Articles: myocardial-injury.
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Emerg Med Australas · Apr 2014
ReviewReview article: Elevated troponin: Diagnostic gold or fool's gold?
Troponin is a highly sensitive biomarker of myocardial injury and has been used extensively in everyday clinical practice in the community as well as in hospitals for the diagnosis of acute myocardial infarction (AMI) and for risk stratification of patients with acute coronary symptoms. Dynamic elevations in biomarkers (troponin) are considered fundamental to the diagnosis of AMI. ⋯ An incorrect diagnosis of myocardial infarction can also lead to the oversight of serious life-threatening alternative causes of troponin elevation (e.g. pulmonary embolism). This article discusses the role of troponin in our everyday clinical practice in the ED.
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Ann Noninvasive Electrocardiol · Mar 2014
Observational StudyDiagnostic accuracy of a new cardiac electrical biomarker for detection of electrocardiogram changes suggestive of acute myocardial ischemic injury.
A new cardiac "electrical" biomarker (CEB) for detection of 12-lead electrocardiogram (ECG) changes indicative of acute myocardial ischemic injury has been identified. Objective was to test CEB diagnostic accuracy. ⋯ CEB detects acute myocardial ischemic injury with high diagnostic accuracy. CEB is instantly constructed from three ECG leads on the cardiac monitor and displayed instantly allowing immediate cost-effective identification of patients with acute ischemic injury during cardiac rhythm monitoring.
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To measure concentrations of high-sensitivity cardiac troponin (HS-cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis (RA) and to examine correlates. ⋯ HS-cTnT and NTproBNP are increased in patients with RA, independent of CV risk factors. The association between HS-cTnT, NT-proBNP, and CRP, together with the correlation between HS-cTnT and disease activity, support the link between myocardial injury/dysfunction and inflammation.
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J. Mol. Cell. Cardiol. · Nov 2013
Cyclic nucleotide phosphodiesterase 3A1 protects the heart against ischemia-reperfusion injury.
Phosphodiesterase 3A (PDE3A) is a major regulator of cAMP in cardiomyocytes. PDE3 inhibitors are used for acute treatment of congestive heart failure, but are associated with increased incidence of arrhythmias and sudden death with long-term use. We previously reported that chronic PDE3A downregulation or inhibition induced myocyte apoptosis in vitro. ⋯ To further verify the anti-apoptotic effects of PDE3A1, we performed in vitro apoptosis study in isolated adult TG and WT cardiomyocytes. We found that the apoptotic rates stimulated by hypoxia/reoxygenation or H2O2 were indeed significantly reduced in TG myocytes, and the differences between TG and WT myocytes were completely reversed in the presence of the PDE3 inhibitor milrinone. These together indicate that PDE3A1 negatively regulates β-AR signaling and protects against I/R injury by inhibiting cardiomyocyte apoptosis.