Coronary angiography-related myocardial injury as detected by high-sensitivity cardiac troponin T assay

2016 ◽  
Vol 12 (3) ◽  
pp. 337-344 ◽  
Author(s):  
Haitham Abu Sharar ◽  
Daniel Wohlleben ◽  
Mehrshad Vafaie ◽  
Arnt V. Kristen ◽  
H. Christian Volz ◽  
...  
Keyword(s):  
Coronary Angiography ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T

scholarly journals High-Sensitivity Troponin as a Predictor of Cardiac Events and Mortality in the Stable Dialysis Population

2014 ◽  
Vol 60 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Hicham Cheikh Hassan ◽  
Kenneth Howlin ◽  
Andrew Jefferys ◽  
Stephen T Spicer ◽  
Ananthakrishnapuram N Aravindan ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Cardiac Event ◽  
Clinical Utility ◽  
Myocardial Injury ◽  
Prospective Observational Study ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Cardiac Events ◽  
Over Time

Abstract BACKGROUND High-sensitivity cardiac troponin T (hs-cTnT) is a biomarker used in diagnosing myocardial injury. The clinical utility and the variation of this biomarker over time remain unclear in hemodialysis (HD) and peritoneal dialysis (PD) patients. We sought to determine whether hs-cTnT concentrations were predictive of myocardial infarction (MI) and death and to examine hs-cTnT variability over a 1-year period. METHODS A total of 393 nonacute HD and PD patients (70% HD and 30% PD) were followed in a prospective observational study for new MI and death. RESULTS Median hs-cTnT was 57 ng/L (interquartile range, 36–101 ng/L) with no observed difference between HD and PD patients (P = 0.11). Incremental increases in mortality (P = 0.024) and MI (P = 0.001) were observed with increasing hs-cTnT quartiles. MI incidence increased significantly across quartiles in both HD and PD patients (P = 0.012 and P = 0.025, respectively), whereas mortality increased only in HD patients (P = 0.015). For every increase of 25 ng/L in hs-cTnT, the unadjusted hazard ratio (HR) was 1.10 for mortality in the whole group (95% CI, 1.04–1.16, P = 0.001) and 1.16 for MI (95% CI, 1.08–1.23, P < 0.001). Adjusted HR for mortality was 1.07 (95% CI, 1.01–1.15, P = 0.04) and 1.14 for MI (95% CI, 1.06–1.22, P < 0.001). Changes in hs-cTnT from baseline concentrations after 1 year were minimal (55 ng/L vs 53 ng/L, P = 0.22) even in patients who had an MI (P = 0.53). CONCLUSIONS hs-cTnT appears to have a useful role in predicting MI and death in the dialysis population. Over a 1-year period concentrations remained stable even in patients who sustained a new cardiac event.

The shocking lack of significant increases in high sensitivity troponin values after cardioversion

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R Lobo ◽  
R.D White ◽  
L.J Donato ◽  
Y.M Cha ◽  
R.M Melduni ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin T ◽  
High Sensitivity ◽  
High Energy ◽  
Funding Source ◽  
Cardiac Troponin T ◽  
Private Industry ◽  
Cumulative Energy ◽  
Dc Cardioversion

Abstract Background and introduction Cardioversion is commonly used to terminate cardiac arrhythmias. Some previous reports have suggested that cardioversion results in myocardial injury as evidenced by increased levels of cardiac troponin. However, many of these studies were done years ago with less sensitive troponin assays and monophasic waveform defibrillators. Purpose To determine if external direct current (DC) cardioversion with biphasic rectilinear waveform shocks results in myocardial injury as assessed by high sensitivity cardiac troponin T (hs-cTnT) and I (hs-cTnI). Methods Patients scheduled for elective DC cardioversion for atrial fibrillation or atrial flutter were recruited. Plasma samples for measurement of hs-cTnT and hs-cTnI were obtained pre-cardioversion and as late as feasible but at least 6 hours post-cardioversion [median of 9 (7–11) hours]. Results A total of 96 patients were recruited. One patient was excluded because the pre-cardioversion sample was hemolysed. Median (25th–75th interquartile range) cumulative energy delivered was 121.6J (62.4–277.4J) and median highest energy individual shock was 121.0J (62.1–146.2J). A total of 39 (41.1%) patients received more than 1 shock, 23 (24.2%) patients received a cumulative energy of 300J or higher and 5 (5.3%) patients received a cumulative energy of 1,000J or more. The median pre-cardioversion hs-cTnT value was 11.48 (7.19–18.38) ng/L and the median hs-cTnI value was 5.1 (2.0–9.4) ng/L. Median post-cardioversion hs-cTnT value were 12.46 (7.98–20.28) ng/L and hs-cTnI value were 6.3 (3.5–10.0) ng/L. Wilcoxon-Signed ranks test showed a statistically significant change between the pre-and-post cardioversion hs-cTnT values (Z=−4.237, p<0.001) and hs-cTnI values (Z=−4.822, p<0.001). In only 5 (hs-cTnT) and 4 patients (hs-cTnI) was there an increase of >5 ng/L. There were 5 cases where the post-cardioversion values of both hs-cTnT and hs-cTnI were above the 50% reference change value. There was no relation between the change in hs-cTn values and sex, number of shocks, total energy delivered (even in those who received more than 1,000J), highest energy per shock, total current delivered, highest current delivered per shock or transthoracic impedance. Conclusion(s) There is a statistically significant but very small change in median hs-cTnT and hs-cTnI values (1 ng/L and 1.2 ng/L respectively) after DC cardioversion. The results were similar even in patients where high energy shocks were delivered and did not vary based on the pre cardioversion baseline value. Patients who have marked troponin elevations after cardioversion should be assessed for other causes of myocardial injury. It should not be assumed that they have myocardial injury from the cardioversion alone. Figure 1 Funding Acknowledgement Type of funding source: Other. Main funding source(s): Dr. Allan Jaffe has substantial research funds from both grants and private industry. Funds were used to pay for blood sample collection and analysis of high sensitivity cardiac troponin T at Mayo Clinic. Abbott Laboratories donated reagents for the high sensitivity cardiac troponin I analysis.

