Document Detail


Myocardial function after fetal cardiac bypass in an ovine model.
MedLine Citation:
PMID:  20884028     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Fetal cardiac surgery might improve the prognosis of certain complex congenital heart defects that have significant associated mortality and morbidity in utero or after birth. An important step in translating fetal cardiac surgery is identifying potential mechanisms leading to myocardial dysfunction after bypass. The hypothesis was that fetal cardiac bypass results in myocardial dysfunction, possibly because of perturbation of calcium cycling and contractile proteins.
METHODS: Midterm sheep fetuses (n = 6) underwent 30 minutes of cardiac bypass and 120 minutes of monitoring after bypass. Sonomicrometric and pressure catheters inserted in the left and right ventricles measured myocardial function. Cardiac contractile and calcium cycling proteins, along with calpain, were analyzed by means of immunoblotting.
RESULTS: Preload recruitable stroke work (slope of the regression line) was reduced at 120 minutes after bypass (right ventricle: baseline vs 120 minutes after bypass, 38.6 ± 6.8 vs 20.4 ± 4.8 [P = .01]; left ventricle: 37 ± 7.3 vs 20.6 ± 3.9, respectively [P = .01]). Tau (in milliseconds), a measure of diastolic relaxation, was increased in both ventricles (right ventricle: baseline vs 120 minutes after bypass, 32.7 ± 4.5 vs 67.8 ± 9.4 [P < .01]); left ventricle: 26.1 ± 3.2 vs 63.2 ± 11.2, respectively [P = .01]). Cardiac output was lower and end-diastolic pressures were higher in the right ventricle, but not in the left ventricle, after bypass compared with baseline values. Right ventricular troponin I was degraded by increased calpain activity, and protein levels of sarco(endo)plasmic reticulum calcium ATPase were reduced in both ventricles.
CONCLUSIONS: Fetal cardiac bypass was associated with myocardial dysfunction and disruption of calcium cycling and contractile proteins. Minimizing myocardial dysfunction after cardiac bypass is important for successful fetal surgery to repair complex congenital heart defects.
Authors:
Jodie Y Duffy; Orlando Petrucci; R Scott Baker; Christopher T Lam; Casey A Reed; Danielle J Everman; Pirooz Eghtesady
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Publication Detail:
Type:  Journal Article     Date:  2010-09-29
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  141     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-22     Completed Date:  2011-05-16     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  961-8, 968.e1     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2011 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calpain / metabolism
Cardiac Surgical Procedures / adverse effects*
Cardiopulmonary Bypass / adverse effects*
Excitation Contraction Coupling
Female
Fetal Heart / metabolism,  physiopathology,  surgery*
Models, Animal
Myocardial Contraction
Pregnancy
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
Sheep
Time Factors
Troponin I / metabolism
Ventricular Dysfunction, Left / etiology*,  metabolism,  physiopathology
Ventricular Dysfunction, Right / etiology*,  metabolism,  physiopathology
Ventricular Function, Left
Ventricular Function, Right
Ventricular Pressure
Grant Support
ID/Acronym/Agency:
R01 HL098634/HL/NHLBI NIH HHS; R21 HL093683/HL/NHLBI NIH HHS; R21 HL093683-01A1/HL/NHLBI NIH HHS; R21 HL093683-01A1S1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Troponin I; EC 3.4.22.-/Calpain; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases
Comments/Corrections

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