An early diagnosis of atherosclerosis, particularly in subclinical status, can play a remarkable role in reducing mortality and morbidity. Because of coronary artery calcification (CAC) nature in radiation exposure, finding biomarkers associated with CAC could be useful in identifying individuals at high risk of CAC score. In this review, we focused on the association of cardiac troponins (hs-cTns) and CAC to achieve insight into the pathophysiology of CAC. In October 2022, we systematically searched Web of Science, Scopus, PubMed, and Embase databases to find human observational studies which have investigated the association of CAC with cardiac troponins. To appraise the included articles, we used the Newcastle Ottawa scale (NOS). Out of 520 records, 10 eligible studies were included. Based on findings from longitudinal studies and cross-sectional analyses, troponin T and I were correlated with occurrence of CAC and its severity. Two of the most important risk factors that affect the correlation between hs-cTns serum levels and CAC were age and gender. The elevation of cardiac troponins may affect the progression of CAC and future cardiovascular diseases. Verifying the association between cardiac troponins and CAC may lead to identify individuals exposed to enhanced risk of cardiovascular disease (CVD) complications and could establish innovative targets for pharmacological therapy.

Hypertrophic cardiomyopathy (HCM) is characterized by unexplained left ventricular hypertrophy and is classically caused by pathogenic or likely pathogenic variants (P/LP) in genes encoding sarcomere proteins. Not all subclinical variant carriers will manifest clinically overt disease because penetrance (proportion of sarcomere or sarcomere-related P/LP variant carriers who develop disease) is variable, age dependent, and not reliably predicted.
A systematic search of the literature was performed. We used random-effects generalized linear mixed model meta-analyses to contrast the cross-sectional prevalence and penetrance of sarcomere or sarcomere-related genes in 2 different contexts: clinically-based studies on patients and families with HCM versus population or community-based studies. Longitudinal family/clinical studies were additionally analyzed to investigate the rate of phenotypic conversion from subclinical to overt HCM during follow-up.
In total, 455 full-text manuscripts and articles were assessed. In family/clinical studies, the prevalence of sarcomere variants in patients diagnosed with HCM was 34%. The penetrance across all genes in nonproband relatives carrying P/LP variants identified during cascade screening was 57% (95% CI, 52%-63%), and the mean age at HCM diagnosis was 38 years (95% CI, 36%-40%). Penetrance varied from ≈32% for MYL3 (myosin light chain 3) to ≈55% for MYBPC3 (myosin-binding protein C3), ≈60% for TNNT2 (troponin T2) and TNNI3 (troponin I3), and ≈65% for MYH7 (myosin heavy chain 7). Population-based genetic studies demonstrate that P/LP sarcomere variants are present in the background population but at a low prevalence of <1%. The penetrance of HCM in incidentally identified P/LP variant carriers was also substantially lower at ≈11%, ranging from 0% in Atherosclerosis Risk in Communities to 18% in UK Biobank. In longitudinal family studies, the pooled phenotypic conversion across all genes was 15% over an average of ≈8 years of follow-up, starting from a mean of ≈16 years of age. However, short-term gene-specific phenotypic conversion varied between ≈12% for MYBPC3 and ≈23% for MYH7.
The penetrance of P/LP variants is highly variable and influenced by currently undefined and context-dependent genetic and environmental factors. Additional longitudinal studies are needed to improve our understanding of true lifetime penetrance in families and in the community and to identify drivers of the transition from subclinical to overt HCM.

BACKGROUND: Patients with end-stage renal disease (ESRD) have an increased risk of cardiovascular disease, but interpreting cardiac troponin is difficult in this population. The effect of renal replacement therapy (RRT) is important to consider when interpreting serial cardiac troponin T (cTnT) results for patients with ESRD suspected of acute coronary syndrome (ACS). The aim of this systematic review is to answer how low-flux hemodialysis (LF-HD), high-flux hemodialysis (HF-HD), and hemodiafiltration (HDF) affect the blood concentration of high-sensitive cardiac troponin T (hs-cTnT).
METHODS: Several databases were searched and identified records were evaluated independently by two of the authors. Pre- and postdialysis hs-cTnT concentrations together with other relevant data were extracted from the included studies. The quality (potential bias and applicability issues) were assessed for each of the included studies.
RESULTS: The literature search identified 2,540 records and 15 studies were included. The relative pre- to postdialysis change of hs-cTnT varied from -41 to 29%. LF-HD increased the hs-cTnT concentration with relative changes between 2 and 17%. HDF decreased the concentration with relative changes from -41% to -9%. Both increases and decreases were seen for HF-HD (-16% to 12%).
CONCLUSIONS: In this systematic review, we found LF-HD to increase the hs-cTnT concentration and HDF to decrease the concentration. Results for HF-HD and unspecified HD are more heterogeneous. Because of the differences between the included studies, a meta-analysis was not meaningful. This systematic review can help with the assessment of patients with ESRD suspected of ACS in relation to hemodialysis/HDF treatment.