scholarly journals HIGH-SENSITIVITY CARDIAC TROPONIN T FOR THE DETECTION OF MYOCARDIAL INJURY AND RISK STRATIFICATION IN COVID-19

2021 ◽  
Vol 77 (18) ◽  
pp. 3145
Author(s):  
Laura De Michieli ◽  
Olatunde Ola ◽  
Jonathan Knott ◽  
Ashok Akula ◽  
Ramila Mehta ◽  
...  
Keyword(s):  
Risk Stratification ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin T ◽  
High Sensitivity ◽  
Cardiac Troponin T

scholarly journals Relationship Between Myocardial Injury During Index Hospitalization for SARS‐CoV‐2 Infection and Longer‐Term Outcomes

2021 ◽  
Author(s):  
Brittany Weber ◽  
Hasan Siddiqi ◽  
Guohai Zhou ◽  
Jefferson Vieira ◽  
Andy Kim ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin T ◽  
Cardiac Injury ◽  
High Sensitivity ◽  
Cardiac Biomarkers ◽  
Study Cohort ◽  
Cardiac Troponin T ◽  
Index Hospitalization ◽  
The Relationship

Background Myocardial injury in patients with COVID‐19 is associated with increased mortality during index hospitalization; however, the relationship to long‐term sequelae of SARS‐CoV‐2 is unknown. This study assessed the relationship between myocardial injury (high‐sensitivity cardiac troponin T level) during index hospitalization for COVID‐19 and longer‐term outcomes. Methods and Results This is a prospective cohort of patients who were hospitalized at a single center between March and May 2020 with SARS‐CoV‐2. Cardiac biomarkers were systematically collected. Outcomes were adjudicated and stratified on the basis of myocardial injury. The study cohort includes 483 patients who had high‐sensitivity cardiac troponin T data during their index hospitalization. During index hospitalization, 91 (18.8%) died, 70 (14.4%) had thrombotic complications, and 126 (25.6%) had cardiovascular complications. By 12 months, 107 (22.2%) died. During index hospitalization, 301 (62.3%) had cardiac injury (high‐sensitivity cardiac troponin T≧14 ng/L); these patients had 28.6%, 32.2%, and 33.2% mortality during index hospitalization, at 6 months, and at 12 months, respectively, compared with 4.1%, 4.9%, and 4.9% mortality for those with low‐level positive troponin and 0%, 0%, and 0% for those with undetectable troponin. Of 392 (81.2%) patients who survived the index hospitalization, 94 (24%) had at least 1 readmission within 12 months, of whom 61 (65%) had myocardial injury during the index hospitalization. Of 377 (96%) patients who were alive and had follow‐up after the index hospitalization, 211 (56%) patients had a documented, detailed clinical assessment at 6 months. A total of 78 of 211 (37.0%) had ongoing COVID‐19–related symptoms; 34 of 211 (16.1%) had neurocognitive decline, 8 of 211 (3.8%) had increased supplemental oxygen requirements, and 42 of 211 (19.9%) had worsening functional status. Conclusions Myocardial injury during index hospitalization for COVID‐19 was associated with increased mortality and may predict who are more likely to have postacute sequelae of COVID‐19. Among patients who survived their index hospitalization, the incremental mortality through 12 months was low, even among troponin‐positive patients.

scholarly journals Drug-Induced Rhabdomyolysis with Elevated Cardiac Troponin T

2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
Gro Egholm ◽  
Manan Pareek
Keyword(s):  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin T ◽  
Myocardial Necrosis ◽  
High Sensitivity ◽  
Cardiac Troponin T ◽  
Drug Induced ◽  
Definitive Evidence ◽  
Positive Results

The essential role of cardiac troponin in the diagnosis of acute myocardial infarction has led to the development of high-sensitivity assays, which are able to detect very small amounts of myocardial necrosis. The high-sensitivity cardiac troponin T assay, however, is not entirely specific for myocardial injury. This case report describes a 48-year-old woman, who, two years after cardiac transplantation, presented with rhabdomyolysis. During the course of the disease, her troponin T level was elevated on repeated occasions, but other definitive evidence of myocardial injury was not found. Asymptomatic cardiac troponin T elevations during rhabdomyolysis may be due to either cardiac involvement or false positive results stemming from skeletal muscle injury.

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