Role of galectin‐3 in subclinical myocardial impairment in psoriasis

Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu. Objective We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibros...

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Published inJournal of the European Academy of Dermatology and Venereology Vol. 33; no. 1; pp. 136 - 142
Main Authors Kotwica, T., Relewicz, J., Rojek, A., Tupikowska‐Marzec, M., Kabaj, M., Karolko, B., Maj, J., Bednarek‐Tupikowska, G., Kosmala, W., Szepietowski, J.C., Przewlocka‐Kosmala, M.
Format Journal Article
LanguageEnglish
Published England 01.01.2019
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Online AccessGet full text
ISSN0926-9959
1468-3083
1468-3083
DOI10.1111/jdv.15211

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Abstract Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu. Objective We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. Methods We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty‐five age‐ and sex‐matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e′ velocity and E/e′ ratio. Laboratory measurements encompassed blood Gal‐3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). Results Patients with psoriasis were characterized by elevated Gal‐3 (12.3 [9.3–13.4] vs. 6.3 [5.5–9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0–29.0] vs. 8.5 [6.0–13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7–10.6] vs. 1.9 [1.5–4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal‐3 tertiles. Significant associations between GLS and age (beta = −0.21, P < 0.04), Gal‐3 (beta = −0.27, P < 0.01), CRP (beta = −0.22, P < 0.03), ESR (beta = −0.25, P < 0.01), waist circumference (beta = −0.22, P < 0.03) and waist‐to‐hip ratio (beta = −0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal‐3 (beta = −0.24, P < 0.01) and ESR (beta = −0.21, P < 0.03). Regression‐based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal‐3. Conclusions Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal‐3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.
AbstractList Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu.BACKGROUNDPsoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu.We sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.OBJECTIVEWe sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis.We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).METHODSWe enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR).Patients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3.RESULTSPatients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3.Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.CONCLUSIONSSubclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.
Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu. We sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). Patients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3. Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.
Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease‐associated pro‐inflammatory milieu. Objective We sought to investigate the relationship of galectin‐3 (Gal‐3) – a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. Methods We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty‐five age‐ and sex‐matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e′ velocity and E/e′ ratio. Laboratory measurements encompassed blood Gal‐3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). Results Patients with psoriasis were characterized by elevated Gal‐3 (12.3 [9.3–13.4] vs. 6.3 [5.5–9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0–29.0] vs. 8.5 [6.0–13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7–10.6] vs. 1.9 [1.5–4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal‐3 tertiles. Significant associations between GLS and age (beta = −0.21, P < 0.04), Gal‐3 (beta = −0.27, P < 0.01), CRP (beta = −0.22, P < 0.03), ESR (beta = −0.25, P < 0.01), waist circumference (beta = −0.22, P < 0.03) and waist‐to‐hip ratio (beta = −0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal‐3 (beta = −0.24, P < 0.01) and ESR (beta = −0.21, P < 0.03). Regression‐based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal‐3. Conclusions Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal‐3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.
Author Rojek, A.
Szepietowski, J.C.
Karolko, B.
Przewlocka‐Kosmala, M.
Bednarek‐Tupikowska, G.
Kosmala, W.
Kabaj, M.
Tupikowska‐Marzec, M.
Kotwica, T.
Maj, J.
Relewicz, J.
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Notes The authors declare no conflict of interests.
This work was financially supported by internal University grant Pbmn127.
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Snippet Background Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the...
Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated...
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StartPage 136
SubjectTerms Adult
Aged
Asymptomatic Diseases
Blood Sedimentation
C-Reactive Protein - metabolism
Case-Control Studies
Diastole
Echocardiography
Female
Galectin 3 - blood
Humans
Male
Middle Aged
Psoriasis - blood
Systole
Ventricular Dysfunction, Left - blood
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - physiopathology
Waist Circumference
Waist-Height Ratio
Title Role of galectin‐3 in subclinical myocardial impairment in psoriasis
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjdv.15211
https://www.ncbi.nlm.nih.gov/pubmed/30098067
https://www.proquest.com/docview/2087593342
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