The Annals of Thoracic Surgery, Vol 29, 539-545, Copyright © 1980 by The Society of Thoracic Surgeons
Does cardioplegic arrest compromise long-term left ventricular function?
KV Arom, FL Grover and JK Trinkle
This study was undertaken to evaluate the chronic, long-term effect of
global ischemia produced by cold potassium cardioplegia during
cardiopulmonary bypass. Fifteen dogs underwent either control thoracotomy
and chronic instrumentation(Group A) or cardiopulmonary bypass and 60
minutes of cold cardioplegic arrest (Group B). With the dogs conscious,
hemodynamic variables and left ventricular studies were recorded weekly for
12 weeks postoperatively, both at rest and during volume overload with
saline solution. At rest, the heart rate in Group B was 18% higher and
stroke volume was 14% lower than Group A. With volume overload, cardiac
output and maximum rate of rise of left ventricular pressure in Group B
rose only from 3.7 +/- 0.6 to 7.1 +/- 0.8 liters per minute and 2,410 +/-
220 to 2,730 +/- 130 mm Hg per second, respectively, compared with 3.9 +/-
0.6 to 10.4 +/- 0.8 liters per minute and 2,740 +/- 230 to 3,890 +/- 350 mm
Hg, respectively, in Group A (p less than 0.01). In Group B, the other
variables reached a plateau sooner than in Group A (48 versus 110 seconds).
The left ventricular function curve showed a mild decrease in functional
capacity and depressed contractility. Therefore, one hour of cardioplegic
cardiac arrest caused no depression of function at rest. Mild depression of
left ventricular function was demonstrated up to 7 weeks postoperatively
during acute volume overload.
