title: Myocardial function after fetal cardiac bypass in an ovine model.
abstract: 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.affiliation: Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
authors.forename: Jodie Y
authors.initials: JY
authors.lastname: Duffy
authors.forename: Orlando
authors.initials: O
authors.lastname: Petrucci
authors.forename: R Scott
authors.initials: RS
authors.lastname: Baker
authors.forename: Christopher T
authors.initials: CT
authors.lastname: Lam
authors.forename: Casey A
authors.initials: CA
authors.lastname: Reed
authors.forename: Danielle J
authors.initials: DJ
authors.lastname: Everman
authors.forename: Pirooz
authors.initials: P
authors.lastname: Eghtesady
mesh_terms: D000818:Animals; D002154:Calpain / Q000378:metabolism; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D056966:Excitation Contraction Coupling; D005260:Female; D005318:Fetal Heart / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D023421:Models, Animal; D009200:Myocardial Contraction; D011247:Pregnancy; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D012756:Sheep; D013997:Time Factors; D019210:Troponin I / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right; D017725:Ventricular Pressure
chemical_list: D019210:Troponin I; D002154:Calpain; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases