scholarly journals Endocan: A Key Player of Cardiovascular Disease

2022 ◽  
Vol 8 ◽  
Author(s):  
Jinzhi Chen ◽  
Liping Jiang ◽  
Xiao-Hua Yu ◽  
Mi Hu ◽  
Yang-Kai Zhang ◽  
...  

Endothelial dysfunction is considered to be an early change in atherosclerosis. Endocan, also known as endothelial cell specific molecule-1, is a soluble proteoglycan mainly secreted by endothelial cells. Inflammatory factors such as IL-1β and TNF-α can up regulate the expression of endocan and then affect the expression of cell adhesion molecules, such as ICAM-1 and VCAM-1, which play an important role in promoting leukocyte migration and inflammatory response. Elevated plasma levels of endocan may reflect endothelial activation and dysfunction, and is considered to be a potential immuno-inflammatory marker that may be related to cardiovascular disease. In the case of hypertension, diabetes, angina pectoris and acute myocardial infarction, the increase or decrease of serum endocan levels is of great significance. Here, we reviewed the current research on endocan, and emphasis its possible clinical value as a prognostic marker of cardiovascular disease. Endocan may be a useful biomarker for the prognosis of cardiovascular disease, but more research is needed on its mechanism of action.

2018 ◽  
Vol 24 (4) ◽  
pp. 414-426 ◽  
Author(s):  
Patrick Proctor ◽  
Massoud A. Leesar ◽  
Arka Chatterjee

Thrombolytic therapy kick-started the era of modern cardiology but in the last few decades it has been largely supplanted by primary percutaneous coronary intervention (PCI) as the go-to treatment for acute myocardial infarction. However, these agents remain important for vast populations without access to primary PCI and acute ischemic stroke. More innovative uses have recently come up for the treatment of a variety of conditions. This article summarizes the history, evidence base and current use of thrombolytics in cardiovascular disease.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 144.1-144
Author(s):  
R. Mazzucchelli ◽  
S. Rodriguez-Martin ◽  
A. García-Vadillo ◽  
M. Gil ◽  
A. Rodríguez-Miguel ◽  
...  

Background:There is some evidence from epidemiological studies suggesting that CS and glucosamine could play a role in cardiovascular disease (CVD) prevention (1-4).Studies to date have included prevalent users, therefore a bias that overestimates protection cannot be excluded.Objectives:To test the hypothesis that chondroitin sulphate (CS) or glucosamine reduce the risk of acute myocardial infarction (AMI).Methods:Case-control study nested in a primary cohort composed of patients aged 40 to 99 years, with at least one year of follow-up in the BIFAP database during the 2002-2015 study period. From this cohort of patients, we identified incident cases of AMI and randomly selected five controls per case, matched by exact age, gender, and index date. Adjusted odds ratios (AOR) and their corresponding 95% confidence interval (CI)) were calculated through a conditional logistic regression. Only new users of CS or glucosamine were considered.Results:A total of 23,585 incident cases of AMI and 117,405 controls were included. The mean age was 67.0 (SD 13.4) years and 71.75% were male, in both groups. 558 (2.37%) cases and 3,082 (2.62%) controls used or had used CS. The current use of CS was associated with a lower risk of AMI (AOR 0.57; 95%CI: 0.46–0.72) and disappeared after discontinuation (recent and past users). The reduced risk among current users was observed in both short-term (<365 days AOR 0.58; 95%CI: 0.45-0.75) and long-term users (>364 days AOR 0.56; 95%CI 0.36-0.87), in both sexes (men, AOR=0.52; 95%CI:0.38-0.70; women, AOR=0.65; 95%CI: 0.46-0.91), in individuals over or under 70 years of age (AOR=0.54; 95%CI:0.38-0.77, and AOR=0.61; 95%CI:0.45-0.82, respectively) and in individuals at intermediate (AOR=0.65; 95%CI:0.48-0.91) and high cardiovascular risk (AOR=0.48;95%CI:0.27-0.83), but not in those at low risk (AOR=1.11; 95%CI:0.48-2.56). In contrast, the current use of glucosamine was not associated with either increased or decreased risk of AMI (AOR= 0.86; CI95% 0.66-1.08)Conclusion:Our results support a cardioprotective effect of CS, while no effect was observed with glucosamine. The highest protection was found among subgroups at higher cardiovascular risk.References:[1]Ma H, Li X, Sun D, Zhou T, Ley SH, Gustat J, et al. Association of habitual glucosamine use with risk of cardiovascular disease: prospective study in UK Biobank. BMJ. 2019;365(Journal Article):l1628.[2]de Abajo FJ, Gil MJ, Garcia Poza P, Bryant V, Oliva B, Timoner J, et al. Risk of nonfatal acute myocardial infarction associated with non-steroidal antiinflammatory drugs, non-narcotic analgesics and other drugs used in osteoarthritis: a nested case-control study. PharmacoepidemiolDrug Saf. 2014;23(11):1128–38.[3]Li Z-H, Gao X, Chung VC, Zhong W-F, Fu Q, Lv Y-B, et al. Associations of regular glucosamine use with all-cause and cause-specific mortality: a large prospective cohort study. Ann Rheum Dis. 2020 Apr 6;annrheumdis-2020-217176.[4]King DE, Xiang J. Glucosamine/Chondroitin and Mortality in a US NHANES Cohort. J Am Board Fam Med. 2020 Dec;33(6):842–7.Disclosure of Interests:Ramón Mazzucchelli Speakers bureau: UCB, Lilly, Grant/research support from: Pfizer, Roche, Amgen, Sara Rodriguez-Martin: None declared, Alberto García-Vadillo: None declared, Miguel Gil: None declared, Antonio Rodríguez-Miguel: None declared, Diana Barreira-Hernández: None declared, Alberto García-Lledó: None declared, Francisco de Abajo: None declared


