Myocardial strain/stress changes identified by echocardiography may reveal early sepsis-induced myocardial dysfunction
Objective To perform early assessment of sepsis-induced myocardial dysfunction (SIMD) using strain/stress echocardiography. Methods A canine model of SIMD was established using intravenous injection of lipopolysaccharide (LPS, 2 mg/kg). Thirteen dogs were included, comprising an LPS-treated SIMD gro...
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Published in | Journal of international medical research Vol. 46; no. 4; pp. 1439 - 1454 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.04.2018
Sage Publications Ltd SAGE Publishing |
Subjects | |
Online Access | Get full text |
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Summary: | Objective
To perform early assessment of sepsis-induced myocardial dysfunction (SIMD) using strain/stress echocardiography.
Methods
A canine model of SIMD was established using intravenous injection of lipopolysaccharide (LPS, 2 mg/kg). Thirteen dogs were included, comprising an LPS-treated SIMD group (n = 7) and saline control group (n = 6). SIMD was assessed at various time-points using cardiac measurements including haemodynamics and echocardiography.
Results
Systolic and radial ventricular wall stress and circular ventricular wall stress (WSsc) were significantly lower in the sepsis group versus the control group at all time-points. Logistic regression analysis revealed an inverse correlation between stress rate of the front-posterior and bottom wall and left ventricle systolic wall strength. In contrast, a positive correlation was found between the mean velocity of circumferential fibre shortening (mVCF) or heart rate-adjusted mVCF (RVCF) and WSsc. Using regression equations, predicted values for mVCF and RVCF in animals with sepsis were significantly higher than measured values at 4- 5- and 6-h time-points.
Conclusions
These findings will further the understanding of pathophysiological alterations in SIMD at the early stage of sepsis, and suggest that strain rate may reflect the nature of myocardial contractility. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0300-0605 1473-2300 |
DOI: | 10.1177/0300060517737434 |