UNASSIGNED: To estimate the effectiveness and cost-effectiveness of a high-sensitivity troponin I (hsTnI) guided cardiovascular risk assessment program in women in Croatia.
UNASSIGNED: An observational study of a voluntary program for cardiovascular disease (CVD) risk assessment in women aged above 45 years with no specific symptoms, no confirmed or known coronary artery disease was conducted (WHP). Participants were stratified into three categories according to their hsTnI level. Subjects in the moderate or high-risk class were referred to cardiac work-up and invasive cardiovascular investigation as appropriate. Study information were applied to a discrete-event simulation model to estimate the cost-effectiveness of WHP against current practice. The number of CVD events and deaths, costs, and quality-adjusted life years (QALY) were assessed over 10 years from a societal perspective.
UNASSIGNED: Of 1034 women who participated in the program, 921 (89.1%), 100 (9.7%), and 13 (1.3%) subjects fall into the low, moderate, and high-risk class. Of 26 women referred for angiography, significant coronary artery disease (CAD) was diagnosed in 12 women (46.1%). WHP gained 15.8 (95%CI 12.8; 17.2) QALYs per 1000 subjects, increased costs by 490€ (95%CI 487; 500), decreased CVD-related mortality by 40%. At a willingness-to-pay threshold of 45,000 €/QALY, WHP was cost-effective with a probability of 90%. Model results were most sensitive to utility weights and cost of medical prevention.
UNASSIGNED: Assessing the cardiovascular risk in asymptomatic women with hsTnI and guiding those at higher risk to further cardiac testing, identified individuals with CAD, could reduce CVD related burden, and would be cost-effective.

Numerous studies have been published suggesting that troponin levels are related to adverse outcomes in chronic cardiac and non-cardiac conditions. Our study investigated whether troponin levels gathered from unselected blood samples taken during outpatient care are associated with adverse outcomes in a population with stable coronary artery disease. In a cohort of 949 patients with stable coronary artery disease, an average age of 67.5 ± 9.5 years, 69.5% male, 52.1% diabetics, 51.6% with previous myocardial infarction, and 57.9% with triple-vessel disease, 21.7% of patients encountered new events during an average period of monitoring of 2.07 ± 0.81 years. Troponin I/99th percentile categorized into tertiles emerged as an independent predictor of death and combined events risk (hazard ratio: 2.02 (1.13-3.60), p = 0.017; 2.30 (1.37-3.88, p = 0.002, respectively). A troponin ratio > 0.24 was able to identify 53.3% of patients at risk of death and heart failure hospitalization. In patients with stable coronary artery disease who are adherent to treatment, troponin levels are independently associated with death and heart failure hospitalization in a medium-term follow-up.

UNASSIGNED: Acute Myocardial injury defined by increased troponin I level is associated with poor in-hospital outcomes and cardiovascular complications in patients with COVID-19. The current study was designed to determine the implications and clinical outcome of myocardial injury in COVID-19.
UNASSIGNED: This retrospective study included hospitalized COVID-19 patients. Myocardial injury was defined by high sensitivity Troponin I (hs-TNI)≥26ng/l. Cardiac biomarkers, inflammatory markers and clinical data were systemically collected and analyzed. Hazard ratio for in-hospital mortality and logistic regression for predictors of acute myocardial injury were analyzed.
UNASSIGNED: Of the 1821 total patients with COVID-19, 293(16.09%) patients died and 1528 (83.91%) patients survived. Patients who died had significantly higher association with presence of cardiovascular risk factors, severe CTSS ( CT severity score ) and myocardial injury as compared to survived group. 628 (34.5%) patients had evidence of myocardial injury and they had statistically significant association with cardiovascular risk factors, in-hospital mortality, procalcitonin; higher hospital, and ICCU stay. We found significant hazard ratio of diabetes (HR=2.66, (CI:1.65-4.29)), Severe CT score (HR=2.81, (CI:1.74-4.52)), hs-TNI≥26 ng/l (HR=4.68, (CI:3.81-5.76)) for mortality. Severe CTSS score (OR=1.95, CI: 1.18-3.23, P=0.01) and prior CVD history (OR=1.65, CI:1.00-2.73, P=0.05) were found significant predictors of myocardial injury in regression analysis.
UNASSIGNED: Almost one third of hospitalized patients had evidence of acute myocardial injury during hospitalization. Acute myocardial injury is associated with higher hospital and ICCU stay, mortality, higher in-hospital infection which indicates more severe disease and the poor in-hospital outcomes.

