High-workload endurance training may increase serum ischemia-modified albumin concentrations

2005 ◽  
Vol 43 (7) ◽  
Author(s):  
Giuseppe Lippi ◽  
Giorgio Brocco ◽  
Gian Luca Salvagno ◽  
Martina Montagnana ◽  
Francesco Dima ◽  
...  
Keyword(s):  
Endurance Training ◽  
Myocardial Injury ◽  
Troponin T ◽  
Acute Chest Pain ◽  
Medium Term ◽  
Ischemia Modified Albumin ◽  
Coronary Syndrome ◽  
High Workload ◽  
Cobalt Binding ◽  
Creatine Kinase Isoenzyme Mb

AbstractThe measurement of cardiac troponins has emerged as the biochemical “gold standard” for the diagnosis and management of patients with acute chest pain. However, earlier markers should support investigation strategies, as several patients with acute coronary syndrome might present with non-diagnostic concentrations. Ischemia-modified albumin (IMA), measured by the albumin cobalt binding (ACB) assay, was recently proposed for early detection of myocardial ischemia. To establish the potential influence of endurance training on the diagnostic approach to patients with suspected myocardial injury, cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK-MB), myoglobin and IMA were evaluated in healthy individuals subjected to different aerobic workloads. The concentrations of both IMA and CK-MB were significantly increased in athletes subjected to high-workload endurance training, whereas the concentration of cTnT and myoglobin was not influenced by physical exercise in the medium term. Taken together, our results demonstrate that demanding aerobic physical activity might influence the generation of IMA, which might be increased in the medium term following high-workload endurance training, while the concentration of other conventional markers of myocardial injury remains non-diagnostic.

scholarly journals Copeptin Does Not Add Diagnostic Information to High-Sensitivity Troponin T in Low- to Intermediate-Risk Patients with Acute Chest Pain: Results from the Rule Out Myocardial Infarction by Computed Tomography (ROMICAT) Study

2011 ◽  
Vol 57 (8) ◽  
pp. 1137-1145 ◽  
Author(s):  
Mahir Karakas ◽  
James L Januzzi ◽  
Julia Meyer ◽  
Hang Lee ◽  
Christopher L Schlett ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Chest Pain ◽  
Predictive Value ◽  
Troponin T ◽  
Cardiac Computed Tomography ◽  
Acute Chest Pain ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Intermediate Risk ◽  
Coronary Syndrome

PURPOSE Copeptin, a stable peptide derived from the AVP precursor, has been linked to presence and severity of myocardial ischemia. We sought to evaluate the predictive value of copeptin and its incremental value beyond that of high-sensitivity cardiac troponin T (hs-cTnT) in patients with acute chest pain and low to intermediate risk for acute coronary syndrome (ACS). METHODS We recruited patients who presented with acute chest pain to the emergency department and had a negative initial conventional troponin T test (<0.03 μg/L). In all patients, hs-cTnT and copeptin measurements were taken. Each patient also underwent cardiac computed tomography (CT) and coronary angiography. RESULTS Baseline copeptin concentrations, in contrast to hs-cTnT, were not significantly higher in patients with ACS than in those without (P = 0.24). hs-cTnT showed an earlier rise in patients with ACS than copeptin, when analyses were stratified by time. A copeptin concentration ≥7.38 pmol/L had a negative predictive value (NPV) of 94% and a sensitivity of 51%, whereas hs-cTnT (≥13.0 pg/mL) had a NPV of 96% and a sensitivity of 63%. The combination of copeptin and hs-cTnT resulted in a lower diagnostic accuracy than hs-cTnT alone. Finally, on cardiac CT, copeptin concentrations were not associated with coronary artery morphology, although they were related to the presence of left ventricular dysfunction (P = 0.02). CONCLUSIONS Among patients with acute chest pain and low to intermediate risk for ACS, copeptin concentrations are not independently predictive of ACS and do not add diagnostic value beyond that of hs-cTnT measurements.

scholarly journals Incremental Value of High-Sensitivity Cardiac Troponin T for Risk Prediction in Patients with Suspected Acute Myocardial Infarction

2011 ◽  
Vol 57 (9) ◽  
pp. 1318-1326 ◽  
Author(s):  
Willibald Hochholzer ◽  
Tobias Reichlin ◽  
Raphael Twerenbold ◽  
Claudia Stelzig ◽  
Kirsten Hochholzer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Risk Score ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Acute Chest Pain ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Coronary Syndrome

