IJC metabolic & endocrine最新文献

{"title":"Liquid fructose supplementation in LDL-R−/− mice fed a western-type diet enhances lipid burden and atherosclerosis despite identical calorie consumption","authors":"Natalia Hutter ,&nbsp;Miguel Baena ,&nbsp;Gemma Sangüesa ,&nbsp;Alberto Dávalos ,&nbsp;María Jesús Latasa ,&nbsp;Joan Carles Escolà-Gil ,&nbsp;Rosa María Sánchez ,&nbsp;Núria Roglans ,&nbsp;Marta Alegret ,&nbsp;Juan Carlos Laguna","doi":"10.1016/j.ijcme.2015.10.002","DOIUrl":"10.1016/j.ijcme.2015.10.002","url":null,"abstract":"<div><h3>Background</h3><p>Studies on humans have related the high consumption of fructose, especially in the form of sugar-sweetened beverages, to obesity, fatty liver, and hypercholesterolemia, all risk factors for atherosclerosis, and cardiovascular disease. We aimed to determine whether supplementation of liquid fructose (SLF), in either a normal, healthy chow or a Western-style chow, promoted the appearance of atherosclerosis in a rodent model.</p></div><div><h3>Methods</h3><p>LDL receptor knockout mice were fed for twelve weeks with normal chow, normal chow plus <em>ad libitum</em> 15% fructose solution, Western chow, or Western chow plus <em>ad libitum</em> 15% fructose solution (W<!--> <!-->+<!--> <!-->F). Food and liquid intake and body weight were periodically monitored. At the end of the study, plasma and hepatic lipids, liver histology and expression of genes related to lipid handling were analyzed and histological and immunohistological analyses of atherosclerosis at the aortic origin was performed.</p></div><div><h3>Results</h3><p>Total calorie intake was significantly increased in Western-fed <em>vs</em> normal chow-fed mice, but was not modified by SLF. SLF significantly increased body weight, visceral adiposity, plasma lipids and liver cholesterol content in Western-fed mice, probably due to an increase in <em>de novo</em> lipid synthesis. Aortic atherosclerotic total lesion area was significantly correlated to plasma lipids, being highest in W<!--> <!-->+<!--> <!-->F mice. Further, SLF induced higher immunostaining for macrophages and oxidized-LDL receptor, independently of lesion area and caloric burden.</p></div><div><h3>Conclusions</h3><p>SLF, without changing total calorie intake, increases atherosclerosis, visceral adipose tissue and cholesterol burden in a background of overweight LDL receptor knockout mice consuming an unhealthy, Western-type solid rodent chow.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"9 ","pages":"Pages 12-21"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.10.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87629792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Untreated diabetes mellitus, but not impaired fasting glucose, is associated with increased left ventricular mass and concentric hypertrophy in an elderly, healthy, Swedish population","authors":"Manan Pareek ,&nbsp;Abdellatif Aharaz ,&nbsp;Mette Lundgren Nielsen ,&nbsp;Oke Gerke ,&nbsp;Margrét Leósdóttir ,&nbsp;Jacob Eifer Møller ,&nbsp;Niels Holmark Andersen ,&nbsp;Peter M. Nilsson ,&nbsp;Michael Hecht Olsen","doi":"10.1016/j.ijcme.2015.10.005","DOIUrl":"10.1016/j.ijcme.2015.10.005","url":null,"abstract":"<div><h3>Background/objectives</h3><p>To examine whether higher fasting plasma glucose (FPG) levels were independently associated with left ventricular (LV) mass and/or geometry in elderly, otherwise healthy subjects.</p></div><div><h3>Methods</h3><p>We tested cross-sectional associations between echocardiographically determined LV mass/geometric patterns, cardiovascular risk factors, and FPG categorized as normal fasting glucose (NFG), impaired fasting glucose (IFG), and untreated diabetes mellitus (DM), in 486 men and 207 women aged 56–79<!--> <!-->years without overt cardiovascular disease, who received no cardiovascular, anti-diabetic, or lipid-lowering drugs and had a preserved LV ejection fraction &gt;<!--> <!-->50%.</p></div><div><h3>Results</h3><p>Unadjusted mean LV mass index (LVMI) was significantly greater among subjects with DM than those without (90<!