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
F Kahles ◽  
R.W Mertens ◽  
M.V Rueckbeil ◽  
M.C Arrivas ◽  
J Moellmann ◽  
...  

Abstract Background GLP-1 and GLP-2 (glucagon-like peptide-1/2) are gut derived hormones that are co-secreted from intestinal L-cells in response to food intake. While GLP-1 is known to induce postprandial insulin secretion, GLP-2 enhances intestinal nutrient absorption and is clinically used for the treatment of patients with short bowel syndrome. The relevance of the GLP-2 system for cardiovascular disease is unknown. Purpose The aim of this study was to assess the predictive capacity of GLP-2 for cardiovascular prognosis in patients with myocardial infarction. Methods Total GLP-2 levels, NT-proBNP concentrations and the Global Registry of Acute Coronary Events (GRACE) score were assessed at time of admission in 918 patients with myocardial infarction, among them 597 patients with NSTEMI and 321 with STEMI. The primary composite outcome of the study was the first occurrence of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke (3-P-MACE) with a median follow-up of 311 days. Results Kaplan-Meier survival plots (separated by the median of GLP-2 with a cut-off value of 4.4 ng/mL) and univariable cox regression analyses found GLP-2 values to be associated with adverse outcome (logarithmized GLP-2 values HR: 2.87; 95% CI: 1.75–4.68; p&lt;0.0001). Further adjustment for age, sex, smoking, hypertension, hypercholesterolemia, diabetes mellitus, family history of cardiovascular disease, hs-Troponin T, NT-proBNP and hs-CRP levels did not affect the association of GLP-2 with poor prognosis (logarithmized GLP-2 values HR: 2.96; 95% CI: 1.38–6.34; p=0.0053). Receiver operating characteristic curve (ROC) analyses illustrated that GLP-2 is a strong indicator for cardiovascular events and proved to be comparable to other established risk markers (area under the curve of the combined endpoint at 6 months; GLP-2: 0.72; hs-Troponin: 0.56; NT-proBNP: 0.70; hs-CRP: 0.62). Adjustment of the GRACE risk estimate by GLP-2 increased the area under the receiver-operating characteristic curve for the combined triple endpoint after 6 months from 0.70 (GRACE) to 0.75 (GRACE + GLP-2) in NSTEMI patients. Addition of GLP-2 to a model containing GRACE and NT-proBNP led to a further improvement in model performance (increase in AUC from 0.72 for GRACE + NT-proBNP to 0.77 for GRACE + NT-proBNP + GLP-2). Conclusions In patients admitted with acute myocardial infarction, GLP-2 levels are associated with adverse cardiovascular prognosis. This demonstrates a strong yet not appreciated crosstalk between the heart and the gut with relevance for cardiovascular outcome. Future studies are needed to further explore this crosstalk with the possibility of new treatment avenues for cardiovascular disease. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): German Society of Cardiology (DGK), German Research Foundation (DFG)


2017 ◽  
Author(s):  
John K. Roberts ◽  
John P. Middleton

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes. 