BACKGROUND: This study aimed to demonstrate potential measures to discern interference and establish an algorithm for identifying interference in an hs-cTnT assay with a clinical discrepancy.
METHODS: Laboratory error and disease factors were first excluded. Then, a serial dilution test, polyethylene glycol (PEG) precipitation, and heterophile antibody blocking reagents (HBRs) were performed to confirm the interference substance. In addition, high-speed centrifugation and western blot were tried.
RESULTS: The sample diluted linearly (R2 = 0.9966). However, there was a dramatic reduction in the concentration of hs-cTnT concentration to a normal level after both PEG precipitation and HBR1 treatment. The results were inconclusive in high-speed centrifugation and western blot assay.
CONCLUSIONS: This study elucidated a heterophile antibody interference in measurement of hs-cTnT alone on a Roche analyzer.

Biosensors are valuable tools for the detection of biological species, including cells, pathogens, proteins, and other biological molecules. Biosensing devices integrated with microfluidics not only allow for easier sample preparation, portability, and reduced detection time and cost but also offer unique features such as label-free detection and improved sensitivity. Cardiovascular diseases (CVDs), particularly acute myocardial infarction, which is considered one of the main causes of death, are currently diagnosed by electrocardiography (ECG), which has been proven to be inadequate. To overcome the limitations of ECG, the efficient detection of cardiac biomarkers and specifically the measurement of cardiac troponins (cTnT and cTnI) are suggested. This review aims to expound on microfluidics, the most recent materials to develop these devices, and their application in medical diagnosis, particularly in CVD detection. Moreover, we will explore some of the prevalent and last readout methods to investigate in-depth electrochemical label-free detection methods for CVDs, primarily based on voltammetry and electrochemical impedance spectroscopy, with the main focus on structural details.

BACKGROUND: Marathon running is an extreme sport with a distance of about 42 kilometers. Its relationship to high-sensitivity cardiac troponin (hs-cTn) remains controversial.
OBJECTIVE: As the gold standard for detecting myocardial injury, the trends of hs-cTn before and after a marathon were investigated and analyzed.
METHODS: A literature search was conducted in PubMed, EMBASE, and Cochrane Library databases by combing the keywords marathon and troponin, and studies regarding high-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT) concentrations before and after marathon running (not for half-marathon and ultra-marathon) were included. \"Quality Assessment Tool for Before-After (Pre-Post) Studies With No Control Group\" were used to assess the risk of bias. Statistical analysis was performed using Review Manager, presenting data as mean values and 95% confidence intervals (CIs). Sensitivity analysis and subgroup analysis were performed if there was high heterogeneity among studies based on I2 statistic.
RESULTS: A total of 13 studies involving 824 marathoners were included in this systematic review and meta-analysis. Both hs-cTnI (MD 68.79 ng/L, [95% CI 53.22, 84.37], p< 0.001) and hs-cTnT (MD 42.91 ng/L, [95% CI 30.39, 55.43], p< 0.001) were elevated after running a marathon, but the concentration of hs-cTnT returned to baseline after 72 to 96 h post-race (MD 0.11 ng/L, [95% CI -1.30, 1.52], p= 0.88). The results of subgroup analysis demonstrated that the 99th percentile upper reference limit of hs-cTnT might be the source of heterogeneity.
CONCLUSIONS: The concentrations of hs-cTnI and hs-cTnT were increased after marathon running, but the change of hs-cTnT is usually not seen as irreversible myocardial injury.

The diagnosis of cardiac contusion, caused by blunt chest trauma, remains a challenge due to the non-specific symptoms it causes and the lack of ideal tests to diagnose myocardial damage. A cardiac contusion can be life-threatening if not diagnosed and treated promptly. Several diagnostic tests have been used to evaluate the risk of cardiac complications, but the challenge of identifying patients with contusions nevertheless remains.
To evaluate the accuracy of diagnostic tests for detecting blunt cardiac injury (BCI) and its complications, in patients with severe chest injuries, who are assessed in an emergency department or by any front-line emergency physician.
A targeted search strategy was performed using Ovid MEDLINE and Embase databases from 1993 up to October 2022. Data on at least one of the following diagnostic tests: electrocardiogram (ECG), serum creatinine phosphokinase-MB level (CPK-MB), echocardiography (Echo), Cardiac troponin I (cTnI) or Cardiac troponin T (cTnT). Diagnostic tests for cardiac contusion were evaluated for their accuracy in meta-analysis. Heterogeneity was assessed using the I2 and the QUADAS-2 tool was used to assess bias of the studies.
This systematic review yielded 51 studies (n = 5,359). The weighted mean incidence of myocardial injuries after sustaining a blunt force trauma stood at 18.3% of cases. Overall weighted mean mortality among patients with blunt cardiac injury was 7.6% (1.4-36.4%). Initial ECG, cTnI, cTnT and transthoracic echocardiography TTE all showed high specificity (> 80%), but lower sensitivity (< 70%). TEE had a specificity of 72.1% (range 35.8-98.2%) and sensitivity of 86.7% (range 40-99.2%) in diagnosing cardiac contusion. CK-MB had the lowest diagnostic odds ratio of 3.598 (95% CI: 1.832-7.068). Normal ECG accompanied by normal cTnI showed a high sensitivity of 85% in ruling out cardiac injuries.
Emergency physicians face great challenges in diagnosing cardiac injuries in patients following blunt trauma. In the majority of cases, joint use of ECG and cTnI was a pragmatic and cost-effective approach to rule out cardiac injuries. In addition, TEE may be highly accurate in identifying cardiac injuries in suspected cases.