--> <!-->+/−<!--> <!-->26<!--> <!-->g/m² vs. 85<!--> <!-->+/−<!--> <!-->20<!--> <!-->g/m², p<!--> <!-->=<!--> <!-->0.01), as were both relative wall thickness (RWT) (0.43<!--> <!-->+/−<!--> <!-->0.09 vs. 0.40<!--> <!-->+/−<!--> <!-->0.08, p<!--> <!-->=<!--> <!-->0.01) and prevalence of concentric LV hypertrophy (LVH) (11% vs. 6%, p<!--> <!-->=<!--> <!-->0.03). However, only RWT remained significantly associated with the presence of DM after multivariable adjustment (p<!--> <!-->=<!--> <!-->0.04). Interaction analyses revealed that greater LVMI/LVH was predominantly associated with higher levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) among subjects with IFG or DM, but not NFG.</p></div><div><h3>Conclusions</h3><p>Subjects with untreated DM had higher values of LVMI and a greater prevalence of concentric LVH, but the associations were not independent of other risk factors. NT-proBNP was primarily associated with greater LV size in subjects with IFG or DM.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"9 ","pages":"Pages 39-47"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.10.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72525881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Cardio-renal Syndrome (CRS)","authors":"Enrico V. Scabbia,&nbsp;Luca Scabbia","doi":"10.1016/j.ijcme.2014.10.013","DOIUrl":"10.1016/j.ijcme.2014.10.013","url":null,"abstract":"<div><p>The presence of impaired kidney function during heart failure and vice versa is a frequent occurrence. This situation is defined “Cardio-renal Syndrome”.</p><p>In the Cardio-renal Syndrome (CRS) are included 5 different sub-syndromes defined on the basis of the organ primitively responsible: Acute Cardio-renal Syndrome (Type 1), Chronic Cardio-renal Syndrome (Type 2), Acute Reno-cardiac Syndrome (Type 3), Chronic Renal-cardiac Syndrome (Type 4) and Secondary Cardio-renal Syndrome (Type 5).</p><p>The physiopathologic mechanisms underlying CRS are still partially obscure, but, a key role seems to be played by the renin-angiotensin-aldosterone axis.</p><p>Therapeutic strategies involved in CRS treatment include the use of diuretics, ACE inhibitors, Angiotensin Receptor Blockers and β-Blockers, emphasizing the role of a proper use of medication indicated for the treatment of cardiac decompensation.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"9 ","pages":"Pages 1-4"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2014.10.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80563489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electrocardiographic characteristics in the underweight and obese in accordance with the World Health Organization classification","authors":"Satoshi Kurisu,&nbsp;Hiroki Ikenaga,&nbsp;Noriaki Watanabe,&nbsp;Tadanao Higaki,&nbsp;Takashi Shimonaga,&nbsp;Ken Ishibashi,&nbsp;Yoshihiro Dohi,&nbsp;Yukihiro Fukuda,&nbsp;Yasuki Kihara","doi":"10.1016/j.ijcme.2015.10.006","DOIUrl":"10.1016/j.ijcme.2015.10.006","url":null,"abstract":"<div><h3>Objective</h3><p>It is clinically important to recognize how the underweight or obese affects electrocardiogram (ECG). We assessed the effects of body mass index (BMI) on QRS axis or R-wave heights.</p></div><div><h3>Methods</h3><p>From daily outpatient electrocardiograms with sinus rhythm, 203 were selected. The patients were classified into four groups: underweight (&lt;<!--> <!-->18.5<!--> <!-->kg/m²), normal weight (18.5–24.9<!--> <!-->kg/m²), overweight (25–29.9<!--> <!-->kg/m²) and obese (≥<!--> <!-->30<!--> <!-->kg/m²).</p></div><div><h3>Results</h3><p>With increasing BMI, QRS axis shifted rightward to leftward. There was a significant inverse correlation between BMI and QRS axis (r<!--> <!-->=<!--> <!-->−<!--> <!-->0.60, p<!--> <!-->&lt;<!--> <!-->0.001). Multivariate linear regression analysis among age, female, BMI, hypertension, left ventricular internal dimension and left ventricular mass (LVM) revealed that BMI was an independent determinant of QRS axis (β<!