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Ann Thorac Surg 2003;75:1937-1941
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Fetal myocardial protection is markedly improved by reduced cardioplegic calcium content

^a Department of Surgery, New York University School of Medicine, New York, New York, USA
^b Department of Cardiothoracic Surgery, University of Cologne Medical Center, Cologne, Germany
^c Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California, USA

Accepted for publication December 31, 2002.

^* Address reprint requests to Dr Malhotra, New York University School of Medicine, Department of Surgery, 530 First Avenue, NB-15N1, New York, NY 10016, USA
e-mail: spmalhotra{at}yahoo.com

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.

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