Assessment of Inflammatory Biomarkers in Pulmonary Arteries of Chagasic and Non-Chagasic Heart Transplant Recipients

• Published in: Brazilian Journal of Transplantation Vol. 27; no. 1
• Main Authors: Silva, Marcus Vinícius de Paula da, Alves, Ildernandes Vieira, Alves, Antonielle Rodrigues Pereira, Lemos, Virginia Soares, Carmo, Gabriel Assis Lopes do, Castilho, Fábio o Morato de, Gelape, Cláudio Léo
• Format: Journal Article
• Language: English
• Published: 11-07-2024
• ISSN: 2764-1589; 2764-1589
• DOI: 10.53855/bjt.v27i1.561_ENG

In Brazil, Chagas cardiomyopathy is the third most common cause of indication for heart transplantation (HTx). Pulmonary arterial hypertension (PAH) is a severe condition frequently present in patients with terminal heart failure that worsens the prognosis of patients undergoing HTx. The etiological mechanism of PAH is multifactorial, with increased ventricular filling pressure being one of the main ones. Recently, however, several studies have sought to demonstrate the role of the local inflammatory process in contributing to the stiffening of the pulmonary arteries and the emergence or worsening of PAH in the heart failure (HF) setting. Objectives: To evaluate the inflammatory process in the pulmonary arteries of chagasic HTx (HTx-C) and non-chagasic (HTx-NC) patients, with and without PAH, through the tissue concentration of inflammatory cytokines obtained at the time of HTx. Methods: The levels of interleukins (IL)-6,IL-1β, TNF-α, and CD68 and CD66b neutrophils were measured in fragments of the pulmonary arteries of HTx-C and HTx-NC patients with and without PAH. Results: No statistically significant difference (p≥ 0.05) between the inflammatory biomarkers measured in HTx-C and HTx-NC pulmonary arteries, with or without PAH. Conclusion: We observed that HTx-C and HTx-NC patients present the same levels of inflammatory markers expressed in the pulmonary artery tissue, whether or not they have PAH. This fact suggests that PAH in HTx-C and HTx-NC patients is a process that is related to HF itself and not to the patients’ inflammatory profile.