The primary objective was to determine rapid rule-out (RRO) criteria for the outcome of myocardial infarction (MI) using the Beckman Coulter Access high-sensitivity cardiac troponin I (hs-cTnI) assay. Secondary objectives were to explore cut-points for rapid rule-in (RRI) and amount of change at 3-h (3-h delta) indicative of MI.
A retrospective study included ED patients with suspected MI between June and September 2019. hs-cTnI levels were performed at baseline and after 3 h. The performance benchmark for RRO criteria was a negative predictive value (NPV) for MI with a lower 95% confidence limit >99%, and for RRI and 3-h delta cut-points was a positive predictive value (PPV) for MI >70%. Delta calculation required rising hs-cTnI levels, with at least one above the 99th percentile of the upper reference limit. Analyses utilised receiver operating characteristic (ROC) curves and contingency tables.
Baseline hs-cTnI levels from 935 patients were available for RRO analyses. Of tested criteria, baseline hs-cTnI <6 ng/L (females) or <11 ng/L (males) plus symptom onset >2 h met the performance benchmark (NPV: 100% [95% confidence interval 99-100]). hs-cTnI levels were available for RRI and 3-h delta analyses from 935 and 52 patients, respectively. A 3-h delta cut-point >35 ng/L met the performance benchmark (PPV: 81% [95% confidence interval 58-95]) but no RRI cut-point did so.
For the Beckman Coulter Access hs-cTnI assay, RRO criteria of baseline hs-cTnI <6 ng/L (females) or <11 ng/L (males) plus symptom onset >2 h met our performance benchmark. A 3-h delta cut-point >35 ng/L met the performance benchmark, but poor precision means further adequately powered research is required.

UNASSIGNED: The aim of the present study is to assess multimodality imaging findings according to systemic biomarkers, high-sensitivity troponin I (hsTnI) and B-type natriuretic peptide (BNP) levels, in low-flow, low-gradient aortic stenosis (LFLG-AS).
UNASSIGNED: Elevated levels of BNP and hsTnI have been related with poor prognosis in patients with LFLG-AS.
UNASSIGNED: Prospective study with LFLG-AS patients that underwent hsTnI, BNP, coronary angiography, cardiac magnetic resonance (CMR) with T1 mapping, echocardiogram and dobutamine stress echocardiogram. Patients were divided into 3 groups according to BNP and hsTnI levels: Group 1 (n = 17) when BNP and hsTnI levels were below median [BNP < 1.98 fold upper reference limit (URL) and hsTnI < 1.8 fold URL]; Group 2 (n = 14) when BNP or hsTnI were higher than median; and Group 3 (n = 18) when both hsTnI and BNP were higher than median.
UNASSIGNED: 49 patients included in 3 groups. Clinical characteristics (including risk scores) were similar among groups. Group 3 patients had lower valvuloarterial impedance (P = 0.03) and lower left ventricular ejection fraction (P = 0.02) by echocardiogram. CMR identified a progressive increase of right and left ventricular chamber from Group 1 to Group 3, and worsening of left ventricular ejection fraction (EF) (40 [31-47] vs. 32 [29-41] vs. 26 [19-33]%; p < 0.01) and right ventricular EF (62 [53-69] vs. 51 [35-63] vs. 30 [24-46]%; p < 0.01). Besides, there was a marked increase in myocardial fibrosis assessed by extracellular volume fraction (ECV) (28.4 [24.8-30.7] vs. 28.2 [26.9-34.5] vs. 31.8 [28.9-35.5]%; p = 0.03) and indexed ECV (iECV) (28.7 [21.2-39.1] vs. 28.8 [25.4-39.9] vs. 44.2 [36.4-51.2] ml/m2, respectively; p < 0.01) from Group 1 to Group 3.
UNASSIGNED: Higher levels of BNP and hsTnI in LFLG-AS patients are associated with worse multi-modality evidence of cardiac remodeling and fibrosis.

