Sepsis-associated diastolic dysfunction without elevated plasma B-type natriuretic peptide

Sturgess, D. J., Haluska, B. A., Masci, P., Jones, M. and Venkatesh, B. (2008). Sepsis-associated diastolic dysfunction without elevated plasma B-type natriuretic peptide. In: Jean-Louis Vincent, 28th International Symposium on Intensive Care and Emergency Medicine. 28th International Symposium on Intensive Care and Emergency Medicine, Brussels, Belgium, (S175-S176). 18-21 March 2008.


Author Sturgess, D. J.
Haluska, B. A.
Masci, P.
Jones, M.
Venkatesh, B.
Title of paper Sepsis-associated diastolic dysfunction without elevated plasma B-type natriuretic peptide
Conference name 28th International Symposium on Intensive Care and Emergency Medicine
Conference location Brussels, Belgium
Conference dates 18-21 March 2008
Proceedings title 28th International Symposium on Intensive Care and Emergency Medicine   Check publisher's open access policy
Journal name Critical Care   Check publisher's open access policy
Place of Publication Current Science
Publisher Philadelphia, PA, United States
Publication Year 2008
Year available 2008
Sub-type Published abstract
Open Access Status Link (no DOI)
ISSN 1364-8535
1466-609X
Editor Jean-Louis Vincent
Volume 12
Issue S1
Start page S175
End page S176
Total pages 212
Language eng
Formatted Abstract/Summary
Introduction: Plasma B-type natriuretic peptide concentration (BNP) is a marker of cardiac dysfunction [1]. It is unclear why
extremely high concentrations have been reported in sepsis with preserved systolic function [2]. This study sought to evaluate
relationships between BNP and in vivo diastolic function in a rat cecal ligation and perforation (CLP) model of sepsis.

Methods: With institutional ethics committee approval (UQ AEC Protocol 675/05), 24 male Sprague–Dawley rats (518 ± 56 g)
were studied. Rats were assigned to CLP (n = 12), sham surgery (sham, n = 6) or anaesthesia without surgery (control, n = 6). Echocardiography (15 MHz rodent probe) and venous blood sampling (BNP enzyme immunoassay) were performed prior to intervention (baseline; T0) and 18–22 hours following intervention (final; T2).

Results: Prior to final evaluation, three CLP rats (25%) and one sham rat (during anaesthesia) died. Baseline differences between groups (ANOVA) were demonstrated for heart rate (HR) (CLP 340 ± 36 bpm, sham 351 ± 19 bpm, control 300 ± 12 bpm; P = 0.02), peak passive to active diastolic transmitral velocity ratio (E/A) (CLP 1.7 ± 0.65, sham 1.26 ± 0.27, control 2.34 ± 0.59; P = 0.048) and A velocity (CLP 0.574 ± 0.13 m/s, sham 0.733 ± 0.33 m/s, control 0.411 ± 0.07 m/s; P = 0.03). BNP was not significantly different between groups (CLP 0.676 ± 0.179 ng/ml; sham 0.719 ± 0.202 ng/ml; control 0.503 ± 0.006 ng/ml; P = 0.07). At T2, CLP was compared with sham and control (ANCOVA with adjustment for baseline values). Compared with control rats, CLP rats demonstrated higher HR (CLP 402 ± 46 bpm, control 305 ± 11 bpm; P = 0.003), higher A velocity (CLP 0.802 ± 0.152 m/s, control 0.501 ± 0.103 m/s; P = 0.01), and lower E/A (CLP 1.02 ± 0.23, control 1.74 ± 0.46; P = 0.004). BNP was not significantly different in the CLP group (CLP 0.743 ± 0.225 ng/ml, sham 0.756 ± 0.213 ng/ml (P = 0.3), control 0.509 ± 0.026 ng/ml (P = 0.7)). At T2, multiple linear regression with backward elimination yielded HR as the only independent predictor of BNP (adjusted r2 = 0.56, P < 0.001).

Conclusions:
In this model, sepsis was associated with echocardiographic evidence of diastolic dysfunction resembling
clinical sepsis without an associated increase in BNP. HR was an independent predictor of BNP, accounting for 56% of variation.
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Conference Paper
Collection: School of Pharmacy Publications
 
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Created: Sat, 21 May 2016, 20:26:29 EST by Dr David Sturgess on behalf of School of Pharmacy