title: Increased cardiac work provides a link between systemic hypertension and heart failure.
abstract: The spontaneously hypertensive rat (SHR) is an established model of human hypertensive heart disease transitioning into heart failure. The study of the progression to heart failure in these animals has been limited by the lack of longitudinal data. We used MRI to quantify left ventricular mass, volume, and cardiac work in SHRs at age 3 to 21 month and compared these indices to data from Wistar-Kyoto (WKY) controls. SHR had lower ejection fraction compared with WKY at all ages, but there was no difference in cardiac output at any age. At 21 month the SHR had significantly elevated stroke work (51 ± 3 mL.mmHg SHR vs. 24 ± 2 mL.mmHg WKY; n = 8, 4; P < 0.001) and cardiac minute work (14.2 ± 1.2 L.mmHg/min SHR vs. 6.2 ± 0.8 L.mmHg/min WKY; n = 8, 4; P < 0.001) compared to control, in addition to significantly larger left ventricular mass to body mass ratio (3.61 ± 0.15 mg/g SHR vs. 2.11 ± 0.008 mg/g WKY; n = 8, 6; P < 0.001). SHRs showed impaired systolic function, but developed hypertrophy to compensate and successfully maintained cardiac output. However, this was associated with an increase in cardiac work at age 21 month, which has previously demonstrated fibrosis and cell death. The interplay between these factors may be the mechanism for progression to failure in this animal model.
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand alexander.wilson@auckland.ac.nz.|Department of Physiology, University of Auckland, Auckland, New Zealand.
authors.forename: Alexander J
authors.initials: AJ
authors.lastname: Wilson
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
authors.forename: Vicky Y
authors.initials: VY
authors.lastname: Wang
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.|Department of Physiology, University of Auckland, Auckland, New Zealand.
authors.forename: Gregory B
authors.initials: GB
authors.lastname: Sands
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.|Department of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.
authors.forename: Alistair A
authors.initials: AA
authors.lastname: Young
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.|Department of Engineering Science, University of Auckland, Auckland, New Zealand.
authors.forename: Martyn P
authors.initials: MP
authors.lastname: Nash
authors.affiliation: Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.|Department of Physiology, University of Auckland, Auckland, New Zealand.
authors.forename: Ian J
authors.initials: IJ
authors.lastname: LeGrice
mesh_terms: D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D018450:Disease Progression; D006321:Heart / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006333:Heart Failure / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006352:Heart Ventricles / Q000033:anatomy & histology / Q000000981:diagnostic imaging*; D006973:Hypertension / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D023421:Models, Animal; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology; D020257:Ventricular Remodeling
keywords: Cardiomyopathy; heart failure; hypertension; hypertrophy; ventricular dysfunction; ventricular remodeling