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 inJournal of international medical research Vol. 46; no. 4; pp. 1439 - 1454
Main Authors Wang, Xiaoting, Su, Longxiang, Yang, Rongli, Zhang, Hongmin, Liu, Dawei
Format Journal Article
LanguageEnglish
Published London, England SAGE Publications 01.04.2018
Sage Publications Ltd
SAGE Publishing
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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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ISSN:0300-0605
1473-2300
DOI:10.1177/0300060517737434