Effect of inferior caval valve implantation on circulating immune cells and inflammatory mediators in severe tricuspid regurgitation.

BACKGROUND: Interventional valve implantation into the inferior vena cava (CAVI) lowers venous congestion in patients with tricuspid regurgitation (TR). We evaluated the impact of a reduction of abdominal venous congestion following CAVI on circulating immune cells and inflammatory mediators. METHODS: Patients with severe TR were randomized to optimal medical therapy (OMT) + CAVI (n = 8) or OMT (n = 10). In the OMT + CAVI group, an Edwards Sapien XT valve was implanted into the inferior vena cava. Immune cells and inflammatory mediators were measured in the peripheral blood at baseline and three-month follow-up. RESULTS: Leukocytes, monocytes, basophils, eosinophils, neutrophils, lymphocytes, B, T and natural killer cells and inflammatory markers (C-reactive protein, interferon-gamma, interleukin-2, -4, -5, -10, and tumor necrosis factor-alpha) did not change substantially between baseline and three-month follow-up within the OMT + CAVI and OMT group. CONCLUSION: The present data suggest that reduction of venous congestion following OMT + CAVI may not lead to substantial changes in systemic inflammation within a short-term follow-up. CLINICAL TRIAL REGISTRATION: NCT02387697.

Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction.

Increased TNF-α levels following acute myocardial infarction (AMI) contribute to impaired recovery of myocardial function. Interaction of inactive rhomboid protein 2 (iRhom2) with TNF-α converting enzyme (TACE) is required for TNF-α shedding from immune cells. We hypothesized that iRhom2 expression increases in circulating monocytes following AMI. Transcript levels of iRhom2, TACE and TNF-α were evaluated by quantitative real-time PCR in isolated monocytes of 50 AMI patients at admission (d1) and 3 days (d3) after. We observed a significant increase in levels of iRhom2 mRNA expression in monocytes between d1-3, while TNF-α and TACE mRNA expression remained unchanged. At d3, iRhom2 mRNA expression positively correlated with levels of intermediate monocytes or serum TNF-α, and negatively with LV systolic function. iRhom2 may contribute to regulation of post-infarction inflammation and is associated with LV dysfunction following AMI. iRhom2 modulation should be evaluated as a potential therapeutic strategy to attenuate cardiac remodeling following AMI.