Effects of afterload on regional left ventricular torsion

To determine if left ventricular torsion, as measured by magnetic resonance tissue tagging, is afterload dependent in a canine isolated heart model in which neurohumoral responses are absent, and preload is constant. In ten isolated, blood perfused, ejecting, canine hearts, three afterloads were stu...

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Bibliographic Details
Published in:Cardiovascular research 1996-06, Vol.31 (6), p.917-925
Main Authors: MACGOWAN, G. A, BURKHOFF, D, WEISS, J. L, SHAPIRO, E. P, ROGERS, W. J, SALVADOR, D, AZHARI, H, HEES, P. S, ZWEIER, J. L, HALPERIN, H. R, SIU, C. O, LIMA, J. A. C
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Computers
Dogs
Fundamental and applied biological sciences. Psychology
Heart
Heart - anatomy & histology
Heart - physiology
Heart Ventricles
Magnetic Resonance Imaging
Models, Cardiovascular
Perfusion
Stroke Volume - physiology
Torsion Abnormality
Vertebrates: cardiovascular system
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Summary:To determine if left ventricular torsion, as measured by magnetic resonance tissue tagging, is afterload dependent in a canine isolated heart model in which neurohumoral responses are absent, and preload is constant. In ten isolated, blood perfused, ejecting, canine hearts, three afterloads were studied, while keeping preload constant: low afterload, high afterload (stroke volume reduced by approx. 50% of low afterload), and isovolumic loading (infinite afterload). There were significant effects of afterload on both torsion (P < 0.05) and circumferential shortening (P < 0.0005). Between low and high afterloads, at the anterior region of the endocardium only, where torsion was maximal, there was a significant reduction in torsion (15.1 +/- 2.2 degrees to 7.8 +/- 1.8 degrees, P < 0.05). Between high afterload and isovolumic loading there was no significant change in torsion (7.8 +/- 1.8 degrees to 6.2 +/- 1.5 degrees, P = NS). Circumferential shortening at the anterior endocardium was significantly reduced both between low and high afterload (-0.19 +/- 0.02 to -0.11 +/- 0.02, P < 0.0005), and also between high afterload and isovolumic loading (-0.11 +/- 0.02 to 0.00 +/- 0.02, P < 0.05). Plots of strains with respect to end-systolic volume demonstrated a reduction in both torsion and shortening with afterload-induced increases in end-systolic volume. Torsion, but not circumferential shortening, persisted at isovolumic loading. Maximal regional torsion of the left ventricle is afterload dependent. The afterload response of torsion appears related to the effects of afterload on end-systolic volume.
ISSN:0008-6363
1755-3245
DOI:10.1016/0008-6363(96)00042-9