Predictive value of galectin-3 for incident cardiovascular disease and heart failure in the population-based FINRISK 1997 cohort

2015 ◽  
Vol 192 ◽  
pp. 33-39 ◽  
Author(s):  
Annika Jagodzinski ◽  
Aki S. Havulinna ◽  
Sebastian Appelbaum ◽  
Tanja Zeller ◽  
Pekka Jousilahti ◽  
...  
Author(s):  
Raimund Pechlaner ◽  
Stefan Kiechl ◽  
Manuel Mayr ◽  
Peter Santer ◽  
Siegfried Weger ◽  
...  

AbstractThe expression of the key iron regulatory hormone hepcidin is regulated by iron availability, inflammation, hormones, hypoxia, and anaemia. Increased serum concentrations of hepcidin have recently been linked to atherosclerosis. We studied demographic, haematologic, biochemical, and dietary correlates of serum hepcidin levels and its associations with incident cardiovascular disease and with carotid atherosclerosis.Serum hepcidin concentrations were measured by tandem mass spectrometry in samples taken in 2000 from 675 infection-free participants of the prospective population-based Bruneck study (age, mean±standard deviation, 66.0±10.2; 48.1% male). Blood parameters were measured by standard methods. Dietary intakes of iron and alcohol were surveyed with a food frequency questionnaire. Carotid atherosclerosis (365 cases) was assessed by ultrasound and subjects were observed for incident stroke, myocardial infarction, or sudden cardiac death (91 events) until 2010.Median (interquartile range) hepcidin levels were 2.27 nM (0.86, 4.15). Most hepcidin correlates were in line with hepcidin as an indicator of iron stores. Independently of ferritin, hepcidin was related directly to physical activity (p=0.024) and fibrinogen (p<0.0001), and inversely to alcohol intake (p=0.006), haemoglobin (p=0.027), and γ-glutamyltransferase (p<0.0001). Hepcidin and hepcidin-to-ferritin ratio were not associated with prevalent carotid atherosclerosis (p=0.43 and p=0.79) or with incident cardiovascular disease (p=0.62 and p=0.33).In this random sample of the general community, fibrinogen and γ-glutamyltransferase were the most significant hepcidin correlates independent of iron stores, and hepcidin was related to neither atherosclerosis nor cardiovascular disease.


2019 ◽  
Vol 46 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Xiao Zhong ◽  
Xiaoqian Qian ◽  
Guangping Chen ◽  
Xiang Song

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Andreea M Rawlings ◽  
Christie M Ballantyne ◽  
Rebecca F Gottesman ◽  
Ron C Hoogeveen ◽  
Timothy M Hughes ◽  
...  

Background: Cerebrovascular disease is often the consequence of cardiac disease. Our aim was to examine associations of biomarkers of cardiovascular disease, high sensitivity troponin T (hs-cTnT), NT-proBNP, and galectin-3, with cerebrovascular signs: lacunar infarcts, lobar and subcortical microhemorrhages, cortical infarcts, and white matter hyperintensity (WMH) volume. We also examined total cortical and Alzheimer’s Disease (AD) signature region volumes. Methods: We conducted a cross-sectional analysis of 1748 ARIC participants from the 2011-2013 exam who had biomarker measurements, completed a brain MRI, and did not have a clinical history of stroke. We used linear regression to model brain volumes, modeled as Z scores, and logistic regression for all other outcomes; biomarkers were log transformed. We repeated analyses excluding persons with coronary heart disease, atrial fibrillation, and heart failure. Results: The mean age of participants was 76, 62% were female, and 21% were Black. All biomarkers were associated with total cortical volume. Each standard deviation increase in log hs-cTnT was associated with lower total cortical volume (adjusted beta = -0.08, 95% CI: -0.12, -0.05); results for the other biomarkers were similar (Figure). All biomarkers were associated with lobar microhemorrhages. Hs-cTnT and NT-proBNP were associated with WMH volume, but galectin-3 was not. No biomarker was associated with subcortical microhemorrhages or cortical infarcts. Results were similar in persons without coronary heart disease, atrial fibrillation, or heart failure (conditions associated with cerebral thromboembolism). Conclusions: In persons free of clinical cardiovascular disease, biomarkers of cardiac stretch, strain, and fibrosis were associated cerebral small vessel disease and reduced cortical volume, but not in a specific pattern suggestive of AD pathogenesis. This suggests subclinical vascular insults affect brain structure through mixed pathogenic processes.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
D. A. Lebedev ◽  
E. A. Lyasnikova ◽  
E. Yu Vasilyeva ◽  
A. Yu Babenko ◽  
E. V. Shlyakhto