--> <!-->=<!--> <!-->−<!--> <!-->0.52, p<!--> <!-->&lt;<!--> <!-->0.0001). Although LVM increased with increasing BMI, R-wave heights in leads V4-5 were similar among the underweight, normal weight and overweight. R-wave heights in leads V4-5 were significantly lower paradoxically in the obese than other groups. With increasing BMI, Sokolow–Lyon index corrected by LVM decreased progressively.</p></div><div><h3>Conclusions</h3><p>Our results suggest that the underweight or obese is strongly associated with QRS axis or R-wave heights.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"9 ","pages":"Pages 61-65"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.10.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89938483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of aldosterone receptor blocker therapy in hypertension and heart failure","authors":"Giuseppina Santese,&nbsp;Cosimo Stefanio,&nbsp;Gianluca Belletti,&nbsp;Maria Boiani,&nbsp;Antonietta Schipani,&nbsp;Rosanna Trane,&nbsp;Fabio Zacà","doi":"10.1016/j.ijcme.2014.10.010","DOIUrl":"10.1016/j.ijcme.2014.10.010","url":null,"abstract":"<div><p>The aldosterone receptor blocker therapy as an “add-on” to hypotensive therapy is an excellent therapeutic strategy that has proved to be particularly effective in treating refractory hypertension, hypertension with organ damage and overweight hypertensive patients. Aldosterone receptor blockers are extremely useful in inhibiting hormonal activation linked with heart failure: they have cardioprotective effects not only during full-blown heart failure, but also in its early stages, and this effect can be observed even more frequently in heart failures with metabolic syndrome. The use of molecules such as canrenone with a favorable tolerability profile ensures a better tolerability ratio by providing benefits linked to fewer drug interactions, lower incidence of side effects and improved therapy adherence.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 34-37"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2014.10.010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88384450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of febuxostat and allopurinol on the inflammation and cardiac function in chronic heart failure patients with hyperuricemia","authors":"Akihiro Nakagomi ,&nbsp;Yoshiyuki Saiki ,&nbsp;Satsuki Noma ,&nbsp;Keiichi Kohashi ,&nbsp;Taichirou Morisawa ,&nbsp;Munenori Kosugi ,&nbsp;Yoshiki Kusama ,&nbsp;Hirotsugu Atarashi ,&nbsp;Wataru Shimizu","doi":"10.1016/j.ijcme.2015.07.001","DOIUrl":"10.1016/j.ijcme.2015.07.001","url":null,"abstract":"<div><h3>Background</h3><p>An elevated uric acid (UA) level is associated with an increased risk of adverse outcomes in patients with chronic heart failure (CHF). Febuxostat and allopurinol lower the UA levels and attenuate the expression of an inflammatory marker, monocyte chemoattractant protein (MCP)-1. However, a direct comparison of the effects of febuxostat and allopurinol on the inflammation and cardiac function in CHF patients with hyperuricemia has not yet been performed.</p></div><div><h3>Methods</h3><p>A total of 61 CHF patients with hyperuricemia who had a mean left ventricular ejection fraction (LVEF) of 37.1<!--> <!-->±<!--> <!-->6.7% were randomly assigned to receive febuxostat (n<!--> <!-->=<!--> <!-->31) or allopurinol (n<!--> <!-->=<!--> <!-->30).</p></div><div><h3>Results</h3><p>The MCP-1 levels and LVEF at baseline were comparable between the groups. However, after 12<!--> <!-->months of treatment, the febuxostat group achieved significantly higher percent decreases in the UA and MCP-1 levels from baseline than those of the allopurinol group (p<!--> <!-->&lt;<!--> <!-->0.001). The LVEF in both groups had improved after 12<!--> <!-->months; however, a greater percent increase in the LVEF from baseline was observed in the febuxostat group than that in the allopurinol group (p<!--> <!-->&lt;<!--> <!