Background and Objectives: In patients with acute heart failure (AHF), there is no definite evidence on the relationship between high-sensitivity cardiac troponin (hs-cTnI) and the left ventricular ejection fraction (LVEF) comparing the reduced and preserved EF conditions. Materials and Methods: Between January and April 2022, we retrospectively analyzed the data from 386 patients admitted to the emergency departments (ED) of five hospitals in Rome, Italy, for AHF. The criteria for inclusion were a final diagnosis of AHF; a cardiac ultrasound and hs-cTnI evaluations in the ED; and age > 18 yrs. We excluded patients with acute coronary syndrome (ACS). Based on echocardiography and hs-cTnI evaluations, the patients were grouped for (1) preserved (HFpEF) or (2) reduced LVEF (HFrEF) and a a) negative (within the normal range value) or b) positive (above the normal range value) of hs-cTnI, respectively. Results: There was a significant negative relationship between a positive test for hs-cTnI and LVEF. When compared to the group with a negative hs-cTnI test, the patients with a positive test, both from the HFpEF and HFrEF subgroups, were significantly more likely to have an adverse outcome, such as being admitted to the intensive care unit (ICU) or dying in the ED. Moreover, a reduced ejection fraction was linked with a final disposition to a higher level of care. Conclusions: In patients admitted to the ED for AHF without ACS, there is a negative relationship between hs-cTnI and a reduced LVEF, although a significant percentage of patients with a preserved LVEF also resulted to have high levels of hs-cTnI. In the absence of ACS, hs-cTnI seems to be a reliable biomarker of myocardial injury in AHF in the ED and should be considered as a risk stratification parameter for these subjects regardless of the left ventricular function. Further larger prospective studies are needed to confirm these preliminary data.

OBJECTIVE: Atrial fibrillation (AF) is becoming increasingly common. Traditional cardiovascular risk factors (CVRF) do not explain all AF cases. Blood-based biomarkers reflecting cardiac injury such as high-sensitivity troponin I (hsTnI) may help close this gap.
METHODS: We investigated the predictive ability of hsTnI for incident AF in 45,298 participants (median age 51.4 years, 45.0% men) across European community cohorts in comparison to CVRF and established biomarkers (C-reactive protein, N-terminal pro B-type natriuretic peptide).
RESULTS: During a median follow-up of 7.7 years, 1734 (3.8%) participants developed AF. Those in the highest hsTnI quarter (≥4.2 ng/L) had a 3.91-fold (95% confidence interval (CI) 3.30, 4.63; p < .01) risk for developing AF compared to the lowest quarter (<1.4 ng/L). In multivariable-adjusted Cox proportional hazards models a statistically significant association was seen between hsTnI and AF (hazard ratio (HR) per 1 standard deviation (SD) increase in log10(hsTnI) 1.08; 95% CI 1.01, 1.16; p = .03). Inclusion of hsTnI did improve model discrimination (C-index CVRF 0.811 vs. C-index CVRF and hsTnI 0.813; p < .01). Higher hsTnI concentrations were associated with heart failure (HR per SD 1.37; 95% CI 1.12, 1.68; p < .01) and overall mortality (HR per SD 1.24; 95% CI 1.09, 1.41; p < .01).
CONCLUSIONS: hsTnI as a biomarker of myocardial injury does not improve prediction of AF incidence beyond classical CVRF and NT-proBNP. However, it is associated with the AF-related disease heart failure and mortality likely reflecting underlying subclinical cardiovascular impairment.

UNASSIGNED: Prior studies support the utility of high sensitivity troponin I (hsTnI) for cardiovascular disease (CVD) risk stratification among asymptomatic populations; however, only two prior studies examined women separately. The association between hsTnI and breast arterial calcification is unknown.
UNASSIGNED: Cohort study of 2896 women aged 60-79 years recruited after attending mammography screening between 10/2012 and 2/2015. BAC status (presence versus absence) and quantity (calcium mass mg) was determined using digital mammograms. Pre-specified endpoints were incident coronary heart disease (CHD), ischemic stroke, heart failure and its subtypes and all CVD.
UNASSIGNED: After 7.4 (SD = 1.7) years of follow-up, 51 CHD, 30 ischemic stroke and 46 heart failure events were ascertained. At a limit of detection of 1.6 ng/L, 98.3 of the cohort had measurable hsTnI concentration. HsTnI in the 4-10 ng/L range were independently associated of CHD (adjusted hazard ratio[aHR] = 2.78; 95% CI, 1.48-5.22; p = 0.002) and all CVD (aHR = 2.06; 95% CI, 1.37-3.09; p = 0.0005) and hsTnI over 10 ng/L was independently associated with CHD (aHR = 4.75; 95% CI, 1.83-12.3; p = 0.001), ischemic stroke (aHR = 3.81; 95% CI, 1.22-11.9; p = 0.02), heart failure (aHR = 3.29; 95% CI, 1.33-8.13; p = 0.01) and all CVD (aHR = 4.78; 95% CI, 2.66-8.59; p < 0.0001). No significant association was found between hsTnI and BAC. Adding hsTnI to a model containing the Pooled Cohorts Equation resulted in significant and clinical important improved calibration, discrimination (Δ Cindex = 6.5; p = 0.02) and reclassification (bias-corrected clinical NRI = 0.18; 95% CI, -0.13-0.49 after adding hsTnI categories).
UNASSIGNED: Our results support the consideration of hsTnI as a risk enhancing factor for CVD in asymptomatic women that could drive preventive or therapeutic decisions.

