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The Journal of Thoracic and Cardiovascular Surgery, Vol 95, 223-229, Copyright © 1988 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
PJ del Nido, DA Mickle, GJ Wilson, LN Benson, RD Weisel, JG Coles, GA Trusler and WG Williams
Postoperative low cardiac output is the most common cause of death in
patients undergoing elective repair of tetralogy of Fallot. The incidence
is much higher than in elective adult bypass operations for coronary artery
disease. To explain this difference, we investigated 16 children having
elective repair of tetralogy (mean age 6.3 years). Myocardial biopsy
specimens obtained during bypass before arrest, at the end of cold arrest
by blood cardioplegia, and after 30 minutes of reperfusion were studied for
adenosine triphosphate and lactate levels. Myocardium was submitted for
microscopic study shortly after the onset of ischemia. The operation was
successful in reducing right ventricular- pulmonary artery gradients from
82 +/- 28 to 9 +/- 1 mm Hg, yet seven patients required significant
inotropic support (dopamine, greater than 5 micrograms/kg/min) for more
than 24 hours and 12 patients needed prolonged use of digoxin and diuretics
for right ventricular failure. Tissue levels of adenosine triphosphate and
lactate in the tetralogy groups were compared with those in 20 adults with
coronary artery disease having similar myocardial protection techniques.
Adenosine triphosphate levels in the tetralogy group decreased during
cross- clamping (41 +/- 8 minutes) from 24 +/- 3 to 16 +/- 2 mmol/kg dry
weight (mean +/- 1 standard error), with a marked further drop after
reperfusion to 9 +/- 2 mmol/kg (p less than 0.01). Adenosine triphosphate
levels in the group with coronary disease also decreased from 20 +/- 1 to
16 +/- 1 mmol/kg after a longer cross-clamp time (70 +/- 17 minutes) but
remained at 15 +/- 2 mmol/kg after reperfusion. Tissue lactate levels in
the tetralogy group rose markedly during ischemia and remained elevated
after reperfusion. In contrast, lactate levels in the group with coronary
disease rose moderately during ischemia and returned to normal early on
reperfusion. Microscopic study revealed focal myocyte necrosis in tetralogy
of Fallot. Our findings, which demonstrate inadequate myocardial protection
of patients with tetralogy during repair, with depression of adenosine
triphosphate and increased lactate during ischemia and reperfusion, suggest
a defect in oxidative metabolism. The drop in adenosine triphosphate after
reperfusion in the patients with tetralogy implicates reperfusion injury as
a mechanism of myocardial damage.
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Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot
Division of Cardiovascular Surgery, Hospital for Sick Children, Toronto, Ontario, Canada.
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