Open AccessIncreased cardiac work provides a link between systemic hypertension and heart failure
Author(s) -
Wilson Alexander J.,
Wang Vicky Y.,
Sands Gregory B.,
Young Alistair A.,
Nash Martyn P.,
LeGrice Ian J.
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13104
Subject(s) - medicine , ejection fraction , heart failure , cardiology , stroke volume , hypertensive heart disease , cardiac function curve , cardiac hypertrophy , muscle hypertrophy , spontaneously hypertensive rat , cardiac fibrosis , cardiac output , fibrosis , endocrinology , blood pressure
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 SHR s 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). SHR s 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.