Novel Biomarkers for Cardiovascular Risk in Obese Patients

2018

Diabetes Updates

Obesity remains a leading cause of cardiovascular (CV) events and diabetes worldwide. Although there are at least two main body-size phenotypes (metabolically healthy and metabolically non-healthy) of individuals with established obesity, the cardiometabolic risk amongst these patients' populations extremely distinguishes. The review is discussed the controversies regarding obese paradox and the probabilities to stratify the patients with established obesity in cardiometabolic risk. It is suggested that the biomarkers could predict CV events in patients depending on obese phenotypes. The role of metabolic biomarkers, progenitor cells, natriuretic peptides, inflammatory cytokines and galectin-3 are discussed.

Section: Endothelial Progenitor Cell Dysfunctionmentioning

confidence: 99%

The obesity phenotypes: emerging role of cardiac biomarkers

2018

Diabetes Updates

“…Fourth, age and metabolic comorbidities including diabetes mellitus, rheumatic diseases, hypertension may lead to kidney insuffi ciency prior to HF manifestation and worse nature evolution of HF [4].…”

Section: Short Communicationmentioning

confidence: 99%

Serum uric acid as a metabolic regulator of endothelial function in heart failure

2017

Arch Clin Hypertens

Citation: Berezin AE (2017) Serum uric acid as a metabolic regulator of endothelial function in heart failure. Arch Clin Hypertens 3(1): 027-029. DOI: http://dx.doi.org/10.17352/ach.000016 AbstractThe development of heart failure (HF) associated with elevated level of serum uric acid (SUA). Additionally, the majority of individuals with traditional cardiovascular risk factors contributing in HF risk exhibited increased levels of SUA. Although SUA lowering drugs are widely used in patients with symptomatic hyperuricemia and gout beyond their etiologies, there is no agreement of SUA below target level 6.0 mg/dL in asymptomatic individuals with kidney injury and CV disease and data of ones in heart failure (HF) are suffi ciently controversial. First SUA plays an important role in inducing oxidative stress, infl ammation, neurohumoral activation, and endothelial dysfunction. Secondary, SUA may act as antioxidant contributing in restoring of vascular function. Moreover, SUA is able to epigenetically regulate a survival of endothelial precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory phenomenon into repair capability of cell precursors. However, elevated SUA level was found a predictor of adverse clinical outcomes of HF. The short communication is depicted the importance of new clinical data to confi rm the emerging reparative ability of SUA in HF and its role as promising target for treatment in cardiac failure. Short Communication Serum uric acid as a metabolic regulator of endothelial function in heart failureAlexander E Berezin* Short CommunicationThere is a large body of evidence regarding the role of serum uric acid (SUA) in pathogenesis of cardiovascular diseases (CVD) including heart failure (HF). Although SUA levels above the current international reference limit equal 6.0 mg/dL are highly prevalent in chronic kidney disease (CKD), hyperuricemia strongly associates with in-hospital CV mortality independently from CKD etiology and renal function in individuals admitted to the hospital due to several causes, i.e. acute myocardial infarction, stroke, hypertensive emergencies, acute / chronic heart failure, arrhythmia, shock and sepsis.In contrast, hypouricemia did not associate with increased mortality rate in patient populations with established CVD [1]. In HF an elevated SUA level was found due to several mechanisms including an increased activity of xanthine oxidase (XO), which is a key enzyme in uric acid synthesis and is under control of infl ammatory cytokines / chemokines, some growth factors, and intermediates (blood glucose). Whether SUA could be an independent predictor of HF development is not fully clear. Recent clinical studies and some meta-analysis have shown that elevated SUA levels were associated with an increased risk of incident HF, observed in majority of patients with established chronic HF and relate to adverse clinical outcomes in HF [8][9][10][11]. However, the impact of uric acid on all-cause mortality and HF-related dea...

“…Thus, the EPCs may enhance the balance between heart and vascular injury and repair that is critical for the maintenance of cardiac remodeling, heart function, intimal integrity, endothelial function, and prevention of CV complications [97,98]. All these findings elucidate that EPCs dysfunction could be an alternative therapeutic target to promoting heart and vessels repair in patients with DM.…”

Section: The Concept Of Impaired Cardiac and Vessel Reparation In Diabetes: Role Of Epcsmentioning

confidence: 99%

Altered endothelial reparation and diabetes-Induced endothelial progenitor cell dysfunction

2016

Cardiovasc Disord Med

Self Cite

Diabetes mellitus (DM) is considered a leading cause of premature cardiovascular (CV) mortality and morbidity in general population and in individuals with known CV disease. Recent animal and clinical studies have shown that reduced number and weak function of endothelial progenitor cells (EPCs) may not only indicate to higher CV risk, but contribute to the impaired heart and vessels reparation in patients with DM. Moreover, EPCs having a protective impact on the vasculature may mediate the functioning of other organs and systems. Therefore, EPCs dysfunction is probably promising target for DM treatment strategy, while the role of restoring of EPCs number and functionality in CV risk diminish and reduce of DM-related complications is not fully clear. The aim of the review is summary of knowledge regarding EPCs dysfunction in DM patients.