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Ann Thorac Surg 2005;79:1093-1094
© 2005 The Society of Thoracic Surgeons
Department of PediatricsHO85, Penn State College of Medicine, 500 University Dr, PO Box 850, Hershey, PA 17033
(E-mail: aundar{at}psu.edu).
We read with great interest the article on left ventricular pressure and volume unloading during support with a pulsatile versus a nonpulsatile left ventricular assistence device by Klotz and associates [1]. They concluded that left ventricular pressure unloading is similar for both pulsatile and nonpulsatile left ventricular assist devices and that pulsatile flow significantly improves left ventricular volume unloading compared with nonpulsatile (continuous) flow. We have a few comments on this important investigation.
One [24] of us previously has suggested that hemodynamic energy levels should be included in all investigations before making any comparisons of different perfusion modes. Generation of pulsatile flow depends on energy gradient [25]. It is well documented that pulsatile flow generates significantly higher hemodynamic energy compared with nonpulsatile flow during long-term support [24]. We suggest that the energy equivalent pressure (EEP) formula of Shepard and colleagues [5] is the best tool to precisely quantify the hemodynamic energy levels of different perfusion systems or different types of pulsatility.
The EEP formula is based on the ratio between the area beneath the hemodynamic power curve (
fpdt) and the area beneath the pump flow curve (
fdt) during each pulse cycle:
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We have concerns about the hemodynamic data after implantation of the left ventricular assist devices. First, according to Table 2 in the study by Klotz and associates, pump output and cardiac output (CO) in the nonpulsatile group were 3.6 ± 0.9 L/min and 5.1 ± 1.0 L/min, respectively. The difference between pump output and cardiac output in this group is 41.6%. However, in the pulsatile group, the difference is only 9.8% (5.1 L/min versus 5.6 L/min). Therefore, the native hearts were ejecting significantly more in the nonpulsatile group than in the pulsatile group. How do Klotz and co-workers explain this significant difference? What is the possible mechanism?
Second, the CO after implantation in the nonpulsatile group and the pump flow rate in the pulsatile group are identical (5.1 ± 1.0 L/min). Is this just a coincidence, or is it a typing error? We also believe that the right atrial pressure in the nonpulsatile group after implantation (77.7 ± 6.2 mm Hg in Table 2) must be a typographical error. What is the correct value?
Finally, MAP was significantly lower in the nonpulsatile group than in the pulsatile group after implantation (77.7 ± 6.2 mm Hg versus 104.6 ± 13.6 mm Hg). Have Klotz and colleagues tried to increase CO by changing the revolutions per minute of the nonpulsatile pump?
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