HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Yoshiya Toyoda Masahiro Yamaguchi Yutaka Okita Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Toyoda, Y. Articles by Okita, Y. Search for Related Content PubMed PubMed Citation Articles by Toyoda, Y. Articles by Okita, Y. Related Collections Congenital - acyanotic Congenital - cyanotic Myocardial protection

J Thorac Cardiovasc Surg 2003;125:1242-1251
© 2003 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease

Cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric cardiac surgery

From the Division of Cardiac Surgery, Kobe Children's Hospital, Kobe, Japan,^a and the Kobe University Graduate School of Medicine, Kobe, Japan.^b

Received for publication May 30, 2002. Revisions requested July 8, 2002; revisions received Aug 11, 2002. Accepted for publication Aug 16, 2002. Address for reprints: Masahiro Yamaguchi, MD, Kobe Children's Hospital, Division of Cardiothoracic Surgery, 1-1-1 Takakuradai, Sum ku, Kobe, Hyogo 654-0081, Japan.

Objectives: Terminal warm blood cardioplegia has been shown to enhance myocardial protection in adult patients. However, the cardioprotective effects and the mechanisms of terminal warm blood cardioplegia in pediatric heart surgery were still unknown.
Methods: One hundred three consecutive patients were prospectively randomized to one of two groups. In the control group (n = 52), myocardial protection was achieved with intermittent hyperkalemic cold blood cardioplegia and topical cardiac cooling. In the terminal warm blood cardioplegia group (n = 51), this was supplemented with terminal warm blood cardioplegia before the aorta was declamped. Arterial and coronary sinus blood samples were analyzed to determine myocardial energy metabolism and tissue injury.
Results: There were no significant differences between the two groups in age (5.5 ± 0.6 years in the control group vs 5.6 ± 0.5 years in the terminal warm blood cardioplegia group), body weight (17.2 ± 1.4 kg in the control group vs 19.8 ± 1.7 kg in the terminal warm blood cardioplegia group), percentage of cyanotic heart diseases (50% in the control group vs 51% in the terminal warm blood cardioplegia group), number of patients who required right ventriculotomy (33% in the control group vs 39% in the terminal warm blood cardioplegia group), cardiopulmonary bypass time (194 ± 12.1 minutes in the control group vs 177 ± 8.6 minutes in the terminal warm blood cardioplegia group), aortic crossclamp time (83.3 ± 5.9 minutes in the control group vs 82.3 ± 5 minutes in the terminal warm blood cardioplegia group), lowest rectal temperature (27.4 ± 0.3°C in the control group vs 28.1 ± 0.3°C in the terminal warm blood cardioplegia group), and myocardial temperature (9.6 ± 0.6°C in the control group vs 9.6 ± 0.7°C in the terminal warm blood cardioplegia group). Spontaneous defibrillation occurred after reperfusion in 80% in the terminal warm blood cardioplegia group, which was significantly (P < .05) higher than the control group (62%). The lactate extraction rate at 60 minutes of reperfusion was significantly (P < .05) higher in the terminal warm blood cardioplegia group (9.0 ± 2.8%) than the control group (-3.3 ± 2.4%). The postreperfusion values of cardiac troponin T (7.4 ± 0.6 ng/mL vs 11.2 ± 1.0 ng/mL at 6 hours; 4.6 ± 0.6 ng/mL vs 9.3 ± 1.6 ng/mL at 18 hours) and heart-type fatty acid binding protein (137 ± 28 ng/mL vs 240 ± 30 ng/mL at 2 hours; 88 ± 19 ng/mL vs 162 ± 26 ng/mL at 3 hours) were significantly (P < .05 vs the control group) lower in the terminal warm blood cardioplegia group.
Conclusion: Terminal warm blood cardioplegia enhances myocardial protection in pediatric cardiac surgery by an improvement in aerobic energy metabolism and a reduction of myocardial injury or necrosis.

This article has been cited by other articles:

				N. Yoshimura, Y. Oshima, M. Yoshida, H. Murakami, H. Matsuhisa, and M. Yamaguchi Continuous Hemodiafiltration During Cardiopulmonary Bypass in Infants Asian Cardiovasc Thorac Ann, October 1, 2007; 15(5): 376 - 380. [Abstract] [Full Text] [PDF]

				C. Rergkliang, A. Chetpaophan, V. Chittithavorn, P. Vasinanukorn, and V. Chowchuvech Terminal Warm Blood Cardioplegia in Mitral Valve Replacement: Prospective Study Asian Cardiovasc Thorac Ann, April 1, 2006; 14(2): 134 - 138. [Abstract] [Full Text] [PDF]

				K. Amark, H. Berggren, K. Bjork, A. Ekroth, R. Ekroth, K. Nilsson, and J. Sunnegardh Blood Cardioplegia Provides Superior Protection in Infant Cardiac Surgery Ann. Thorac. Surg., September 1, 2005; 80(3): 989 - 994. [Abstract] [Full Text] [PDF]

				T. Hasegawa, M. Yamaguchi, N. Yoshimura, and Y. Okita The dependence of myocardial damage on age and ischemic time in pediatric cardiac surgery J. Thorac. Cardiovasc. Surg., January 1, 2005; 129(1): 192 - 198. [Abstract] [Full Text] [PDF]

				T. Hasegawa, N. Yoshimura, S. Oka, Y. Ootaki, Y. Toyoda, and M. Yamaguchi Evaluation of heart fatty acid-binding protein as a rapid indicator for assessment of myocardial damage in pediatric cardiac surgery J. Thorac. Cardiovasc. Surg., June 1, 2004; 127(6): 1697 - 1702. [Abstract] [Full Text] [PDF]