title: Does reduced myocardial efficiency in systemic hypertensive-hypertrophy correlate with increased left-ventricular wall thickness?
abstract: Elevated systemic blood pressure, and the attendant development of pathologic left ventricular (LV) hypertrophy, ultimately culminates in heart failure and death. In clinical studies, a reduction of myocardial efficiency has been implicated in systemic hypertensive-hypertrophy. However, it is uncertain whether reduced efficiency correlates with LV wall thickness. Hence, we performed experiments on isolated working hearts of spontaneously hypertensive rats (SHRs)-a widely-used experimental model of human hypertensive-hypertrophy. We contrasted their mechanoenergetic performance with that of Wistar controls at two ages: Adult (9 months) and Aged (post-18 months). The use of animal hearts allowed us to perform experiments over a wide range of afterloads. We found that mechanoenergetic performance (coronary and aortic flows, work output and oxygen consumption) declined with age. The peak efficiency of the Adult SHR was essentially similar to that of Control, but that for the Aged SHR was lower, compared with that of age-matched Wistar rats. All variables, including peak efficiency, obtained from the failing Aged SHR hearts (which also developed right ventricular hypertrophy), were greatly reduced. Our data reveal that peak efficiency of the Aged SHR, upon transitioning from compensated hypertrophy to failure, diminishes sharply, arising from compromised flows-both aortic and coronary. We further show that the reduction of myocardial efficiency in hypertensive-hypertrophy does not correlate with LV wall thickness, but instead is inversely correlated with whole-heart mass. The latter relation may serve as a prognostic and diagnostic tool in the clinical setting.
authors: Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand.
authors: June-Chiew
authors: JC
authors: Han
authors: Department of Physiology, The University of Auckland, Auckland, New Zealand.
authors: Carolyn J
authors: CJ
authors: Barrett
authors: 1] Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand [2] Department of Engineering Science, The University of Auckland, Auckland, New Zealand.
authors: Andrew J
authors: AJ
authors: Taberner
authors: 1] Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand [2] Department of Physiology, The University of Auckland, Auckland, New Zealand.
authors: Denis S
authors: DS
authors: Loiselle
mesh_terms: D000367:Age Factors; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar