Osteopontin and galectin-3 as biomarkers of maladaptive right ventricular remodeling in pulmonary hypertension

2021 ◽  
Author(s):  
Stanislav Keranov ◽  
Oliver Dörr ◽  
Leili Jafari ◽  
Christoph Liebetrau ◽  
Till Keller ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Dilated Cardiomyopathy ◽  
Ventricular Hypertrophy ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Potential Biomarker ◽  
Lv Remodeling ◽  
Galectin 3 ◽  
Right Ventricular Remodeling

Aim: This study assessed the utility of osteopontin (OPN) and galectin-3 (Gal-3) as biomarkers of maladaptive right ventricular remodeling in pulmonary hypertension (PH). Materials & methods: We examined plasma levels of OPN and Gal-3 in patients with PH (n = 62), dilated cardiomyopathy (n = 34), left ventricular hypertrophy (LVH; n = 47), and controls without right ventricle (RV) or LV abnormalities (n = 38). Results: OPN and Gal-3 levels were higher in PH, dilated cardiomyopathy and LVH than in the controls. OPN concentrations in PH patients with maladaptive RV were significantly higher than in those with adaptive RV. Gal-3 did not differentiate between adaptive and maladaptive RV remodeling in PH. OPN and Gal-3 levels did not correlate with parameters of LV remodeling. Conclusion: OPN is a potential biomarker of RV maladaptation.

Repeated lung injury due to alpha-naphthylthiourea causes right ventricular hypertrophy in rats

1984 ◽  
Vol 56 (2) ◽  
pp. 388-396 ◽  
Author(s):  
N. S. Hill ◽  
R. F. O'Brien ◽  
S. Rounds
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Vascular Reactivity ◽  
Tween 80 ◽  
Left Ventricular ◽  
Right Ventricular Hypertrophy ◽  
Arterial Blood

Acute lung injury due to alpha-naphthylthiourea (ANTU) is associated with increased permeability edema, transient pulmonary hypertension, and increased vascular reactivity. We sought to determine whether repeated administration of ANTU caused right ventricular hypertrophy. Rats were injected weekly for 4 wk with ANTU or an equivalent volume of the vehicle Tween 80. Rats injected repeatedly with ANTU in doses of 5–10 mg/kg body wt had increased ratios of right ventricular to left ventricular plus septal weights. The right ventricular hypertrophy in ANTU-treated rats was associated with right ventricular systolic hypertension. Repeated injections of ANTU also caused transient pulmonary edema after each dose, as evidenced by increased wet-to-dry lung weight ratios after 4 h, which returned to normal by 24 h. Lungs isolated from ANTU-injected rats had greater pressor responses to hypoxia and to angiotensin II than lungs from Tween 80-injected rats. Pressure-flow curves of isolated lungs, arterial blood gases, and hematocrits were similar in rats treated repetitively with ANTU or Tween alone. Lung histology was also similar in ANTU and control lungs, as were measurements of arterial medial thickness and ratios of numbers of arteries/100 alveoli, indicating that substantial vascular remodeling had not occurred. Thus, four weekly ANTU injections in rats caused right ventricular hypertrophy, probably due to pulmonary hypertension. We speculate that the pulmonary hypertension was due, at least in part, to sustained vasoconstriction, which somehow resulted from repeated acute lung injury.

Is Right Ventricular Remodeling in Pulmonary Hypertension Dependent on Etiology? An Echocardiographic Study

2015 ◽  
Vol 33 (4) ◽  
pp. 546-554 ◽  
Author(s):  
Sorin Giusca ◽  
Elena Popa ◽  
Mihaela Silvia Amzulescu ◽  
Ioana Ghiorghiu ◽  
Ioan Mircea Coman ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Echocardiographic Study ◽  
Right Ventricular Remodeling

scholarly journals Possible new options and benefits to detect myocarditis, right ventricular remodeling and coronary anomalies by echocardiography in systematic preparticipation screening of athletes

2020 ◽  
Vol 36 (10) ◽  
pp. 1855-1885 ◽  
Author(s):  
Tom Döbel ◽  
Stephan Stöbe ◽  
Robert Percy Marshall ◽  
Pierre Hepp ◽  
Sven Fikenzer ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Image Acquisition ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Post Processing ◽  
Coronary Anomalies ◽  
Cardiac Abnormalities ◽  
Normal Ranges ◽  
Right Ventricular Remodeling

Abstract Exclusion of cardiac abnormalities should be performed at the beginning of the athlete’s career. Myocarditis, right ventricular remodeling and coronary anomalies are well-known causes of life-threatening events of athletes, major cardiovascular events and sudden cardiac death. The feasibility of an extended comprehensive echocardiographic protocol for the detection of structural cardiac abnormalities in athletes should be tested. This standardized protocol of transthoracic echocardiography includes two- and three-dimensional imaging, tissue Doppler imaging, and coronary artery scanning. Post processing was performed for deformation analysis of all compounds including layer strain. During 2017 and 2018, the feasibility of successful image acquisition and post processing analysis was retrospectively analyzed in 54 male elite athletes. In addition, noticeable findings inside the analyzed cohort are described. The extended image acquisition and data analyzing was feasible from 74 to 100%, depending on the used modalities. One case of myocarditis was detected in the present cohort. Coronary anomalies were not found. Right ventricular size and function were within normal ranges. Isovolumetric right ventricular relaxation time showed significant regional differences. One case of hypertrophic cardiomyopathy and two subjects with bicuspid aortic valves were found. Due to the excessive cardiac stress in highly competitive sports, high-quality and precise screening modalities are necessary, especially with respect to acquired cardiac diseases like acute myocarditis and pathological changes of left ventricular and RV geometry. The documented feasibility of the proposed extended protocol underlines the suitability to detect distinct morphological and functional cardiac alterations and documents the potential added value of a comprehensive echocardiography.

Abstract 622: Cd44 Plays an Important Role in Regulating Heart Failure Induced Lung Vascular Remodeling and Who Type-2 Pulmonary Hypertension

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Xinyu Weng ◽  
Wenhui Yue ◽  
Dongzhi Wang ◽  
Huan Wang ◽  
Yawei Xu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Vascular Remodeling ◽  
Lung Inflammation ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Ventricular Failure

End-stage left ventricular failure or chronic heart failure (CHF) causes severe lung inflammation, vascular remodeling, WHO type-2 pulmonary hypertension, and right ventricular hypertrophy. However, the molecular mechanism of CHF-induced lung inflammation and remodeling is largely unknown. CD44 is a member of the hyaluronate receptor family of cell adhesion molecules, which has been shown to play a selective role in controlling macrophage and lymphocyte migration. Here we demonstrated that end-stage CHF causes a dramatic increase of CD44 expression in heart and lung in human and mice. Histological staining shows that CD44 is predominantly expressed in leukocytes such as macrophages. Flow cytometry analysis further demonstrates that CD44 is predominantly expressed in F4/80 positive macrophages, CD4+, and CD8+ T cells. CD44 expression is dramatically increased in activated T cell subsets. To further determine the physiological role of CD44 in CHF-induced lung remodeling and type-2 pulmonary hypertension, we studied the effect of CD44 blockade on type-2 pulmonary hypertension development in a group of mice with existing moderate left ventricular failure without apparent lung remodeling. Interestingly, we found that blockade CD44 with blocking antibodies (Abs) significantly attenuate the development of lung vascular and interstitial leukocyte infiltration, lung vascular remodeling, fibrosis, and increase of right ventricular hypertrophy. Blockade CD44 signaling also significantly attenuated further decline of left ventricular ejection fraction in mice with existing LV failure. In addition, we demonstrated that induction of T regulatory cells with IL-2 and IL-2 Abs complex significantly attenuated the infiltration of CD44 positive leukocytes in lung tissue, lung vascular remodeling, lung fibrosis, and right ventricular hypertrophy in mice with existing moderate left ventricular failure. Together, these data indicate an important role of CD44 in left ventricular failure-induced lung inflammation, and type-2 pulmonary hypertension, suggesting that inhibition of CD44 may attenuate heart failure progression and type-2 pulmonary hypertension.

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