The need for pulsatility in the circulation during long-term mechanical support has been a subject of debate. We compared histological changes in calf renal arteries subjected to various degrees of pulsatile circulation in vivo. We addressed the hypothesis that the local reninangiotensin system (RAS) may be implicated in these histological changes.
Methods and Results
Sixteen calves were implanted with devices giving differing degrees of pulsatile circulation: six had a continuous flow left ventricular assist device (LVAD); six had a continuous flow right ventricular assist device (RVAD); and four had a pulsatile total artificial heart (TAH). Six other calves were histological and immunohistochemical controls. In the LVAD group, the pulsatility index was significantly lower (0.28 ± 0.07 LVAD vs 0.56 ± 0.08 RVAD, vs 0.53 ± 0.10 TAH; p < 0.01), and we observed severe periarteritis in all cases in the LVAD group. The number of angiotensin II type 1 receptor (AT1R)-positive cells and angiotensin converting enzyme (ACE)-positive cells in periarterial areas was significantly higher in the LVAD group (AT1R: 350 ± 139 LVAD vs 8 ± 6 RVAD, vs 3 ± 2 TAH, vs 3 ± 2 in control; p < 0.001 and ACE: 325 ± 59 LVAD vs 6 ± 4 RVAD, vs 6 ± 5 TAH, vs 3 ± 1 control; p < 0.001).
The reduced pulsatility produced by a continuous flow LVAD implantation induced severe periarteritis in the kidney. The local RAS was upregulated in the inflammatory cells only in the continuous flow LVAD group.
We compared histological changes in calf renal arteries subjected to various degrees of pulsatile circulation; continuous flow left ventricular assist device (LVAD), continuous flow right ventricular assist device, pulsatile total artificial heart and control. We observed severe periarteritis, and upregulation of local renin angiotensin system only in the LVAD group. The necessity of maintaining pulsatility in the systemic circulation during long-term mechanical support has been a subject of debate. Recently, simpler and smaller continuous flow blood pumps have become more prevalent. The diminished pulsatility created by support from a continuous flow left ventricular assist device (LVAD) is physiologically abnormal, and some changes to the morphology of the aortic wall and the renal artery have been reported.1,2 Continuous flow LVAD support has been reported to cause renal cortical artery hypertrophy and inflammatory cell infiltration in the renal cortex.2 However, the mechanisms leading to those morphological changes are still unclear.