BACKGROUND High-sensitivity cardiac troponin assays have better analytical precision and sensitivity than earlier-generation assays when measuring cardiac troponin at low concentrations. We evaluated whether use of a high-sensitivity assay could further improve risk stratification compared with a standard cardiac troponin assay. METHODS We enrolled consecutive patients presenting with acute chest pain, 30% of whom were diagnosed with acute coronary syndrome. Blood samples were drawn at the time of presentation. We measured cardiac troponin T with a standard fourth-generation assay (cTnT) and a high-sensitivity assay (hs-cTnT) (both Roche Diagnostics) and followed the patients for 24 months. RESULTS Of the 1159 patients, 76 died and 42 developed an acute myocardial infarction (AMI). Prognostic accuracy of hs-cTnT for death was significantly higher [area under ROC curve (AUC) 0.79, 95% CI 0.74–0.84] than that of cTnT (AUC 0.69, 95% CI 0.62–0.76; P < 0.001). After adjustment for Thrombolysis in Myocardial Infarction (TIMI) risk score (that included the cTnT assay result), hs-cTnT above the 99th percentile (0.014 μg/L) was associated with a hazard ratio for death of 2.60 (95% CI 1.42–4.74). Addition of hs-cTnT to the risk score improved the reclassification of patients (net reclassification improvement 0.91; 95% CI 0.67–1.14; P < 0.001). Subgroup analyses showed that this effect resulted from the better classification of patients without AMI at time of testing. hs-cTnT outperformed cTnT in the prediction of AMI during follow-up (P=0.02), but was not independently predictive for this endpoint. CONCLUSIONS Concentrations of hs-cTnT >0.014 μg/L improve the prediction of death but not subsequent AMI in unselected patients presenting with acute chest pain.

scholarly journals Copeptin as a Prognostic Marker in Acute Chest Pain and Suspected Acute Coronary Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Beata Morawiec ◽  
Damian Kawecki ◽  
Brygida Przywara-Chowaniec ◽  
Mariusz Opara ◽  
Piotr Muzyk ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Chest Pain ◽  
Troponin T ◽  
Strong Predictor ◽  
Acute Chest Pain ◽  
Coronary Syndrome ◽  
Cerebrovascular Events ◽  
Registration Number ◽  
Cox Analysis

Background. In patients admitted with chest pain and suspected acute coronary syndrome (ACS), it is crucial to early identify those who are at higher risk of adverse events. The study aim was to assess the predictive value of copeptin in patients admitted to the emergency department with chest pain and nonconclusive ECG. Methods. Consecutive patients suspected for an ACS were enrolled prospectively. Copeptin and high-sensitive troponin T (hs-TnT) were measured at admission. Patients were followed up at six and 12 months for the occurrence of death and major adverse cardiac and cerebrovascular events (MACCE). Results. Among 154 patients, 11 patients died and 26 experienced MACCE. Mortality was higher in copeptin-positive than copeptin-negative patients with no difference in the rate of MACCE. Copeptin reached the AUC 0.86 (0.75–0.97) for prognosis of mortality at six and 0.77 (0.65–0.88) at 12 months. It was higher than for hs-TnT and their combination at both time points. Copeptin was a strong predictor of mortality in the Cox analysis (HR14.1 at six and HR4.3 at 12 months). Conclusions. Copeptin appears to be an independent predictor of long-term mortality in a selected population of patients suspected for an ACS. The study registration number is ISRCTN14112941.

scholarly journals Subarachnoid haemorrhage mimicking as myocardial infarction

2017 ◽  
Vol 5 (2) ◽  
pp. 707
Author(s):  
Amanjeet S. Kindra ◽  
Abhimanyu Pandit ◽  
Suryanarayanan Bhaskar
Keyword(s):  
Myocardial Infarction ◽  
Subarachnoid Haemorrhage ◽  
Myocardial Injury ◽  
Artery Aneurysm ◽  
Acute Chest Pain ◽  
Anterior Communicating Artery ◽  
Ecg Changes ◽  
Coronary Syndrome ◽  
History Of ◽  
Reversible Condition

Electrocardiographic (ECG) changes due to subarachnoid haemorrhage (SAH) are seen frequently and mimic acute myocardial infarction. For appropriate therapeutic management it is very important to distinguish acute coronary syndrome from neurogenic myocardial injury, which is a reversible condition. A 35 year old male presented to us with history of acute chest pain, ECG suggestive of anterolateral myocardial infarction for which he underwent anticoagulant therapy. It was subsequently diagnosed to be a case of SAH due to ruptured anterior communicating artery aneurysm.

