The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 643-650, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Contracture of the newborn myocardium after prolonged prearrest cooling
D Shum-Tim, CI Tchervenkov, T Hosseinzadeh and RC Chiu
Division of Cardiovascular and Thoracic Surgery, Montreal General Hospital/The Montreal Children's Hospital McGill University, Quebec, Canada.
Profound hypothermic circulatory arrest is frequently used to facilitate
the surgical repair of congenital heart defects in neonates. Deep
hypothermia is achieved by a period of core systemic cooling during
cardiopulmonary bypass before cardioplegic arrest. There have been
conflicting reports with respect to the consequence of perfusing a
nonarrested newborn heart under hypothermic conditions. This in vitro study
was designed to prolong the clinically simulated hypothermic perfusion
sequence into an extreme condition and to test the hypothesis that
prolonged cold perfusion of the nonarrested newborn myocardium could, in
fact, be detrimental. Twenty-four newborn piglets (5 to 7 days old) were
randomly assigned to four groups and studied in a crystalloid perfused
Langendorff heart model. The first two groups of hearts (n = 6 per group)
were subjected to either 30 minutes (group I) or 90 minutes (group II) of
cold perfusion at 15 degrees C, followed by 90 minutes of ischemia and then
30 minutes of normothermic reperfusion. In a second experiment, group III
hearts subjected to 30 minutes of cold perfusion were compared with group
IV (90 minutes of cold perfusion) without ischemic insult in either case.
Postischemic recovery of isovolumetric developed pressure was significantly
impaired in group II (16.1% +/- 7.4% [II] versus 65.5% +/- 4.8% [I], p <
0.05), and 50% of the hearts had no spontaneous cardiac activity on
reperfusion. End-diastolic pressure showed significant contracture with
prolonged cold perfusion: group II 57.3 +/- 13.9 mm Hg versus group I 14.8
+/- 1.8 mm Hg, p < 0.05. In the absence of ischemia, a similar
relationship was observed between groups IV and III (left ventricular
developed pressure 68.5% +/- 3.6% versus 82.4% +/- 4.2%, p < 0.05, and
left ventricular end-diastolic pressure 23.5 +/- 6.2 mm Hg versus 13.3 +/-
2.6 mm Hg, p = not significant. Ultrastructural examination revealed severe
damage to the myocardial cells and contraction band necrosis in group II
(prolonged cooling and ischemia). These results suggest that prolonged cold
perfusion of the nonarrested newborn heart impairs functional recovery and
is therefore detrimental. When followed by a period of ischemic arrest, it
further potentiates the myocardial injury and induces severe contracture.
This preceding adverse effect of prolonged myocardial cold perfusion before
cardiac arrest may, in part, explain the suboptimal protective effect of
cardioplegia in neonates.