-->0.001). The percent increase in the LVEF from baseline was found to be significantly associated with the percent decrease in MCP-1 (r<!--> <!-->=<!--> <!-->−<!--> <!-->0.634, p<!--> <!-->&lt;<!--> <!-->0.001) in the febuxostat group.</p></div><div><h3>Conclusions</h3><p>These data indicate that febuxostat is more effective than allopurinol in reducing the UA level and inflammation and may improve the cardiac function in CHF patients with hyperuricemia due, at least in part, to reductions in inflammation.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 46-55"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83164016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The eNOS T786C mutation, Prinzmetal's Variant Angina, and amelioration of angina by l-arginine in 59 patients with intractable angina despite calcium channel blocker–nitrate therapy","authors":"Charles J. Glueck ,&nbsp;Marloe Prince ,&nbsp;Parth Shah ,&nbsp;Jaykumar G. Patel ,&nbsp;Ramesh Pandit ,&nbsp;Ping Wang","doi":"10.1016/j.ijcme.2015.05.022","DOIUrl":"10.1016/j.ijcme.2015.05.022","url":null,"abstract":"<div><h3>Background</h3><p>Despite calcium channel blockers — long acting nitrates (CaCH-LAN), ~<!--> <!-->20% of patients with Prinzmetal's Variant Angina (PVA) retain intractable angina. The endothelial nitric oxide synthase (eNOS) T-786C polymorphism, more common in PVA than normal subjects, decreases the conversion of <span>l</span>-arginine to nitric oxide (NO), promoting coronary artery spasm (CAS)-angina.</p></div><div><h3>Methods</h3><p>PCR measures for the eNOS T-786C polymorphism were done in 59 PVA patients with intractable angina despite CaCH-LAN. Using the Seattle Angina Questionnaire (SAQ), effects of 9<!--> <!-->g <span>l</span>-arginine/day were prospectively assessed in 28 patients with ≥<!--> <!-->3 visits, pre-treatment entry and ≥<!--> <!-->2 follow-ups at 1 and 5<!--> <!-->months, and in 31 additional patients with 2 visits, entry and 7.7<!--> <!-->months on <span>l</span>-arginine. This allowed an assessment of response to <span>l</span>-arginine in 59 patients at entry and 12<!--> <!-->months later (last follow-up).</p></div><div><h3>Results</h3><p>In the cohort of 59 patients, 47% of eNOS alleles were mutant vs. 20% in 72 normal controls, <em>p</em> <!-->&lt;<!--> <!-->.0001. Compared to pre-treatment baseline, all 5 SAQ components improved in 28 patients at 1 (<em>p</em> <!-->≤<!--> <!-->.02 for all) and 5<!--> <!-->months (<em>p</em> <!-->≤<!--> <!-->.03 for all) on <span>l</span>-arginine treatment, and improved in the 59 patients after 12<!--> <!-->months on <span>l</span>-arginine, <em>p</em> <!-->≤<!--> <!-->.002 for all. The eNOS mutation was a significant positive independent determinant of reduction in anginal symptoms, <em>p</em> <!-->=<!--> <!-->.0002. Patients hetero- and homozygous for the eNOS mutation had greater improvement in anginal symptoms.</p></div><div><h3>Conclusions</h3><p>In patients with intractable angina despite CaCH-LAN, the eNOS T-786C mutation appears to facilitate CAS via reduced NO production, a condition susceptible to treatment with <span>l</span>-arginine.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 13-19"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.05.022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83209166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomics in atherosclerosis","authors":"Demir Djekic ,&nbsp;Rachel Nicoll ,&nbsp;Mehmed Novo ,&nbsp;Michael Henein","doi":"10.1016/j.ijcme.2014.11.004","DOIUrl":"10.1016/j.ijcme.2014.11.004","url":null,"abstract":"<div><p>It is well established that atherosclerotic cardiovascular disease (ACD) is a leading cause of death in the West. There are several predisposing factors for ACD, which can be divided into two groups: firstly modifiable risk factors, including hypertension, dyslipidaemia, type 2 diabetes mellitus, obesity, smoking and a sedentary lifestyle and secondly the unmodifiable risk factors such as age, gender and heredity. Since single biomarkers are unable to provide sufficient