Ischemic intervals during warm blood cardioplegia in the canine heart evaluated by phosphorus 31-magnetic resonance spectroscopy

• Published in: The Journal of thoracic and cardiovascular surgery Vol. 114; no. 6; pp. 1070 - 1079
• Main Authors: de Oliveira, Nilto Carias, Boeve, Theodore J., Torchiana, David F., Kantor, Howard L., Titus, James S., Schmidt, Christopher J., Lu, Cheng-zai, Kim, Jeehyang, Daggett, Willard M., Geffin, Gillian A.
• Format: Journal Article
• Language: English
• Published: United States Mosby, Inc 01.12.1997; AATS/WTSA
• Subjects: Adenosine Triphosphate - metabolism; Animals; Blood; Cardioplegic Solutions; Dogs; Heart Arrest, Induced - adverse effects; Heart Arrest, Induced - methods; Hemodynamics - physiology; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Myocardial Reperfusion Injury - diagnosis; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - physiopathology; Myocardium - metabolism; Phosphocreatine - metabolism; Time Factors; Ventricular Function, Left - physiology
• ISSN: 0022-5223; 1097-685X
• DOI: 10.1016/S0022-5223(97)70021-7

Objective: Warm blood cardioplegia requires interruption by ischemic intervals to aid visualization. We evaluated the safety of repeated interruption of warm blood cardioplegia by normothermic ischemic periods of varying durations. Methods: In three groups of isolated cross-perfused canine hearts, left ventricular function was measured before and for 2 hours of recovery after arrest, which comprised four 15-minute periods of cardioplegia alternating with three ischemic intervals of 15, 20, or 30 minutes (I 15, I 20, and I 30). Metabolism was continuously measured by phosphorus 31–magnetic resonance spectroscopy. Results: Adenosine triphosphate levels fell progressively as ischemia was prolonged; after recovery, adenosine triphosphate was 99% ± 6%, 90% ± 1% ( p = 0.0004 vs control), and 68% ± 3% ( p = 0.0002) of control levels in I 15, I 20, and I 30, respectively. Intracellular acidosis with ischemia was most marked in I 30. After recovery, left ventricular maximal systolic elastance at constant heart rate and coronary perfusion pressure was maintained in I 15 but fell to 85% ± 3% in I 20, ( p = 0.003) and to 65% ± 6% ( p = 0.003) of control values in I 30, while relaxation (tau) was prolonged only in I 30 ( p = 0.007). Conclusions: Hearts recover fully after three 15-minute periods of ischemia during warm blood cardioplegia, but deterioration, significant with 20-minute periods, is profound when the ischemic periods are lengthened to 30 minutes. This suggests that in the clinical setting warm cardioplegia can be safely interrupted for short intervals, but longer interruptions require caution. (J Thorac Cardiovasc Surg 1997;114:1070-80)