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Ann Thorac Surg 2003;76:1777-1778
© 2003 The Society of Thoracic Surgeons
a Congenital Heart Surgery Service, Texas Children’s Hospital/Baylor College of Medicine, 6621 Fannin St, WT 19345-HHouston, TX, USA 77030
e-mail: aundar{at}bcm.tmc.edu
To the Editor:
I read with interest the article by Saito and associates [1] and have a few comments.
I strongly believe that one of the fundamental reasons for continuing controversy over pulsatile and nonpulsatile perfusion in the acute or chronic setting is the lack of universal quantification of pulsatile and nonpulsatile pressure–flow waveforms [2, 3]. Without a precise quantification, comparisons between pulsatile and nonpulsatile perfusion or different forms of pulsatility (physiologic pulsatile flow versus diminished pulsatile flow such as roller pump pulsatility) regarding pulse pressure are totally inadequate.
It is well documented that the generation of pulsatile flow depends on the energy gradient rather than a pressure gradient [2, 4–7]. Therefore, the precise quantification of pressure–flow waveforms in terms of hemodynamic energy levels is a requirement, not an option. The energy equivalent pressure formula of Shepard and colleagues [4] is the best tool to quantify pulsatile and nonpulsatile pressure–flow waveforms. Using this formula, my associates and I [6] have clearly shown that two different pulsatile pumps with similar pulse-pressure levels have significantly different hemodynamic energy levels in an acute setting. Consequently, the morphology (shape and size) of the waveforms is more important than the level of pulse pressures.
Although Saito and associates noted that there were no significant differences in mean arterial pressure (MAP) between, the control group and the group with a left ventricular assist device before and after implantation, I could not find the exact MAP values after implantation in their report. According to the notes I took during the presentation of their data at the 2002 Annual Meeting of The Society of Thoracic Surgeons, the MAP of the nonpulsatile group was 18% to 20% higher than that of the control group after implantation. If the hemodynamic energy levels had been calculated in each group, it would have been clear that the nonpulsatile group had artificially higher hemodynamic energy levels because of higher MAPs. That was no significant difference in MAPs between groups is most likely a result of the very small sample size. Have Saito and co-workers performed a power analysis to achieve an accurate sample size in both groups? What was the MAP after implantation in each group? Have the authors calculated the hemodynamic energy levels?
There is also a major difference between the setup of Saito and colleagues and all other continuous flow pumps used clinically today. It is well documented that the continuous flow (nonpulsatile) pumps generate diminished pulsatility because the native heart is also working. In fact, in some patients, it is possible to achieve physiologic pulsatility after a few weeks of implantation [8]. In their design, Saito and co-workers achieved 100% nonpulsatile flow. Is this desirable in a clinical setting?
I urge Dr Saito and colleagues to consider using the Energy Equivalent Pressure formula for complete comparisons between their two study groups.
References
This article has been cited by other articles:
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  A. Undar and J. L. Myers Arterial pressure and pump flow rate during long-term pulsatile and nonpulsatile cardiac support. Ann. Thorac. Surg., March 1, 2005; 79(3): 1093 - 1094. [Full Text] [PDF]
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