The Annals of Thoracic Surgery, Vol 42, 675-680, Copyright © 1986 by The Society of Thoracic Surgeons
Temperature-specific effects of adjuvant diltiazem therapy on myocardial energetics following potassium cardioplegic arrest
IB Krukenkamp, NA Silverman, D Sorlie, A Pridjian and S Levitsky
Adjuvant slow calcium channel blockade theoretically minimizes the calcium
influx attendant to potassium-induced cardioplegic arrest, particularly if
clinically acceptable levels of cardiac hypothermia are not maintained. The
present study assessed the efficacy of diltiazem therapy in ameliorating
perturbations of myocardial oxygen consumption that could be attributable
to postischemic intracellular calcium accumulation. In 30 canine hearts,
myocardial oxygen consumption was determined during incremental isovolumic
pressure-volume loading before and 30 minutes after 2 hours of either 20 or
28 degrees C potassium cardioplegic arrest. The intracoronary perfusate in
randomized hearts was modified by the addition of diltiazem, 150
micrograms/kg. Although systolic performance (as defined by peak developed
pressure as compared with balloon volume curves) was unchanged after 20
degrees C ischemia, adjuvant diltiazem therapy prevented the 44 +/- 2% (p
less than .01) decrease in peak developed pressure after 28 degrees C
arrest. Moreover, the 39% augmentation of postischemic myocardial oxygen
consumption at specific peak developed pressure following both 20 and 28
degrees C ischemia was attenuated with diltiazem only after the warmer
ischemic interval. This difference was characterized by a larger (35 +/- 2
vs. 26 +/- 2%; p less than .025) decrease in postischemic oxygen extraction
despite a comparable hyperemia. These data suggest that adjuvant diltiazem
therapy during potassium-induced cardioplegic arrest preserves
energy-efficient pump function only after warmer ischemia, thereby limiting
the clinical application of this myoprotective regimen.