As myocardial fibrosis might be an important contributor to the association of diabetes mellitus with left ventricular (LV) dysfunction and chronic heart failure (HF), we investigated the profile of some proinflammatory, profibrotic biomarkers in patients with type 2 diabetes mellitus (T2DM) at various stages of the cardiovascular disease continuum from absence of clinic since and symptoms to HF with preserved (HFpEF) and midrange ejection fraction (HFmrEF). Material and Methods. Sixty-two patients with T2DM (age 60 [55; 61]), 20 patients without clinical manifestations of HF and 2 groups with clinical manifestations of stable HF, 29 patients with HFpEF, and 13 patients with HFmrEF, were included in the study. The control group consisted of 13 healthy subjects and normal BMI. All patients underwent transthoracic echocardiography, laboratory assessment of N-terminal fragment of the brain natriuretic peptide (Nt-proBNP), highly sensitive C-reactive protein (hsCRP), soluble suppression of tumorigenesis-2 (sST2), galectin-3, C-terminal propeptide of procollagen type I (PICP), N-terminal propeptide of procollagen type III (PIIINP), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of matrix proteinase-1 (TIMP-1). Results. Patients with HFmrEF had higher values of LV volumetric parameters, indexed parameters of LV myocardial mass (LVMM), and higher concentrations of Nt-proBNP (all p < 0.05 ). The concentrations of galectin-3 were greater in patients with HFpEF and HFmrEF compared to patients without HF ( p = 0.01 and p = 0.03 , respectively). PICP and PICP/PIIINP ratio were greater in patients with HFmrEF compared to patients with HFpEF ( p = 0.043 and p = 0.033 , respectively). In patients with T2DM and HF, a relationship was found between galectin-3 and LVMM/body surface area ( r = − 0.58 , p = 0.001 ), PIIINP, TIMP-1, and LV end-diastolic volume ( r = − 0.68 and p = 0.042 and r = 0.38 and p = 0.02 , respectively). Conclusion. The dynamics at various stages of the cardiovascular disease continuum in the serum fibrosis markers may reflect an increase in fibrotic and decrease in antifibrotic processes already at the preclinical stage of HF. At the same time, the changes found in the circulating procollagen levels may indicate a shift in balance towards type I collagen synthesis in HFmrEF compared with HFpEF.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Joseph Yeboah

Abstract 1255 Joseph Yeboah, Gregory L Burke, John R Crouse, Wake Forest Univ Sch of Med, Winston Salem, NC; Joao A Lima, John Hopkins Univ, Baltimore, MD; Craig Johnson, Univ of Washington, Seattle, WA; Joseph F Polak, Tufts-New England Medical Ctr, Boston, MA; Aaron Folsom, Univ of Minnesota, Minneapolis, MN; Wendy Post, John Hopkins Univ, Baltimore, MD; David M Herrington, Wake Forest Univ Sch of Med, Winston Salem, NC Joseph Yeboah, 2008 Finalist and Presenting Author


2019 ◽  
Author(s):  
Pushpa Singh ◽  
Anuradhaa Subramanian ◽  
Nicola Adderley ◽  
Krishna Gokhale ◽  
Rishi Shinghal ◽  
...  

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