H. Matsuura et al., DETRIMENTAL EFFECTS OF INTERRUPTING WARM BLOOD CARDIOPLEGIA DURING CORONARY REVASCULARIZATION, Journal of thoracic and cardiovascular surgery, 106(2), 1993, pp. 357-361
Warm blood cardioplegia has emerged as a substitute for cold blood car
dioplegia as a method of myocardial protection. However, the continuou
s infusion of blood in this technique may obscure the operative field
and necessitate interruption of warm blood cardioplegia. This experime
ntal study was therefore undertaken to determine whether interrupting
warm blood cardioplegia during coronary revascularization would increa
se myocardial damage. In 30 adult pigs, the second and third diagonal
vessels were occluded with snares for 90 minutes. All animals underwen
t cardiopulmonary bypass and 45 minutes of cardioplegic arrest. During
the period of cardioplegic arrest, 10 pigs received intermittent ante
grade/retrograde infusion of cold blood cardioplegic solution (4-degre
es-C), 10 pigs received continuous retrograde infusion of warm blood c
ardioplegic solution (37-degrees-C) at 100 ml/min, and 10 pigs receive
d retrograde infusion of warm blood cardioplegic solution that was int
errupted for three 7-minute periods. After aortic unclamping, the coro
nary snares were released and all hearts were reperfused for 180 minut
es. Interrupting retrograde warm blood cardioplegia resulted in more t
issue acidosis during cardioplegic arrest (6.20 +/- 0.16 interrupted r
etrograde warm blood cardioplegia and 6.45 +/- 0.12 continuous retrogr
ade warm blood cardioplegia, both p < 0.05 compared with 6.98 +/- 0.17
intermittent antegrade and retrograde cold blood cardioplegia), decre
ased echocardiographic wall-motion scores (4 [normal] to -1 [dyskinesi
s]; 2.06 +/- 0.30 interrupted retrograde warm blood cardioplegia, p <
0.05 compared with 3.30 +/- 0.40 intermittent antegrade and retrograde
cold blood cardioplegia, 2.80 +/- 0.40 continuous retrograde warm blo
od cardioplegia), and increased tissue necrosis as measured by the are
a of necrosis/area at risk (38% +/- 5% interrupted retrograde warm blo
od cardioplegia, p < 0.05 compared with 21% +/- 2% intermittent antegr
ade and retrograde cold blood cardioplegia; 25% +/- 2% continuous retr
ograde warm blood cardioplegia). We concluded that interrupting warm b
lood cardioplegia during coronary revascularization diminishes the eff
ectiveness of warm blood cardioplegia and results in increased ischemi
c damage.