Implications for the diagnosis of myocardial infarction.
Rittoo D, et al.
JACC 2014;63:2411-20
Showing posts with label Troponin. Show all posts
Showing posts with label Troponin. Show all posts
Sunday, June 29, 2014
Friday, September 30, 2011
Troponin from skeletal muscle
J Am Coll Cardiol, doi:10.1016/j.jacc.2011.08.026 (Published online 28 September 2011)
Diseased Skeletal Muscle
A Noncardiac Source of Increased Circulating Concentrations of Cardiac Troponin T
Allan S. Jaffe, MD*,,*, Vlad C. Vasile, MD, PhD*,, Margherita Milone, MD, PhD, Amy K. Saenger, PhD*, Kalen N. Olson, PhD and Fred S. Apple, PhD
Dr. Allan S. Jaffe, Cardiovascular Division, Gonda 5, Mayo Clinic and Medical School, 200 First Street SW, Rochester, Minnesota 55905 (Email: Jaffe.Allan@Mayo.edu).
Objectives: The purpose of this study was to determine whether there is immunoreactive cardiac troponin T (cTnT) expression in diseased skeletal muscle that might cause possible false-positive increases in cTnT.
Background: Cardiac troponin (I or T) is the biomarker of choice for the diagnosis of cardiac injury. Recently, we were presented with a case that challenged the specificity of cTnT.
Methods: Patients with myopathies seen in the Neuromuscular Clinic at the Mayo Clinic were screened for increases in cTnT. If present, an assay for cTnI was performed. If normal, skeletal biopsy tissue was obtained for Western blot analysis using the capture and detection antibodies from both the fourth-generation and high-sensitivity cTnT assays. Results were compared with findings in normal cardiac tissue.
Results: Sixteen patients had increases in cTnT but not cTnI. All had a myopathy by clinical evaluation, clinical testing, and biopsy. Four residual biopsy samples were obtained. All 3 antibodies used in the cTnT (M11.7, M7) and high-sensitivity cTnT (5D8, M7) assays were immunoreactive with a 37- to 39-kDa protein in all 4 diseased skeletal muscle biopsy specimens and in cardiac tissue. A second immunoreactive isoform (34 to 36 kDa) was also found in 1 patient. None of the noncardiac control tissues expressed immunoreactive protein.
Conclusions: These results document that there are forms in diseased skeletal muscle that could cause increases in circulating levels of cTnT. These increases could reflect re-expressed isoforms. Clinicians need to be aware of the possibility that noncardiac increases in cTnT may occur and lead to a possible false-positive diagnosis of cardiac injury when skeletal muscle pathology is present.
Diseased Skeletal Muscle
A Noncardiac Source of Increased Circulating Concentrations of Cardiac Troponin T
Allan S. Jaffe, MD*,,*, Vlad C. Vasile, MD, PhD*,, Margherita Milone, MD, PhD, Amy K. Saenger, PhD*, Kalen N. Olson, PhD and Fred S. Apple, PhD
Dr. Allan S. Jaffe, Cardiovascular Division, Gonda 5, Mayo Clinic and Medical School, 200 First Street SW, Rochester, Minnesota 55905 (Email: Jaffe.Allan@Mayo.edu).
Objectives: The purpose of this study was to determine whether there is immunoreactive cardiac troponin T (cTnT) expression in diseased skeletal muscle that might cause possible false-positive increases in cTnT.
Background: Cardiac troponin (I or T) is the biomarker of choice for the diagnosis of cardiac injury. Recently, we were presented with a case that challenged the specificity of cTnT.
Methods: Patients with myopathies seen in the Neuromuscular Clinic at the Mayo Clinic were screened for increases in cTnT. If present, an assay for cTnI was performed. If normal, skeletal biopsy tissue was obtained for Western blot analysis using the capture and detection antibodies from both the fourth-generation and high-sensitivity cTnT assays. Results were compared with findings in normal cardiac tissue.
