Plasma Monocyte Chemoattractant Protein-1 and Pulmonary Vascular Resistance in Chronic Thromboembolic Pulmonary Hypertension

Abstract

The pathogenesis of severe pulmonary hypertension seems to be related to inflammatory response in diseased sites. Monocyte chemoattractant protein-1 (MCP-1) has been reported to play a role in the development of congestive heart failure. In this immunological response, activation and migration of leukocytes including macrophages to the inflammatory region are important factors. We hypothesized that the severity of pulmonary hypertension may be related to MCP-1, which is thought to be upregulated by blood pressure or shear stress in pulmonary vasculature as well as by immunological and inflammatory reactions in chronic thromboembolic pulmonary hypertension (CTEPH). Circulating levels of MCP-1, interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha) were measured by sandwich ELISA in 14 patients with CTEPH. The plasma level of MCP-1 was significantly correlated with pulmonary vascular resistance. In IL-1beta and TNF-alpha, on the other hand, there was no correlation between cytokines and pulmonary hemodynamics. Pathological specimens obtained from the patients with CTEPH undergoing thromboendarterectomy demonstrated immunoreactivity of MCP-1 in endothelium, smooth muscle cells, and macrophages within neointima in the hypertensive large elastic pulmonary artery. We conclude that MCP-1 is upregulated in the remodeling of pulmonary arteries in close association with increased pulmonary vascular resistance in CTEPH.

Neutrophil/Lymphocyte Ratio Can Predict Postoperative Mortality in Patients with Chronic Thromboembolic Pulmonary Hypertension

“…11) Circulating monocyte chemoattractant protein-1 has been found to correlate with PVR in CTEPH patients. 22) Our findings confirm and contribute previous studies, in which used different inflammatory biomarkers, on the usefulness of NLR to correlate preoperative PVR and also to predict mortality. 9,23) In addition, NLR was positively correlated with PVR, supporting the hypothesis that inflammation is an important process on PVR in patients with CTEPH.…”

Dilatation of Bronchial Arteries Correlates With Extent of Central Disease in Patients With Chronic Thromboembolic Pulmonary Hypertension

“…Our previous study showed that monocyte chemoattractant protein-1 is produced in endothelial cells, mononuclear cells, and smooth muscle cells in the fibrinous portion adjacent to the vascular lumen in endarterectomized tissue. 18 Herve and Fadel speculated that macrophages infiltrating the wall of an occluded pulmonary artery stimulate proliferation of the vasa vasorum and lead to delivery of bone marrow-derived endothelial progenitor cells for local vasculogenesis within the nonresolving clots. 6 Other nonhemodynamic factors that are elevated in patients with CTEPH, such as endothelin-1, 19 might play a role in development of dilated BAs.…”

Atorvastatin in Pulmonary Arterial Hypertension (APATH) study

“…Nonetheless, while each may have a different pathobiology and natural history, histopathologic studies suggest a number of similarities in the vascular changes in CTEPH and CHD-PAH to those seen in idiopathic PAH [29,30]. As in PAH, recent work also suggests a role for inflammation in the genesis of CTEPH [31].…”