BACKGROUND
There is a paucity of data on the association between high-sensitivity cardiac troponin (hs-cTn) levels and outcomes in patients with chest pain but no myocardial infarction (MI), or any other condition that may lead to acutely elevated troponin levels.


OBJECTIVES
The authors hypothesized that any detectable high-sensitivity cardiac troponin T (hs-cTnT) level is associated with adverse outcomes.


METHODS
All patients (N = 22,589) >25 years of age with chest pain and hs-cTnT analyzed concurrently in the emergency department of Karolinska University Hospital, Stockholm, Sweden from 2011 to 2014 were eligible for inclusion. After excluding all patients with acute conditions that may have affected hs-cTnT, or MI associated with the visit, or insufficient information to determine whether troponin levels were stable, Cox regression was used to estimate risks for all-cause, cardiovascular, and noncardiovascular mortality, MI, and heart failure at different levels of troponins.


RESULTS
A total of 19,460 patients with a mean age of 54 ± 17 years were included. During a mean follow-up of 3.3 ± 1.2 years, 1,349 (6.9%) patients died. Adjusted hazard ratios (with 95% confidence intervals) for all-cause mortality were 2.00 (1.66 to 2.42), 2.92 (2.38 to 3.59), 4.07 (3.28 to 5.05), 6.77 (5.22 to 8.78), and 9.68 (7.18 to 13.00) in patients with hs-cTnT levels of 5 to 9, 10 to 14, 15 to 29, 30 to 49, and ≥50 ng/l, respectively, compared with patients with hs-cTnT levels <5 ng/l. There was a strong and graded association between all detectable levels of hs-cTnT and risk for MI, heart failure, and cardiovascular and noncardiovascular mortality.


CONCLUSIONS
Among patients with chest pain and stable troponin levels, any detectable level of hs-cTnT is associated with an increased risk of death and cardiovascular outcomes and should merit further attention.

Stable high-sensitivity cardiac troponin T levels and outcomes

The 2021 American Heart Association/American College of Cardiology/American Society of Echocardiography/American College of Chest Physicians/Society for Academic Emergency Medicine/Society of Cardiovascular Computed Tomography/Society for Cardiovascular Magnetic Resonance guidelines for the evaluation and diagnosis of acute chest pain make important recommendations that include the recognition of high-sensitivity cardiac troponin (hs-cTn) as the preferred biomarker, endorsement of 99th percentile upper reference limits to define myocardial injury, and the use of clinical decision pathways, as well as acknowledgment of the uniqueness of women and other patient subsets. Details on how to integrate hs-cTn into clinical practice are less extensively addressed. Clinicians should be aware of some of the analytical aspects related to hs-cTn assays regarding the limit of detection and the limit of quantitation and how they are used clinically, especially for the single sample strategy to rule out acute myocardial infarction. Likewise, it is important for clinicians to understand issues related to the derivation of the 99th percentile upper reference limit; the value of sex-specific 99th percentile upper reference limits; how to use changing concentrations (deltas) to facilitate diagnosis and risk stratification of patients with suspected acute coronary syndrome, including the differentiation of acute from chronic myocardial injury; and how to best integrate the use of hs-cTn with clinical decision pathways. With the use of hs-cTn, conditions such as type 2 myocardial infarction become more common, whereas others such as unstable angina become less frequent but still occur. Sections relating to these issues are included. 

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.122.059678

High-Sensitivity Cardiac Troponin and the 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guidelines for the Evaluation and Diagnosis of Acute Chest Pain

This article proceeds with a discussion of the causes and mechanisms of an elevation in cardiac troponins in pathological conditions not associated with acute myocardial infarction. The second part of the article discusses the causes and mechanisms of cardiac troponins elevation in diabetes mellitus, arterial hypertension, hereditary cardiomyopathies, cardiac arrhythmias (atrial fibrillation, supraventricular tachycardia), acute aortic dissection, and diseases of the central nervous system (strokes, subarachnoidal hemorrhage). The final chapter of this article discusses in detail the false-positive causes and mechanisms of elevated cardiac troponins.

Elevation Mechanisms and Diagnostic Consideration of Cardiac Troponins under Conditions Not Associated with Myocardial Infarction. Part 2.

Introduction and objectives Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. Methods The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. Results In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n = 186), 22% with myocardial injury (n = 41); and ruled out COVID-19 (n = 247), 21.5% with myocardial injury (n = 52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P < .001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P = .001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P = .004). The predictive model analyzed by ROC curves was similar in the 2 groups (P = .701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). Conclusions Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances.

[Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital]

Cardiac troponin I (cTnI) is a biomarker widely related to acute myocardial infarction (AMI), one of the leading causes of death around the world. Point-of-care testing (POCT) of cTnI not only demands a short turnaround time for its detection but the highest accuracy levels to set expeditious and adequate clinical decisions. The analytical technique Surface-enhanced Raman spectroscopy (SERS) possesses several properties that tailor to the POCT format, such as its flexibility to couple with rapid assay platforms like microfluidics and paper-based immunoassays. Here, we analyze the strategies used for the detection of cTnI by SERS considering POCT requirements. From the detection ranges reported in the reviewed literature, we suggest the diseases other than AMI that could be diagnosed with this technique. For this, a section with information about cardiac and non-cardiac diseases with cTnI release, including their release kinetics or cut-off values are presented. Likewise, POCT features, the use of SERS as a POCT technique, and the biochemistry of cTnI are discussed. The information provided in this review allowed the identification of strengths and lacks of the available SERS-based point-of-care tests for cTnI and the disclosing of requirements for future assays design.

A review of cardiac troponin I detection by surface enhanced Raman spectroscopy: Under the spotlight of point-of-care testing

Clinical Features and Prognosis of Patients with Acute and Chronic Myocardial Injury Admitted to the Emergency Department.

BACKGROUND Tachyarrhythmias are very common in emergency medicine, and little is known about the long-term prognostic implications of troponin I levels in these patients. HYPOTHESIS This study aimed to investigate the correlation of cardiac troponin I (cTnI) levels and long-term prognosis in patients admitted to the emergency department (ED) with a primary diagnosis of tachyarrhythmia. METHODS A retrospective cohort study was conducted between January 2012 and December 2013, enrolling patients admitted to the ED with a primary diagnosis of tachyarrhythmia and having documented cTnI measurements. Clinical characteristics and 5-year all-cause mortality were analyzed. RESULTS Of a total of 222 subjects with a primary diagnosis of tachyarrhythmia, 73 patients had elevated levels of cTnI (32.9%). Patients with elevated cTnI levels were older and presented significantly more cardiovascular risk factors. At the 5-year follow-up, mortality was higher among patients with elevated cTnI levels (log-rank test P < 0.001). In the multivariable Cox regression analysis, elevated cTnI was an independent predictor of all-cause death (hazard ratio, 1.95, 95% confidence interval: 1.08-3.50, P = 0.026), in addition to age and prior heart failure. CONCLUSION Patients admitted to the ED with a primary diagnosis of tachyarrhythmia and high cTnI levels have higher long-term mortality rates than patients with low cTnI levels. cTnI is thus a biomarker with predictive capacity for mortality in late follow-up, conferring utility in the risk stratification of this population.

Prognostic implications of troponin I elevation in emergency department patients with tachyarrhythmia.

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Clinical Features and Prognosis of Patients with Acute and Chronic Myocardial Injury Admitted to the Emergency Department.

Prognostic implications of troponin I elevation in emergency department patients with tachyarrhythmia.