PO19-584 ISCHEMIA-MODIFIED ALBUMIN PREDICTS 1-YEAR MORTALITY IN PATIENTS WITH ACUTE CHEST PAIN SUGGESTIVE OF ACUTE CORONARY SYNDROME

2007 ◽  
Vol 8 (1) ◽  
pp. 160
Author(s):  
A. Bouzas-Mosquera ◽  
L. Consuegra-Sanchez ◽  
M.K. Sinha ◽  
P.O. Collinson ◽  
D. Gaze ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Chest Pain ◽  
Acute Chest Pain ◽  
Ischemia Modified Albumin ◽  
Coronary Syndrome

scholarly journals A Case of Acute Myocardial Injury – MINOCA or Myocarditis?

2020 ◽  
Vol 5 (3) ◽  
pp. 120-125
Author(s):  
Camelia Libenciuc ◽  
Răzvan-Andrei Licu ◽  
Istvan Kovacs ◽  
Monica Chitu ◽  
Imre Benedek
Keyword(s):  
Myocardial Injury ◽  
Clinical Presentation ◽  
Young Male ◽  
Acute Chest Pain ◽  
Myocardial Necrosis ◽  
High Sensitivity ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
St Segment ◽  
Acute Myocardial Injury

AbstractMyocardial infarction with non-obstructive coronary arteries (MINOCA) has been defined as clinical presentation of an acute coronary syndrome with laboratory evidence of myocardial necrosis, but with coronary stenosis of less than 50% on coronary angiography. On the other side, myocarditis is an inflammatory response triggered by viral, bacterial, fungal, lymphocytic, eosinophilic, or autoimmune myocardial injury, which may be associated with elevated myocardial necrosis serum biomarkers. We present the case of a young male patient with acute chest pain, ST-segment elevation, and high-sensitivity troponin levels of 22,162 ng/L.

scholarly journals How Safe Is the Outpatient Management of Patients with Acute Chest Pain and Mildly Increased Cardiac Troponin Concentrations?

2012 ◽  
Vol 58 (5) ◽  
pp. 916-924 ◽  
Author(s):  
Christophe Meune ◽  
Tobias Reichlin ◽  
Affan Irfan ◽  
Nora Schaub ◽  
Raphael Twerenbold ◽  
...  
Keyword(s):  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Acute Chest Pain ◽  
High Sensitivity ◽  
Outpatient Management ◽  
Coronary Syndrome ◽  
Risk Patients ◽  
Serial Measurements

Abstract BACKGROUND The appropriate management of patients discharged from the emergency department (ED) with increased high-sensitivity cardiac troponin T (hs-cTnT) but normal or borderline-high conventional cardiac troponin concentrations is unknown. METHODS We investigated 643 consecutive ED patients with acute chest pain who had been discharged for outpatient management after acute myocardial infarction (AMI) had been ruled out by serial measurements of conventional cardiac troponin. hs-cTnT was measured blindly, and we calculated the rates of all-cause mortality (primary endpoint) and subsequent AMI (secondary endpoint) at 30, 90, and 360 days. RESULTS hs-cTnT concentrations were increased (>14 ng/L) in 114 patients (18%) but <30 ng/L in 95% of these patients. Of those 114 patients, 96 (84%) had an adjudicated noncoronary cause of chest pain. Thirty-day mortality (95% CI) was 0.9% (0.1%–6.1%), 90-day mortality was 2.7% (0.9%–8.1%), and 360-day mortality was 5.2% (2.2%–11.9%) in patients with increased hs-cTnT; respective rates (95% CI) of AMI were 0.0%, 1.9% (0.5%–7.2%), and 7.6% (3.7%–15.3%). Increased hs-cTnT was associated with increased mortality and AMI at 90 days (P = 0.006 and P = 0.081, respectively) and 360 days (P = 0.001 for both). CONCLUSIONS hs-cTnT is a strong prognosticator of intermediate and long-term mortality and AMI in low-risk patients discharged from the ED after AMI has been ruled out. The relatively low rate of 30-day events may suggest that patients without acute coronary syndrome and small increases in cardiac troponin are in need of further investigations and treatments, but not necessarily immediate hospitalization.

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