Superior restoration of left ventricular performance after prolonged single-dose del Nido cardioplegia in conjunction with terminal warm blood cardioplegic reperfusion

Objectives: An incomplete restoration of left ventricular contractility after del Nido cardioplegia was noted in our recent study. This study tested the hypothesis that terminal warm blood cardioplegia promotes a prompt restoration of left ventricular performance after a prolonged single-dose del Nido cardioplegia. Methods: Fourteen piglets were subjected to 120 minutes of arrest by del Nido cardioplegia without terminal warm blood cardioplegia (del Nido cardioplegia group; n = 7) or with terminal warm blood cardioplegia before reperfusion (terminal warm blood cardioplegia group; n = 7). The other 7 piglets underwent total cardiopulmonary bypass without ischemia/reperfusion for 150 minutes (control group). Left ventricular function was assessed by percent recovery of end-systolic elastance as the contractility and percent end-diastolic pressure–volume relationship as the compliance using a conductance catheter. Troponin T and the mitochondrial score were also measured. Results: Depressed percent recovery of end-systolic elastance was sustained in the del Nido cardioplegia group, and a prompt restoration of end-systolic elastance was achieved using terminal warm blood cardioplegia (57.9 ± 17.8 vs 94.7 ± 13.1, P < .028). Percent end-diastolic pressure–volume relationship at the early phase was better in the terminal warm blood cardioplegia compared with the del Nido group (88.5 ± 24.0 vs 101.4 ± 16.8, P = .050). Troponin T was higher in the terminal warm blood cardioplegia compared with the control group (0.80% ± 0.21% and 1.49% ± 0.31%, respectively, P = .002). The mitochondrial score was equivalent in all groups. Spontaneous restoration to sinus rhythm was more frequent in the terminal warm blood cardioplegia group than in the del Nido cardioplegia group (6/7 vs 1/7, P < .028). Conclusions: The supplementary use of terminal warm blood cardioplegia achieved prolongation of the safe ischemic time up to 120 minutes for a single-dose application.