Results: Sixteen patients had increases in cTnT but not cTnI. All had a myopathy by clinical evaluation, clinical testing, and biopsy. Four residual biopsy samples were obtained. All 3 antibodies used in the cTnT (M11.7, M7) and high-sensitivity cTnT (5D8, M7) assays were immunoreactive with a 37- to 39-kDa protein in all 4 diseased skeletal muscle biopsy specimens and in cardiac tissue. A second immunoreactive isoform (34 to 36 kDa) was also found in 1 patient. None of the noncardiac control tissues expressed immunoreactive protein.
Conclusions: These results document that there are forms in diseased skeletal muscle that could cause increases in circulating levels of cTnT. These increases could reflect re-expressed isoforms. Clinicians need to be aware of the possibility that noncardiac increases in cTnT may occur and lead to a possible false-positive diagnosis of cardiac injury when skeletal muscle pathology is present.
Tuesday, September 21, 2010
Troponin in Heart Failure - Review article (Adult)
J Am Coll Cardiol, 2010; 56:1071-1078
STATE-OF-THE-ART PAPER
Troponin Elevation in Heart Failure
Prevalence, Mechanisms, and Clinical Implications
Robb D. Kociol, MD*, Peter S. Pang, MD, Mihai Gheorghiade, MD, Gregg C. Fonarow, MD, Christopher M. O'Connor, MD* and G. Michael Felker, MD, MHS*,*
Circulating biomarkers have become increasingly important in diagnosing and risk stratifying patients with heart failure (HF). While the natriuretic peptides have received much focus, there is increasing interest in the role of circulating cardiac troponin (cTn) in detecting myocardial injury (often subclinical) in those with HF. Accumulating evidence suggests that patients with chronic and acute HF may have measurable levels of circulating cTn, whose detection and magnitude may have prognostic implications. Furthermore, as new, more sensitive cTn assays are being developed, larger numbers of HF patients are found to have detectable cTn with a persistent relationship between magnitude and outcome. This knowledge improves our ability to understand the mechanism of worsening HF, improve risk stratification, and detect potential injury related to new therapeutics in HF. As investigators begin to understand the relationship of detectable cTn to HF outcomes, as well as temporal changes in its magnitude, and its relationship to other circulating biomarkers, more insight may be gained into the progressive nature of cardiac dysfunction and the transition from chronic compensated to acute decompensated HF. Ultimately, this information might allow physicians to guide therapy, choose appropriate therapeutics, and improve HF outcomes.
STATE-OF-THE-ART PAPER
Troponin Elevation in Heart Failure
Prevalence, Mechanisms, and Clinical Implications
Robb D. Kociol, MD*, Peter S. Pang, MD, Mihai Gheorghiade, MD, Gregg C. Fonarow, MD, Christopher M. O'Connor, MD* and G. Michael Felker, MD, MHS*,*
Circulating biomarkers have become increasingly important in diagnosing and risk stratifying patients with heart failure (HF). While the natriuretic peptides have received much focus, there is increasing interest in the role of circulating cardiac troponin (cTn) in detecting myocardial injury (often subclinical) in those with HF. Accumulating evidence suggests that patients with chronic and acute HF may have measurable levels of circulating cTn, whose detection and magnitude may have prognostic implications. Furthermore, as new, more sensitive cTn assays are being developed, larger numbers of HF patients are found to have detectable cTn with a persistent relationship between magnitude and outcome. This knowledge improves our ability to understand the mechanism of worsening HF, improve risk stratification, and detect potential injury related to new therapeutics in HF. As investigators begin to understand the relationship of detectable cTn to HF outcomes, as well as temporal changes in its magnitude, and its relationship to other circulating biomarkers, more insight may be gained into the progressive nature of cardiac dysfunction and the transition from chronic compensated to acute decompensated HF. Ultimately, this information might allow physicians to guide therapy, choose appropriate therapeutics, and improve HF outcomes.
Monday, July 5, 2010
Exercise induced Troponin increase - Review
Article
JACC 2010;56:169-176
Review of increase in Troponin increase after strenuous physical exercise. Mechanisms and implications. Worth reading.
JACC 2010;56:169-176
Review of increase in Troponin increase after strenuous physical exercise. Mechanisms and implications. Worth reading.
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