The Physiological Rationale for Incorporating Pulsatility in Continuous-Flow Left Ventricular Assist Devices.

Over the past few decades, left ventricular assist device (LVAD) support has extended the lives of many patients with end-stage heart failure. The most common devices are continuous-flow (CF) LVADs. The use of the CF-LVADs has required that clinicians learn the physiological and clinical consequences of long-term continuous blood flow. While this alteration in the normal physiology still offers advantages from mechanical circulatory support, the lack of pulsatility may also increase the likelihood of adverse events. However, it is currently unknown whether newly evolved devices should incorporate pulsatility. In this article, we discuss the possible benefits of incorporating pulsatility, while maintaining the benefits of the CF-LVAD, to maximize the treatment of patients.

Markers of inflammation in recipients of continuous-flow left ventricular assist devices.

Although the newer continuous-flow left ventricular assist devices (CF-LVADs) provide clinical advantages over the pulsatile pumps, the effects of low pulsatility on inflammation are incompletely understood. The objective of our study was to examine the levels of inflammatory mediators in CF-LVAD recipients compared with both healthy control subjects and heart failure patients who were candidates for CF-LVAD support. Plasma levels of chemokines, cytokines, and inflammatory markers were measured in 18 CF-LVAD recipients and compared with those of 14 healthy control subjects and 14 heart failure patients who were candidates for CF-LVADs. The levels of granulocyte macrophage-colony stimulating factor, macrophage inflammatory proteins-1ß, and macrophage-derived chemokine were significantly higher in the CF-LVAD group compared with both the heart failure and the healthy control groups, whereas no significant differences were observed between the healthy control subjects and the heart failure groups. Compared with the healthy controls, C-reactive protein, interferon gamma-induced protein-10, monocyte chemotactic protein-1, and interleukin-8 levels were significantly higher in both the CF-LVAD and heart failure groups, but no significant differences were observed between the CF-LVAD recipients and the heart failure patients. Inflammatory markers were elevated in CF-LVAD recipients compared with healthy control subjects and the heart failure patients. Further studies should investigate the clinical implications of elevated levels of inflammation in CF-LVAD recipients.