This systematic review and meta-analysis aimed to compare the effects of high-intensity interval exercise (HIIE) with different recovery modes versus moderate-intensity continuous exercise (MICE) on cardiac troponin (cTn) elevation.
A literature search was conducted in four databases: Scopus, PubMed, EBSCO and Web of Science from January 2010 to June 2022. The articles were screened, evaluated for quality before data were extracted. The review protocol was registered at PROSPERO (CRD42021245649). Standardized mean differences (SMD) of peak cTn were analyzed with a 95% confidence interval (95% CI) using Revman 5.4 software.
Six studies satisfied the inclusion criteria with a total of 92 and 79 participants for HIIE and MICE, respectively. Overall, there was no significant difference between HIIE and MICE in the elevation of cardiac troponin T (SMD: 0.41 [95% CI [-0.21, 1.03]], p = 0.20, I 2 = 77%, p for heterogeneity <0.01). In subgroup analysis, HIIE with passive recovery elicits greater release of cardiac troponin T than MICE (SMD: 0.85 [95% CI [0.44, 1.27]], p < 0.01, I 2 = 32%, p for heterogeneity = 0.22). Changes of cardiac troponin T (SMD: 0.41 [95% CI [-0.21, 1.03]], p = 0.20, I 2 = 77%, p for heterogeneity < 0.01) after HIIE with active recovery were not significantly different from those of MICE.
There was no significant difference between HIIE and MICE in the elevation of cardiac troponin T. However, HIIE with passive recovery elicited more cardiac troponin T elevation than MICE, which should be considered when developing exercise programs.

Cardiac troponin I and T are both used for diagnosing myocardial infarction (MI) after coronary artery bypass grafting (CABG), also known as type 5 MI (MI-5). Different MI-5 definitions have been formulated, using multiples of the 99th percentile upper reference limit (10×, 35×, or 70× URL), with or without supporting evidence. These definitions are arbitrarily chosen based on conventional assays and do not differentiate between troponin I and T. We therefore investigated the kinetics of high-sensitivity cardiac troponin I (hs-cTnI) and T (hs-cTnT) following CABG.
A systematic search was applied to MEDLINE and EMBASE databases including the search terms \"coronary artery bypass grafting\" AND \"high-sensitivity cardiac troponin.\" Studies reporting hs-cTnI or hs-cTnT on at least 2 different time points were included. Troponin concentrations were extracted and normalized to the assay-specific URL.
For hs-cTnI and hs-cTnT, 17 (n = 1661 patients) and 15 studies (n = 2646 patients) were included, respectively. Preoperative hs-cTnI was 6.1× URL (95% confidence intervals: 4.9-7.2) and hs-cTnT 1.2× URL (0.9-1.4). Mean peak was reached 6-8 h postoperatively (126× URL, 99-153 and 45× URL, 29-61, respectively). Subanalysis of hs-cTnI illustrated assay-specific peak heights and kinetics, while subanalysis of surgical strategies revealed 3-fold higher hs-cTnI than hs-cTnT for on-pump CABG and 5-fold for off-pump CABG.
Postoperative hs-cTnI and hs-cTnT following CABG surpass most current diagnostic cutoff values. hs-cTnI was almost 3-fold higher than hs-cTnT, and appeared to be highly dependent on the assay used and surgical strategy. There is a need for assay-specific hs-cTnI and hs-cTnT cutoff values for accurate, timely identification of MI-5.

Ventricular noncompaction (VNC) is a cardiomyopathy characterized by overdeveloped ventricular trabeculaes and deep recess, which has been rarely reported.
A 29-year-old Chinese pregnant woman with no obvious fetal abnormality in regular prenatal examination during first and second trimester. However, at 32 weeks of gestation, both obstetric growth scan and fetal echocardiogram revealed an enlarged heart with grid-like changes at the apical region. Eventually, the genetic and autopsy findings indicated the deceased infant with VNC.
Isolated VNC could be detected prenatally, even during the late pregnancy. Fetuses suspected of VNC should be offered genetic tests.