Galectin-3 in Patients with Acute Heart Failure: Preliminary Report on First Polish Experience

Sygitowicz, Grażyna; Tomaniak, Mariusz; Filipiak‬, Krzysztof J.; Kołtowski, Łukasz; Sitkiewicz, Dariusz

doi:10.17219/acem/60527

Cited by 17 publications

(15 citation statements)

References 19 publications

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“…These observations suggest that Fxn along with multiple other downstream candidates causes behavioral deficits in FRDAkd mice. Similarly, for cardiac phenotypes, we identified multiple genes related to cardiac fibrosis that were up-regulated in FRDAkd mice heart ( Figure 8c ), including Lgals3 ( Sygitowicz et al, 2016 ), Icam1 ( Salvador et al, 2016 ) and Timp1 ( Polyakova et al, 2011 )( Figure 8c ). Genes related to iron regulation, included Hfe ( Del-Castillo-Rueda et al, 2012 ), Slc40a1 ( Del-Castillo-Rueda et al, 2012 ), Hmox1 ( Song et al, 2012 ), Tfrc ( Del-Castillo-Rueda et al, 2012 ) and Gdf15 ( Cui et al, 2014 ), all of which are directly involved in hemochromatosis and iron overload ( Figure 8c ).…”

Section: Resultsmentioning

confidence: 81%

Inducible and reversible phenotypes in a novel mouse model of Friedreich’s Ataxia

Chandran

Gao

Swarup

et al. 2017

eLife

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Friedreich's ataxia (FRDA), the most common inherited ataxia, is caused by recessive mutations that reduce the levels of frataxin (FXN), a mitochondrial iron binding protein. We developed an inducible mouse model of Fxn deficiency that enabled us to control the onset and progression of disease phenotypes by the modulation of Fxn levels. Systemic knockdown of Fxn in adult mice led to multiple phenotypes paralleling those observed in human patients across multiple organ systems. By reversing knockdown after clinical features appear, we were able to determine to what extent observed phenotypes represent reversible cellular dysfunction. Remarkably, upon restoration of near wild-type FXN levels, we observed significant recovery of function, associated pathology and transcriptomic dysregulation even after substantial motor dysfunction and pathology were observed. This model will be of broad utility in therapeutic development and in refining our understanding of the relative contribution of reversible cellular dysfunction at different stages in disease.

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Section: Resultsmentioning

confidence: 81%

Inducible and reversible phenotypes in a novel mouse model of Friedreich’s Ataxia

Chandran

Gao

Swarup

et al. 2017

eLife

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“…Finally, galectin‐3 is a marker excreted by macrophages and is specifically involved in remodeling and fibrosis in heart disease. It is elevated in patients with acute heart failure but is better in predicting long‐term outcomes than conveying severity of dyspnea …”

Section: Resultsmentioning

confidence: 99%

Transfusion‐associated circulatory overload—a systematic review of diagnostic biomarkers

et al. 2018

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BACKGROUND: Transfusion-associated circulatory overload (TACO) is the leading cause of transfusionrelated major morbidity and mortality. Diagnosing TACO is difficult because there are no pathognomonic signs and symptoms. TACO biomarkers may aid in diagnosis, decrease time to treatment, and differentiate from other causes of posttransfusion dyspnea such a transfusionrelated acute lung injury. STUDY DESIGN AND METHODS:A systematic review of literature was performed in EMBASE, PubMed, the TRIP Database, and the Cochrane Library, from inception to June 2018. All articles discussing diagnostic markers for TACO were included. Non-English articles or conference abstracts were excluded. RESULTS: Twenty articles discussing biomarkers forTACO were included. The majority investigated B-type natriuretic peptide (BNP) and the N-terminal prohormone cleavage fragment of BNP (NT-proBNP), markers of hydrostatic pressure that can be determined within 1 hour. The data indicate that a post/pretransfusion NT-proBNP ratio > 1.5 can aid in the diagnosis of TACO. Posttransfusion levels of BNP less than 300 or NT-proBNP less than 2000 pg/mL, drawn within 24 hours of the reaction, make TACO unlikely. Cut-off levels that exclude TACO are currently unclear. In critically ill patients, the specificity of natriuretic peptides for circulatory overload is poor. Other biomarkers, such as cytokine profiles, cannot discriminate between TACO and transfusion-related acute lung injury. CONCLUSION:Currently, BNP and NT-proBNP are the primary diagnostic biomarkers researched for TACO. An NT-proBNP ratio greater than 1.5 is supportive of TACO, and low levels of BNP or NT-proBNP can exclude TACO. However, they are unreliable in critically ill patients. Other biomarkers, including cytokines and pulmonary edema fluid-to-serum protein ratio have not yet been sufficiently investigated for clinical use. T ransfusion-associated circulatory overload (TACO) is characterized by acute respiratory distress and pulmonary edema with signs of volume overload following transfusion. 1 It is the foremost cause of transfusion-related mortality in Europe, 2-4 Canada 5 and the United States. 6 TACO is currently underrecognized, 7,8 as it is challenging to diagnose due to lack of pathognomonic signs ABBREVIATIONS: AHF = acute heart failure; ARDS = acute respiratory distress syndrome; BALF = bronchoalveolar lavage fluid; BNP = B-type natriuretic peptide; ICU = intensive care unit; IL = interleukin; NPs = natriuretic peptides; NT-proBNP = N-terminal prohormone of BNP; TACO = transfusion-associated circulatory overload; TNCs = transfused negative controls; TRALI = transfusion-related acute lung injury. From the

