Abstract 16133: High Density Lipoprotein Cholesterol is an Alternative Marker to Troponin for Acute Coronary Syndrome in High Risk Patients

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Anke Nguyen ◽  
Heath Adams ◽  
Natalie Yap ◽  
Julian Gin ◽  
Andrew M Wilson

Introduction: It is well known that high density lipoprotein cholesterol is inversely correlated with the risk of coronary artery disease. However, data is limited regarding the relationship of high density lipoprotein cholesterol in the acute setting of coronary artery disease and particularly how it compares to the most well-known biomarker, cardiac troponin I. Hypothesis: We assessed the hypothesis that high density lipoprotein cholesterol could be used as an alternative marker to troponin for acute coronary syndrome (ACS) in high risk patients. Methods: We analysed 740 patients of the BRAVEHEART cohort presenting for coronary angiography at our institution between October 2009 and March 2014. Of these, 153 patients presented with ACS, including 44 with ST elevation myocardial infarction and 109 with non-ST elevation myocardial infarction, and 587 patients presented without ACS. Binary logistic regression was used to compare high density lipoprotein cholesterol and cardiac troponin I levels as predictors of ACS, independent of age, sex, cardiac risk factors and statin use. Results: Patients presenting with ACS had higher median cardiac troponin I levels (0.34 vs. 0.02 μg/L; p<0.001), higher median serum triglyceride levels (1.5 vs. 1.3 mmol/L, p<0.001) and lower median high density lipoprotein cholesterol levels (0.97 vs. 1.09 mmol/L, p<0.001) than patients without ACS. There was no difference in total cholesterol and low density lipoprotein cholesterol between the two groups. After adjusting for differences in patient variables, the strongest independent predictors of ACS were cardiac troponin I (odds ratio (OR), 1.50; 95% confidence interval (CI), 1.24-1.82; p<0.001) and high density lipoprotein cholesterol (OR, 0.12; 95% CI, 0.04-0.36; p<0.001). Conclusion: In conclusion, high density lipoprotein cholesterol was found to be an independent marker of ACS in high risk patients at our institution. Further studies on high density lipoprotein cholesterol could determine its clinical use in conjunction with troponin levels in patients presenting with ACS.

BMJ Open ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. e019041 ◽  
Author(s):  
Farshid Hajati ◽  
Evan Atlantis ◽  
Katy J L Bell ◽  
Federico Girosi

ObjectivesWe examine the extent to which the adult Australian population on lipid-lowering medications receives the level of high-density lipoprotein cholesterol (HDL-C) testing recommended by national guidelines.DataWe analysed records from 7 years (2008–2014) of the 10% publicly available sample of deidentified, individual level, linked Medicare Benefits Schedule (MBS) and Pharmaceutical Benefits Scheme (PBS) electronic databases of Australia.MethodsThe PBS data were used to identify individuals on stable prescriptions of lipid-lowering treatment. The MBS data were used to estimate the annual frequency of HDL-C testing. We developed a methodology to address the issue of ‘episode coning’ in the MBS data, which causes an undercounting of pathology tests. We used a published figure on the proportion of unreported HDL-C tests to correct for the undercounting and estimate the probability that an HDL-C test was performed. We judged appropriateness of testing frequency by comparing the HDL-C testing rate to guidelines’ recommendations of annual testing for people at high risk for cardiovascular disease.ResultsWe estimated that approximately 49% of the population on stable lipid-lowering treatment did not receive any HDL-C test in a given year. We also found that approximately 19% of the same population received two or more HDL-C tests within the year. These levels of underutilisation and overutilisation have been changing at an average rate of 2% and −4% a year, respectively, since 2009. The yearly expenditure associated with test overutilisation was approximately $A4.3 million during the study period, while the cost averted because of test underutilisation was approximately $A11.3 million a year.ConclusionsWe found that approximately half of Australians on stable lipid-lowering treatment may be having fewer HDL-C testing than recommended by national guidelines, while nearly one-fifth are having more tests than recommended.


Author(s):  
Geraldine Iroh ◽  
Benita Oyoburuoma Weli ◽  
Uyota Anthony Adele ◽  
Ojoye Ngoye Briggs ◽  
Helen Anthony Waribo ◽  
...  

Aim: Assess the effect of tartrazine azo dye on atherogenic indices and markers of cardiac injury in albino rats. Study Design: A total number of 63 rats were used for the study. The study was divided into two phases, 1 and 2, which lasted for 30 and 60 days respectively. Phase 1 had 35 rats, 20 as test and 15 as control, while phase 2 had 28 rats, 16 as test and 12 as control. In each phase the test groups were given 7.5mg/kg of tartrazine orally on daily basis over the stipulated period while the control groups were not treated with tartrazine. Methodology: At the end of the study, 5ml of whole blood was collected from the jugular veins into Lithium Heparin bottles. The sample was spun, plasma collected and analyzed for cardiac Troponin I (cTn-I) and cardiac Troponin T (cTn-T), Total creatinekinase (CK), creatinekinase MM (CK-MM), and creatinekinase MB (CK-MB). Lipid parameters like total cholesterol (TC), High density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C) and Triglyceride (TG) which were also analysed. Atherogenic indices such as atherogenic coefficient (AC), atherogenic index of plasma (AIP), Non High density lipoprotein-cholesterol (nHDL-C), and castelli risk indices 1 and 2 (CRI-1 and CRI-2) were also calculated. In addition, cardiac tissues were collected, fixed in 10% formol saline and examined histologically using Haematoxylin and Eosin stain. Statistical analysis was performed using GraphPad Prism version 8.02. Results: The results obtained indicate significant increases in nHDL-C, total CK and cTn-T after 30 and 60 days of treatment with tartrazine at ADI doses against controls. Other atherogenic indices such as AIP, AC, CRI-1 and CRI-2 as well as markers of cardiac injury such as cTn-I and CK-MB indicated non-significant increases. Conclusion: Orally administered tartrazine over a 60 day period induced cardiac injury as shown by the significant increase in the cTn-T and total CK as well as hypertrophied nuclei of cardiomyocytes. This goes to say chronic administration of tartrazine even at the recommended daily dose could pose the risk of cardiovascular disease. This is also supported by an increase in nHDL cholesterol.


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