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Division of Cardiac Surgery, Johns Hopkins Medical Institutions, Blalock 618, 600 N. Wolfe St, Baltimore, MD 21287
(Email: jconte{at}csurg.jhmi.jhu.edu).
Kimball and associates [1] report on impairment in cellular immunity among patients with left ventricular assist devices (LVADs). The authors appropriately note in their work that infections are the Achilles heel of LVADs.
There are multiple reasons for this to occur. Aside from the fact that humans were not intended to have a power cable exiting their bodies removing the essential barrier function of the skin and providing a portal of entry for microorganisms, cellular immunity is impaired after LVAD implantation. Many authors have previously noted this. These authors asked whether this impairment of cellular immunity lasts longer than 6 months and compared a variety of in vitro immune function tests to transplant candidates without LVADs to elucidate the mechanism(s) of immune impairment.
The authors found that T-cell proliferative responses were impaired due to reduced expression of the cytokines interleukin –2 and tumor necrosis factor-alpha, as well as increased interleukin-10 and more suppressive T-regulatory cells overall. The fact that these findings were noted after 6 months of LVAD use is important, and the authors question whether these changes will last longer or will normalize with longer implantation times. They hypothesize that these effects will last due to the effect of leaching metal on immune function. However, it should be noted that the patients who survived or did not develop infections had a higher (better) proliferative response than those who died or did not develop infections lending some hope that the immune suppression may be limited in scope and duration.
There are many problems with this study. The control and study groups are unbalanced and are poorly defined. The controls were clearly healthier. We have no idea how long the patients were sick, their baseline (healthy) immune status, prior infection history, nutritional status, and so forth. The list could go on and on, and the fact that the study (LVAD) group consisted of two different pumps with very different blood contacting surfaces and biopolymers whose results are reported jointly compounds the problems.
However, we should not throw out the baby with the bath water. Using the authors own words, "By all indicators the LVAD recipients showed an atypical and suboptimal immune response."
The authors recommend antioxidant therapy to scavenge for metallic ions and suppressive antibiotic or antifungal therapy. This is impractical and flies in the face of the multitude of long-term successes we have seen in the LVAD field. If device-related immune suppression is such a big deal, why do patients with artificial joints not have more problems? The development of resistant organisms would be a strong impetus to avoid antibiotics and no one knows what to do about the antioxidant issue. In our program, 6 months is still early postoperatively, and the scores of greater than 2 years plus survivors worldwide, with no infection problems, could argue that the authors are incorrect or that the immune function of LVAD patients returns to normal.
What this article screams out to me is the central problem with the field of mechanical circulatory support. To borrow from the political arena, "It's the drive line stupid!" Until the mechanical device industry develops totally implantable power systems we will have VAD-related infections and this technology will not become mainstream; it is this simple. Our industry partners need to direct their efforts in this area with vigor or our patients and their shareholders will suffer.
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