information about the biochemical pathways responsible for the disease, there is a need for a holistic approach technology, e.g., metabolomics, that provide sufficiently detailed information about the metabolic status and assay results will be able to guide food, drug and lifestyle optimisation. Rather than investigating a single pathway, metabolomics deal with the integrated identification of biological and pathological molecular pathways. Mass spectrometry (MS) and nuclear magnetic resonance (NMR) spectroscopy are the two most commonly used techniques for metabolite profiling. This detailed review concluded that metabolomics investigations seem to have great potential in identifying small groups of disturbed metabolites, which if put together should draw various metabolic routs that lead to the common track pathophysiology. The current evidence in using metabolomics in atherosclerotic cardiovascular disease is also limited, and more well-designed studies remain to be established, which might significantly improve the comprehension of atherosclerosis pathophysiology and consequently management.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 26-30"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2014.11.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79526916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance to antiplatelet drugs. Can it be assessed?","authors":"Rossella Marcucci","doi":"10.1016/j.ijcme.2014.10.012","DOIUrl":"10.1016/j.ijcme.2014.10.012","url":null,"abstract":"<div><p>High platelet reactivity (HPR) during dual antiplatelet therapy is a marker of vascular risk, in particular stent thrombosis in patients with acute coronary syndromes. Genetic determinants (CYP2C19*2 polymorphism), advanced age, female gender, diabetes and reduced ventricular function are related to a higher risk to develop HPR. In addition, inflammation and increased platelet turnover, as revealed by the elevated percentage of reticulate platelets in patients' blood that characterize the acute phase of ACS, are associated with HPR. To overcome the limitation of Clopidogrel, new antiplatelet agents (Prasugrel and Ticagrelor) were synthesized and the demonstration of their superiority over Clopidogrel was obtained in two randomized trials TRITON TIMI 38 and PLATO. Due to the current possibility of choosing between multiple antiplatelet strategies, the future prospect is to include the definition of platelet function during treatment in order to set a tailored therapy, in addition to clinical data and classical risk factors.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 31-33"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2014.10.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72475783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers in acute coronary syndrome","authors":"David del Val Martin,&nbsp;Marcelo Sanmartín Fernández,&nbsp;Jose Luís Zamorano Gómez","doi":"10.1016/j.ijcme.2015.04.003","DOIUrl":"10.1016/j.ijcme.2015.04.003","url":null,"abstract":"<div><h3>Background</h3><p>Biomarkers play an important role in the diagnosis and risk stratification of patients with ischemic heart disease. Currently, troponin continues as the reference biomarker in acute coronary syndromes. However, there are other biomarkers that have shown additional value in improving sensitivity and prognostic information. Several promising molecules are reviewed, some related to cardiomyocyte structure and others working as inflammatory and renal function markers.</p></div><div><h3>Conclusions</h3><p>Although many biomarkers have been shown useful in some studies, further prospective studies are needed to establish their accurate usefulness in routine clinical practice.</p></div>","PeriodicalId":73333,"journal":{"name":"IJC metabolic & endocrine","volume":"8 ","pages":"Pages 20-23"},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ijcme.2015.04.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90047115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}