Fetal myocardial protection is markedly improved by reduced cardioplegic calcium content.
BACKGROUND
Fetal cardiac surgery holds a clear therapeutic benefit in the treatment of lesions that increase in complexity due to pathologic blood flow patterns during development. Fetal and neonatal myocardial physiology differ substantially, particularly in the regulation of myocardial calcium concentration. To examine issues of calcium homeostasis and fetal myocardial protection, a novel isolated biventricular working fetal heart preparation was developed.


METHODS
Hearts from 20 fetal lambs, 115 to 125 days gestation, were harvested and perfused with standard Krebs-Henseleit (K-H) solution. The descending aorta was ligated distal to the ductal insertion and the branch pulmonary arteries were ligated to mimic fetal cardiovascular physiology. Hearts were arrested for 30 minutes with normocalcemic (n = 8), hypocalcemic (n = 6), or hypercalcemic (n = 6) cold crystalloid cardioplegia before reperfusion with K-H solution.


RESULTS
Compared with normocalcemic cardioplegia, hypocalcemic cardioplegia improved preservation of left ventricular (LV) systolic function (88% +/- 2.2% vs 64% +/- 15% recovery of end-systolic elastance, p = 0.02), diastolic function (12% +/- 21% vs 38% +/- 11% increase in end-diastolic stiffness, p = 0.04), and myocardial contractility (97% +/- 9.6% vs 75.2% +/- 13% recovery of preload recruitable stroke work [PRSW], p = 0.04). In contrast, the fetal myocardium was sensitive to hypercalcemic arrest with poor preservation of LV systolic function (37.5% +/- 8.4% recovery of elastance), diastolic function (86% +/- 21% increased stiffness), and overall contractility (32% +/- 13% recovery of PRSW). Myocardial water content was reduced in hearts arrested with hypocalcemic cardioplegia (79% +/- 1.8% vs 83.7% +/- 0.9%, p = 0.0006).


CONCLUSIONS
This study demonstrates the sensitivity of the fetal myocardium to cardioplegic calcium concentration. Hypocalcemic cardioplegia provides superior preservation of systolic, diastolic, and contractile function of the fetal myocardium.
Malhotra
Sunil P
SP
Department of Surgery, New York University School of Medicine, New York, New York 10016, USA. spmalhotra@yahoo.com
Thelitz
Stephan
S
Riemer
R Kirk
RK
Reddy
V Mohan
VM
Suleman
Sam
S
Hanley
Frank L
FL
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003971:Diastole / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005318:Fetal Heart / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D005865:Gestational Age; D005947:Glucose / Q000494:pharmacology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009206:Myocardium / Q000378:metabolism; D011247:Pregnancy; D012756:Sheep; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013599:Systole / Q000187:drug effects / Q000502:physiology; D014325:Tromethamine / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
D002314:Cardioplegic Solutions; C074097:Krebs-Henseleit solution; D014325:Tromethamine; D005947:Glucose; D002118:Calcium