Long-term (≥36 months) LVAD support was associated with significantly lower percentages of total dendritic cells (0.73% vs 1.01%, p<0.01), BDCA3+ myeloid DCs (64.5% vs 71.4%, p<0.01), BDCA2+ plasmacytoid DCs (27.3% vs 31.3%, p=0.01), BDCA4+ plasmacytoid DCs (26.4% vs 30.2%, p=0.02), CD56bright NK cells (3.3% vs 5.2%, p<0.01), and CD19+ B-cells (6.2% vs 14.6%, p<0.01), and higher NK cell terminal differentiation measured by CD57 expression (46.4% vs 39.1%, p=0.03) compared to short-term LVAD support patients.
Observational (n=110)
No
Does long-term LVAD support (≥36 months) cause more detrimental immunological effects compared to short-term LVAD support (12-18 months) in patients with end-stage heart failure?
Long-term LVAD support (≥36 months) is associated with progressive detrimental changes in the innate and adaptive immune systems, including reductions in dendritic cells, B-cells, and immunoregulatory NK cells, compared to short-term support.
Introduction Infection is a common complication following left ventricular assist device (LVAD) implantation that increases the mortality in the post-implantation period. Immunological changes affecting dendritic cells (DCs), natural killer (NK) cells and T-cells have been observed in the first year after implantation, but long-term data are missing. We investigated if long-term LVAD support has stronger effects on the immune system than short-term LVAD support. Methods Blood samples were obtained from patients with 12–18 months of LVAD support (short-term LVAD; n=53) and from patients with ≥36 months of LVAD support (long-term LVAD; n=57). Flow cytometric analyses for CD4 + and CD8 + T-cells, T regs , B cells, NK cells and DCs were performed. Additionally, terminal differentiation and activation of immune cells was quantified. Results Both groups were comparable with regard to sex, age at LVAD implantation, preoperative BMI, etiology of heart failure, NYHA class, left ventricular ejection fraction, INTERMACS, and implant strategy. Platelet counts were lower in the long-term LVAD group (p=0.05). Flow cytometric analyses for CD4 + and CD8 + T-cells, T regs , B-cells, NK cells and DCs revealed that the percentages of total DCs (p0,01), BDCA3 + myeloid DCs (p0.01), BDCA2 + (p=0.01) and BDCA4 + plasmacytoid DCs (p=0.02), CD19 + B-cells (p0.01) and of immunoregulatory CD56 bright NK cells (p0.01) were reduced in long-term compared to short-term LVAD patients. Terminal differentiation of NK cells measured by CD57 expression was higher in long-term than in short-term LVAD patients (p=0.03). Conclusion This cross-sectional observational study revealed that long-term (≥36 months) LVAD support may contribute to detrimental effects on the immune system in comparison to short-term LVAD support. The long-lasting LVAD support may influence DCs, NK cells and B-cells that show a progression of cellular changes.
Dieterlen et al. (Mon,) conducted a observational in Adults (age ≥18 years) with end-stage heart failure supported by HeartMate 3 LVAD for short-term (12–18 months) or long-term (≥36 months) duration (n=110). Long-term LVAD support (≥36 months) vs. Short-term LVAD support (12–18 months) was evaluated on Immunological changes measured by flow cytometric analysis of immune cell populations (dendritic cells, NK cells, B-cells, T-cells). Long-term (≥36 months) LVAD support was associated with significantly lower percentages of total dendritic cells (0.73% vs 1.01%, p<0.01), BDCA3+ myeloid DCs (64.5% vs 71.4%, p<0.01), BDCA2+ plasmacytoid DCs (27.3% vs 31.3%, p=0.01), BDCA4+ plasmacytoid DCs (26.4% vs 30.2%, p=0.02), CD56bright NK cells (3.3% vs 5.2%, p<0.01), and CD19+ B-cells (6.2% vs 14.6%, p<0.01), and higher NK cell terminal differentiation measured by CD57 expression (46.4% vs 39.1%, p=0.03) compared to short-term LVAD support patients.