Abstract

We appreciate Ji and Undar’s kind appraisal of our study on the benefits of pulsatile cardioplegia in failing hearts, because their input to the importance of pulsatile cardiopulmonary bypass is well recognized.1Undar A. Masai T. Yang S.Q. et al.Pulsatile perfusion improves regional myocardial blood flow during and after hypothermic cardiopulmonary bypass in a neonatal piglet model.ASAIO J. 2002; 48: 90-95Crossref PubMed Scopus (56) Google Scholar They propose that energy equivalent pressure (EEP) and surplus hemodynamic energy (SHE) should be reported when studying the effect of pulsatile flow, because the difference between EEP and mean arterial pressure (MAP) conveys the extra energy generated by each pulsatile wave. EEP and MAP are identical and the difference is zero when the pressure wave is perfectly harmonic. Our study did not report those values,2Kassab G.S. Kostelec M. Covell J. Sadeghi A. Hoffman J.I.E. Buckberg G. Myocardial protection in the failing heart under simulated left ventricular restoration: III Effect of pulsatile cardioplegic perfusion.J Thorac Cardiovasc Surg. 2006; 132: 884-890Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar because EEP and MAP were not significantly different for the waveforms used. A recent study by Huo and Kassab3Huo Y. Kassab G.S. Pulsatile blood flow in the entire coronary arterial tree: theory and experiment.Am J Physiol Heart Circ Physiol. 2006; 291: H1074-H1087Crossref PubMed Scopus (61) Google Scholar quantitatively demonstrated this point computationally, based on a full analysis of steady state versus pulsatile flow in the entire coronary arterial tree based on measured anatomical data and experimentally to validate the model. The inlet pressure waveform measured from a porcine model was input into an isolated heart to verify the model predictions and showed excellent agreement between the model and the experiment. Mean flow of both pulsatile and steady-state experiments and mathematical model were not statistically different and were consistent with normal heart microsphere measurements.2Kassab G.S. Kostelec M. Covell J. Sadeghi A. Hoffman J.I.E. Buckberg G. Myocardial protection in the failing heart under simulated left ventricular restoration: III Effect of pulsatile cardioplegic perfusion.J Thorac Cardiovasc Surg. 2006; 132: 884-890Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar The EEP, MAP, and SHE were 75.38 mm Hg, 73.54 mm Hg and 1.84 mm Hg, respectively, providing only a 2.4% SHE/EEP ratio. These calculations and this discussion reflect why our study did not focus on the EEP and SHE parameters. Rather, we believe that a different mechanism is at play because changes occurred only in failing hearts, because no significant changes were found between pulsatile and nonpulsatile cardioplegic flow existed in normal hearts. More importantly, vascular resistance rose in failing hearts in both the beating and cardioplegic states (with and without pulsation) such that factors responsible for initiating such pulsatility effect, such as altered number of vessels, lumen diameter, and vascular length, must be understood as ventricular geometry becomes expanded and spherical. This pulsatility dependency observation implies that dilated heart failure may have impaired coronary flow reserve capacity by limiting coronary autoregulation. This implication reinforces the need to ensure increased perfusion pressure during myocardial protection strategies with the beating and pulsatile or nonpulsatile cardioplegia delivery. Here, a method of pulsatile cardioplegia delivery was introduced to demonstrate the capacity to overcome this limitation of nonpulsatile cardioplegia in failing hearts. Our findings underscore the value of coronary pulsation, either by compression of vessels by the beating heart or by internal stretching by pulsatile cardioplegic flow. Our findings support the work of Undar relating to the significance of pulsatile flow in the use of cardioplegia for cardiac protection. Furthermore, our observations reinforce the importance of studying models that reflect clinical entities, such as heart failure, because the observed enhancement of subendocardial muscle perfusion would have gone undetected in studies of normal hearts. Precise quantification of pressure-flow waveforms during pulsatile and nonpulsatile perfusionThe Journal of Thoracic and Cardiovascular SurgeryVol. 133Issue 5PreviewWe would like to congratulate Kassab and colleagues1 on their experimental design and results concerning pulsatile cardioplegic delivery in improved subendocardial perfusion of the open failing ventricle when compared with nonpulsatile perfusion. We believe that their investigation is a good attempt to use pulsatile flow as a myocardial protective strategy during the cardiopulmonary bypass (CPB) procedure. Such information may be critical to enhance cardioprotective strategies in cardiac patients in the near future. Full-Text PDF

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