2014 ◽  
Vol 42 (1) ◽  
pp. 3-6
Author(s):  
SS Shahina ◽  
JU Ahmed ◽  
S Ahmed ◽  
E Shahriar ◽  
MN Uddin ◽  
...  

Troponin I (cTnI) isoform is cardiac muscle specific protein and shown to have several features as a preferred marker of myocardial injury. It rises early in acute myocardial infarction (AMI) and attains levels that are clearly separated from baseline values. It remains elevated for several days providing a long window for detection of cardiac injury. The objective of the study was to evaluate for the profile of cTnI level among symptomatic AMI patients. The study was conducted at National Institute of Cardiovascular Disease, Dhaka, Bangladesh from July 2007 to June 2008 and total 9552 patients with type 1 or type 2 MI were included. Blood Sample was taken within 3 days of symptoms and cTnI was measured by chemiluminescent immunometric assay method. cTnI was considered positive when the value was >1ng/ml and study population was divided as per age, sex and cTnI level. The mean (+ SD) age of all patients was 55(+ 12.8) years and majority was males (82.20%). Seasonal variation showed highest positive cases in winter. In case of circadian variation positive cTnI results were suggestive of morning peak of AMI. Positive results were obtained in 32.3% of Cases. cTnI is now considered as a better indicator of myocardial injury. Further study in depth is necessary to correlate with clinical symptoms and other diagnostic tests to make a complete profile of AMI according to the latest subtypes. DOI: http://dx.doi.org/10.3329/bmj.v42i1.18969 Bangladesh Med J. 2013 Jan; 42 (1): 3-6


Author(s):  
Sri Anita ◽  
Liong Boy Kurniawan ◽  
Darwati Muhadi

Myocardial infarction is a necrosis of myocardial cells due to lack of blood and oxygen supply caused by obstruction of coronary arteries, mostly due to atherosclerosis processes. Increased inflammatory marker level is associated with poor cardiovascular prognosis. This study was aimed to know whether leukocytes count, differential cell count and the Ratio of Neutrophils-Lymphocytes (RNL) could distinguish between types of Acute Myocardial Infarction (AMI) and to evaluate its correlation with mortality. This was a cross-sectional retrospective study using medical records patients which were diagnosed as AMI by clinicians in Cardiac Centre of the Dr. Wahidin Sudirohusodo Hospital during the period of April 1st, 2015 - May 31st, 2016. Statistical analysis used the Mann-Whitney and Chi-Square test, p<0.05 was considered as significant. The total subjects were 435 patients divided into 289 ST- Elevation Myocardial Infarction (STEMI) and 146 Non-ST-Elevation Myocardial Infarction (NSTEMI). There were significant differences in that mean of leukocytes, neutrophils, lymphocytes, monocytes, eosinophils counts and RNL between STEMI and NSTEMI (p <0.05). Significant differences were also found in leukocyte, neutrophils, lymphocytes, eosinophils, basophils and RNL mean between those who died and survived (p <0.05) and a significant correlation between increased leukocytes, neutrophils, basophils counts with mortality (p <0.05). In conclusion, the number of leukocytes and leukocyte count can be used as diagnostic markers of AMI between STEMI and NSTEMI, as well as prognostic markers among patients who died and survived. Routine blood sampling cohort studies in patients with AMI can avoid the bias of the results obtained. 


Author(s):  
Louise Benning ◽  
Samuel Robinson ◽  
Marie Follo ◽  
Lukas Andreas Heger ◽  
Daniela Stallmann ◽  
...  

2005 ◽  
pp. 1191-1202
Author(s):  
Luciano Babuin ◽  
Allan S. Jaffe

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease. Troponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated.


2017 ◽  
Author(s):  
John K. Roberts ◽  
John P. Middleton

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes. 


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