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Ann Thorac Surg 2003;75:183
© 2003 The Society of Thoracic Surgeons

Invited commentary

Joseph J. DeRose, Jr, MDa

a Columbia University College of Physicians and Surgeons, St. Luke’s-Roosevelt Hospital Center, New York, NY, USA

e-mail: jjd11{at}columbia.edu

Kihara and associates provide an elegant analysis of the medium and small vessel arterial wall pathology associated with continuous flow left ventricular assist devices (LVAD). This report is especially pertinent given the recent clinical trials of three new continuous axial flow LVADs [1–3].

The authors show that decreased pump flow and pulsatilty index result in significant medial smooth muscle cell hypertrophy in the renal arterioles of calves explanted at both 1 and 6 months. The acute effects of nonpulsatile flow have long been known, but the humoral, immunologic, and cellular effects of such long-term support have yet to be established. The arterial wall response described in this study is quite different from the reparative process which occurs following intimal injury. In that situation, medial smooth muscle hyperplasia, migration into the damaged intima, and laying down of extracellular matrix results in intimal repair at the cost of luminal stenosis [4, 5]. The response of the renal arterioles described in Kihara’s report may be mediated by both baroreceptor and humoral signals causing increased smooth muscle size in an attempt to respond to the nonphysiologic flow of continuous flow assistance. The identification of inflammatory cells in the renal cortical matrix also implicates immunologic mechanisms in this smooth muscle cell hypertrophic process. This appears consistent with the recent reports of transient immunologic activation in patients receiving axial flow LVADs pump [6].

How to extrapolate this data to the potential effects of our present axial flow LVADs on small and medium sized arterioles is confounded by two issues: (1) Calf arterial wall physiology is quite different from that found in the human; (2) there are both centrifugal and axial flow systems studied in the present report. Nonetheless, issues concerning arterial wall pathology as well as humoral and and immunologic responses to axial flow support may become critically important in the management of a new, growing population of patients supported with continuous flow LVADs.

References

  1. Frazier O.H., Myers T.J., Gregoric I.D., et al. Initial experience with the Jarvik 2000 implantable axial-flow left ventricular assist system. Circulation 2002;105:2808-2809.[Free Full Text]
  2. Noon G.P., Morely D.L., Irwin S., Abdelsayed S.V., Benkowski R.J., Lynch B.E. Clinical experience with the MicroMed Debakey ventricular assist device. Ann Thorac Surg 2001;71(Suppl 3):S133-138.[Abstract/Free Full Text]
  3. Burke D.J., Burke E., Parsaie F., et al. The Heartmate II: design and development of a fully sealed axial flow left ventricular assist system. Art Organs 2001;25:380-385.
  4. Gibbons G.H., Dzau V.J. The emerging concept of vascular remodeling. N Engl J Med 1994;330:1431-1438.[Free Full Text]
  5. DeRose J.J., Jr, Madigan J., Umana J.P., et al. Retinoic acid suppresses intimal hyperplasia and prevents vessel remodeling following arterial injury. Cardiovasc Surg 1999;7:633-639.[Medline]
  6. Ankersmit H.J., Wieselthaler G., Moser B., et al. Transitory immunologic response after implantation of the DeBakey VAD continuous axial-flow pump. J Thorac Cardiovasc Surg 2002;123:557-561.[Abstract/Free Full Text]



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[Abstract] [Full Text] [PDF]

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