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“…In regards to the other biomarkers in our multi‐marker model, the inclusion of preoperative levels of Galectin‐3 in the model was supported given this biomarkers association with health complications and mortality in patients with heart failure 45, 46. Much work has also been conducted to establish associations between ST2 levels and clinical outcomes before and after cardiovascular procedures in specific populations 47, 48, 49, 50.…”

Section: Discussionmentioning

confidence: 81%

Predictive Ability of Novel Cardiac Biomarkers ST2, Galectin‐3, and NT‐ProBNP Before Cardiac Surgery

Polineni

Parker

Alam

et al. 2018

JAHA

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BackgroundCurrent preoperative models use clinical risk factors alone in estimating risk of in‐hospital mortality following cardiac surgery. However, novel biomarkers now exist to potentially improve preoperative prediction models. An assessment of Galectin‐3, N‐terminal pro b‐type natriuretic peptide (NT‐ProBNP), and soluble ST2 to improve the predictive ability of an existing prediction model of in‐hospital mortality may improve our capacity to risk‐stratify patients before surgery.Methods and ResultsWe measured preoperative biomarkers in the NNECDSG (Northern New England Cardiovascular Disease Study Group), a prospective cohort of 1554 patients undergoing coronary artery bypass graft surgery. Exposures of interest were preoperative levels of galectin‐3, NT‐ProBNP, and ST2. In‐hospital mortality and adverse events occurring after coronary artery bypass graft were the outcomes. After adjustment, NT‐ProBNP and ST2 showed a statistically significant association with both their median and third tercile categories with NT‐ProBNP odds ratios of 2.89 (95% confidence interval [CI]: 1.04–8.05) and 5.43 (95% CI: 1.21–24.44) and ST2 odds ratios of 3.96 (95% CI: 1.60–9.82) and 3.21 (95% CI: 1.17–8.80), respectively. The model receiver operating characteristic score of the base prediction model (0.80 [95% CI: 0.72–0.89]) varied significantly from the new multi‐marker model (0.85 [95% CI: 0.79–0.91]). Compared with the Northern New England (NNE) model alone, the full prediction model with biomarkers NT‐proBNP and ST2 shows significant improvement in model classification of in‐hospital mortality.ConclusionsThis study demonstrates a significant improvement of preoperative prediction of in‐hospital mortality in patients undergoing coronary artery bypass graft and suggests that biomarkers can be used to identify patients at higher risk.

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Galectin-3 in Patients with Acute Heart Failure: Preliminary Report on First Polish Experience

Cited by 17 publications

References 19 publications

Inducible and reversible phenotypes in a novel mouse model of Friedreich’s Ataxia

Inducible and reversible phenotypes in a novel mouse model of Friedreich’s Ataxia

Transfusion‐associated circulatory overload—a systematic review of diagnostic biomarkers

Predictive Ability of Novel Cardiac Biomarkers ST2, Galectin‐3, and NT‐ProBNP Before Cardiac Surgery

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