Background and Objectives: We aimed to compare the time to diagnosis for acute coronary syndromes using high-sensitivity troponin I (hsTnI) and conventional troponin I (TnI) in patients presenting to the emergency department (ED) with chest pain. Materials and Methods: This was an observational prospective study involving patients presenting to the ED of Sant’Andrea Hospital University la Sapienza in Rome (Italy) with chest pain from January to December 2014. Serum troponin was drawn at presentation, and at 3, 6, 9, and/or 12 h if clinically indicated. Depending on date of recruitment, patients had either hsTnI (Abbott Laboratories) or TnI (Abbott Laboratories) performed. The primary endpoint was the time to diagnosis at index visit. Results: A total of 1059 patients were recruited, (673 [63.6%] male, median age 60 years [interquartile range 49−73 years]), out of whom 898 (84.8%) patients were evaluated with hsTnI and 161 (15.2%) with TnI. A total of 393 (37.1%) patients had the diagnosis of acute coronary syndrome in ED. The median time to diagnosis for those evaluated with TnI was 400 min, IQR 120−720 min, while the use of hsTnI led to a significantly shorter time to diagnosis (median 200 min, IQR 100−200 min, p < 0.001). Conclusions: This study confirms that in patients presenting to the emergency department with chest pain, the use of hsTnI is associated with a reduced time to ruling in/out ACS, and, consequently, hsTnI should be routinely used over TnI for more rapid identification of ACS with benefits for patients and related costs.

Early recognition and risk stratification of cardiovascular events are necessary in patients after ischemic stroke. Recent evidence suggests that elevated high-sensitive cardiac troponin is a predictor of mortality and vascular events. Therefore, we aimed to explore the prognostic role of high-sensitive cardiac troponin I (hs-TnI) on mortality and cardiovascular outcomes in patients after ischemic stroke.
From August 2014 to July 2017, 1,506 patients with acute ischemic stroke were pulled consecutively in a retrospective single-center registry. Of these, 1,019 patients were selected and classified into the elevated or non-elevated hs-TnI groups according to hs-TnI level of 99th percentile upper reference limit (URL) at the time of admission for ischemic stroke. The primary outcome was a major adverse cardiac and cerebrovascular event (MACCE) during follow-up.
Among 1,019 patients, 708 patients were non-elevated hs-TnI group (<99th percentile URL of hs-TnI) and 311 patients were elevated hs-TnI group (≥99th percentile URL of hs-TnI). The median follow-up period was 22.5 (interquartile range 5.0-38.8) months. In a multivariable Cox regression model, the elevated hs-TnI group has a higher risk of MACCE (adjusted hazard ratio [HR]: 3.12; 95% confidence interval [CI]: 2.33-4.17; p < 0.01), all-cause mortality (adjusted HR: 4.15; 95% CI: 2.47-6.99; p < 0.01) and readmission caused by coronary revascularization (adjusted HR: 3.12; 95% CI: 1.41-6.90; p < 0.01), heart failure (adjusted HR: 2.76; 95% CI: 1.38-5.51; p < 0.01), and stroke (adjusted HR: 1.73; 95% CI: 1.07-2.78; p = 0.02) compared with the non-elevated hs-TnI group.
Elevated hs-TnI is independently associated with higher mortality and cardiac and cerebrovascular events in patients with ischemic stroke and may serve as a valuable prognostic factor in management after ischemic stroke.