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      The Diagnostic Accuracy of Cardiac Enzymes-Lipid Profile Ratio for Diagnosing Coronary Heart Disease in Chest Pain Patients

      , , ,
      The Open Biochemistry Journal
      Bentham Science Publishers Ltd.

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          Abstract

          Background:

          Lipid abnormalities increase Coronary Heart Disease (CHD) risk. Our developed indexes 1,2 were reported in scientific Journals. Here, we verified and evaluated the cardiac enzymes-lipid profile ratio's diagnostic value for diagnosing CHD patients.

          Methods:

          Lipid profiles and cardiac enzymes were estimated in all chest pain patients. The area under the receiver-operating characteristic curve (AUC) was used to evaluate the markers' diagnostic accuracy.

          Results:

          There were varieties of significant differences (P < 0.01- P < 0.0001) of Creatine Kinase MB (CK-MB) - lipid profile ratio and Troponin I-lipid profile ratio within the groups of chest pain patients. For discriminating between Non-Coronary Chest Pain (NCCP) and Stable Angina (SA) groups, the AUCs were the greatest for CK-MB- High-density Lipoprotein (HDL) ratio (0.62) and for Troponin I-HDL (0.62). Moreover, for discriminating between NCCP and Unstable Angina (UA) groups, the AUC was the greatest for CK-MB-HDL ratio (0.97). Also, for discriminating between NCCP and Acute Myocardial Infarction (AMI) groups, the AUC was the greatest for index 2 (0.99). Similarly, for discriminating between SA and UA groups, the AUC was the greatest for CK-MB-HDL ratio (0.90). For discriminating between SA and AMI groups, the AUC was the greatest for index 2 (0.97). Finally, for discriminating between UA and AMI groups, the AUC was the greatest for index 2 (0.78).

          Conclusion:

          Independent CK-MB-HDL ratio can be used as a good and simple index for diagnosing CHD in chest pain patients and discriminating between the different groups of these patients

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          Most cited references21

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          Dyslipidemia

          Dyslipidemia is an important risk factor for coronary artery disease and stroke. Long-term, prospective epidemiologic studies have consistently shown that persons with healthier lifestyles and fewer risk factors for coronary heart disease, and particularly those with favorable lipid profiles, have reduced incidence of coronary heart disease. Prevention and sensible management of dyslipidemia can markedly alter cardiovascular morbidity and mortality.
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            Cardiac troponins: from myocardial infarction to chronic disease

            Abstract Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of ‘unknown origin’. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasizing the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasizing a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases.
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              Acute Coronary Syndromes: The Way Forward From Mechanisms to Precision Treatment.

              Well into the 21st century, we still triage acute myocardial infarction on the basis of the presence or absence of ST-segment elevation, a century-old technology. Meanwhile, we have learned a great deal about the pathophysiology and mechanisms of acute coronary syndromes (ACS) at the clinical, pathological, cellular, and molecular levels. Contemporary imaging studies have shed new light on the mechanisms of ACS. This review discusses these advances and their implications for clinical management of the ACS for the future. Plaque rupture has dominated our thinking about ACS pathophysiology for decades. However, current evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collection of diseases and obscures other mechanisms that may mandate different management strategies. We propose segmenting coronary artery thrombosis caused by plaque rupture into cases with or without signs of concomitant inflammation. This distinction may have substantial therapeutic implications as direct anti-inflammatory interventions for atherosclerosis emerge. Coronary artery thrombosis caused by plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with of ACS resulting from erosion may permit a less invasive approach to management than the current standard of care. We also now recognize ACS that occur without apparent epicardial coronary artery thrombus or stenosis. Such events may arise from spasm, microvascular disease, or other pathways. Emerging management strategies may likewise apply selectively to this category of ACS. We advocate this more mechanistic approach to the categorization of ACS to provide a framework for future tailoring, triage, and therapy for patients in a more personalized and precise manner.
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                Author and article information

                Journal
                The Open Biochemistry Journal
                TOBIOCJ
                Bentham Science Publishers Ltd.
                1874-091X
                March 22 2021
                March 22 2021
                : 15
                : 1
                : 20-25
                Article
                10.2174/1874091X02115010020
                35037478-1420-4fe9-9012-9523fd005237
                © 2021

                https://creativecommons.org/licenses/by/4.0/legalcode

                History

                Medicine,Chemistry,Life sciences
                Medicine, Chemistry, Life sciences

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