Inflammatory markers in Eisenmenger syndrome and their association with clinical outcomes. A cross-sectional comparative study

Gonzaga, Laion R.A.; Gomes, Walter J.; Rocco, Isadora S.; Matos-Garcia, Bruna C.; Bublitz, Caroline; Viceconte, Marcela; Tatani, Solange Bernardes; Santos, Vinícius Batista; Silva, Célia M.C.; Tulloh, Robert; Arena, Ross; Guizilini, Solange

doi:10.1016/j.ijcard.2021.06.039

Cited by 2 publications

(3 citation statements)

References 24 publications

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“… 32 Notably, in patients with CHD‐PAH, there is an inflammatory profile, especially in Eisenmenger syndrome patients. 33 In contrast, a previous study found that SYN was notably down‐regulated in VSMCs isolated from varicose veins. 19 It has also been reported that SYN is down‐regulated by platelet‐derived growth factor beta (PDGF‐β) and interferon gamma (IFN‐γ), exposure to shear flow stress, and oxidized low‐density lipoprotein (oxLDL) loading.…”

Section: Discussionmentioning

confidence: 83%

“…32 Notably, in patients with CHD-PAH, there is an inflammatory profile, especially in Eisenmenger syndrome patients. 33 In contrast, a…”

Section: Discussionmentioning

confidence: 95%

“…SYN is rarely expressed in portal tract fibroblasts under normal conditions, but is overexpressed in severe inflammatory diseases associated with portal expansion 32 . Notably, in patients with CHD‐PAH, there is an inflammatory profile, especially in Eisenmenger syndrome patients 33 . In contrast, a previous study found that SYN was notably down‐regulated in VSMCs isolated from varicose veins 19 .…”

Section: Discussionmentioning

confidence: 96%

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Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt‐induced pulmonary arterial hypertension

Zhou

2022

ESC Heart Failure

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Aims Although considerable progress has been made in the diagnosis and treatment of congenital heart disease‐associated pulmonary heart hypertension (CHD‐PAH), the clinical prognosis and overall survival of patients with CHD‐PAH remain poor. Therefore, the molecular pathogenesis of CHD‐PAH requires further investigation. The intermediate filament protein synemin (SYN) is reported to modulate phenotypic alterations and varicose vein development, but there is little understanding of its exact functions in CHD‐PAH. Methods and results SYN expression in the pulmonary arterioles of CHD‐PAH patients and shunt‐induced PAH rat models was evaluated using immunohistochemistry and western blot. Cell counts and Transwell migration assays were used to assess the effect of SYN on the proliferation and migration capability of human pulmonary smooth muscle cells (hPASMCs). Adeno‐associated viruses (AAVs) have been used to suppress SYN expression in the pulmonary arterioles of rats. Such rats were further used to construct a shunt‐induced PAH animal model to investigate the function of SYN in PAH and pulmonary vascular remodelling. Compared with the normal control group, SYN expression was found to be clearly up‐regulated in the remodelled pulmonary arterioles of CHD‐PAH and shunt‐induced PAH rat models. In addition, SYN suppression increased the expression of hPASMC contractile‐phenotype markers and decreased the expression of synthetic phenotype markers, in contrast to the control group. SYN suppression also dramatically attenuated the proliferation and migration capability of hPASMCs. Conversely, SYN overexpression promoted phenotypic switch, proliferation, and migration of hPASMCs, whereas these effects were notably alleviated by the protein kinase B (AKT) inhibitor MK‐2206. Furthermore, we confirmed that SYN suppression mitigated PAH and pulmonary vascular remodelling induced by high blood flow in vivo. Conclusions Our findings indicated that SYN may represent a promising therapeutic target in the treatment of CHD‐PAH.

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Section: Discussionmentioning

confidence: 83%

“…32 Notably, in patients with CHD-PAH, there is an inflammatory profile, especially in Eisenmenger syndrome patients. 33 In contrast, a…”

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 96%

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Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt‐induced pulmonary arterial hypertension

Zhou

2022

ESC Heart Failure

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Leukotriene B4 levels in CHD-associated paediatric pulmonary hypertension

Vuran,

Yılmazer,

Gerçeker

et al. 2024

Cardiol Young

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Background: The aim of this study is to evaluate the role of leukotriene B4, an inflammatory mediator, in the development of pulmonary hypertension in paediatric patients with CHD with left-right shunt. Methods: The study included forty patients with CHD with left-right shunts. Based on haemodynamic data obtained from cardiac diagnostic catheterisation, 25 patients who met the criteria for pulmonary arterial hypertension were included in the patient group. The control group comprised 15 patients who did not meet the criteria. The standard cardiac haemodynamic study was conducted. Leukotriene B4 levels were assessed in blood samples taken from both pulmonary arteries and peripheral veins. Results: The median age of patients with pulmonary arterial hypertension was 10 months (range: 3–168), while the median age of the control group was 50 months (range: 3–194). In the pulmonary hypertension group, the median pulmonary artery systolic/diastolic/mean pressures were 38/18/24 mmHg, compared to 26/10/18 mmHg in the control group. Leukotriene B4 levels in pulmonary artery blood samples were significantly higher in the pulmonary arterial hypertension group compared to the controls (p < 0.05). Peripheral leukotriene B4 levels were also elevated in the pulmonary arterial hypertension group in comparison to the control group, though the difference was not statistically significant. Conclusion: The discovery of elevated leukotriene B4 levels in pulmonary artery samples from paediatric patients with pulmonary arterial hypertension secondary to CHD with left-to-right shunt suggests that local inflammation may have a pathological role in the development of pulmonary arterial hypertension.

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Inflammatory markers in Eisenmenger syndrome and their association with clinical outcomes. A cross-sectional comparative study

Cited by 2 publications

References 24 publications

Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt‐induced pulmonary arterial hypertension

Synemin promotes pulmonary artery smooth muscle cell phenotypic switch in shunt‐induced pulmonary arterial hypertension

Leukotriene B4 levels in CHD-associated paediatric pulmonary hypertension

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