying essential hypertension is an increased peripheral vascular resistance. Long-term follow-up of these individuals is now required to determine whether they are at increased risk compared with age-matched normotensive individuals.
authors.affiliation: Clinical Pharmacology Unit, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK. cmm41@cam.ac.uk
authors.forename: Carmel M
authors.initials: CM
authors.lastname: McEniery
authors.lastname: Yasmin
authors.forename: Sharon
authors.initials: S
authors.lastname: Wallace
authors.forename: Kaisa
authors.initials: K
authors.lastname: Maki-Petaja
authors.forename: Barry
authors.initials: B
authors.lastname: McDonnell
authors.forename: James E
authors.initials: JE
authors.lastname: Sharman
authors.forename: Christopher
authors.initials: C
authors.lastname: Retallick
authors.forename: Stanley S
authors.initials: SS
authors.lastname: Franklin
authors.forename: Morris J
authors.initials: MJ
authors.lastname: Brown
authors.forename: R Catherine
authors.initials: RC
authors.lastname: Lloyd
authors.forename: John R
authors.initials: JR
authors.lastname: Cockcroft
authors.forename: Ian B
authors.initials: IB
authors.lastname: Wilkinson
mesh_terms: D000293:Adolescent; D000328:Adult; D001011:Aorta / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D016022:Case-Control Studies; D015331:Cohort Studies; D003187:Compliance; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D011674:Pulse; D013318:Stroke Volume; D014655:Vascular Resistance