Association between Cardiologist Consultation and Mortality of Stable Patients with Elevated Cardiac Troponin at Admission.
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SUBMITTER: Oh AR
PROVIDER: S-EPMC8700380 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:PurposeThe importance of troponin elevation at stroke presentation remains uncertain. We aimed to assess whether baseline ultrasensitive Troponin I (hs-TnI) predicts cardiac complications and outcome in acute stroke patients.MethodStroke patients admitted within 6 h were consecutively enrolled from May 2013 to March 2014. Blood samples were taken at admission to determine hs-TnI by chemiluminescent microparticle immunoassay. hs-TnI > 34.2 pg/ml (male) and >15.6 pg/ml (female) were considered elevated. Complications during in-hospital stay and outcome at 90 days were prospectively recorded. Independent predictors of cardiac complications (heart failure and acute coronary syndrome) and mortality were determined by logistic regression. The additional predictive value of hs-TnI was evaluated by integrated discrimination improvement index. A subanalysis was performed after excluding patients with previous cardiac diseases.FindingsFrom 174 patients, 39(22%) had elevated hs-TnI, having these patients higher incidence of cardiac complications (57% versus 19%, p = 0.004). hs-TnI was an independent predictor of cardiac complications (OR = 16.1 (1.7-150.3)) together with diastolic blood pressure (OR = 0.92 (0.86-0.99)). Addition of hs-TnI to clinical variables significantly improved discrimination (IDI = 15.2% (7.8-22.7)). Subanalysis in patients without previous cardiac diseases showed similar results. Elevated hs-TnI was independently associated with 90 days mortality (OR = 3.6 (1.3-9.4)), but addition of hs-TnI to clinical data did not result in an increased discrimination.DiscussionThe present study confers hs-TnI a 2b level of evidence as a diagnostic tool to predict cardiac complications in stroke. Absence of serial hs-TnI measurements and limited sample size are the main weaknesses of the study.ConclusionPatients with elevated baseline hs-TnI showed a higher frequency of cardiac complications and a higher mortality. Measurement of hs-TnI in acute stroke might be useful to identify patients at a high risk of cardiac complications and death.
| S-EPMC6301235 | biostudies-literature
Project description:BackgroundElevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation.MethodsWe conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 ?g/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation.ResultsOf 133 patients followed for a median of 1.7 years, there were 38 deaths (58% non-cardiac, 39% cardiac, 3% unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95% CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95% CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death.ConclusionElevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.
| S-EPMC4226253 | biostudies-literature
Project description:BackgroundThe clinically meaningful cardiac troponin I (cTnI) threshold associated with the long-term prognosis in patients undergoing elective percutaneous coronary intervention (PCI) is still debated.ObjectiveTo assess the association between different thresholds for post-procedural cTnI and 5-year mortality.MethodsThe study included 4059 consecutive patients with normal baseline cTnI values who underwent elective PCI. The post-procedural cTnI level was measured at 8-48 h after PCI. The main study endpoints were 5-year all-cause mortality and cardiovascular mortality.ResultsA cTnI ≥5 times the upper reference limit (URL) as defined by the fourth universal definition of myocardial infarction (4th UDMI), ≥35 times as defined by the Academic Research Consortium-2 criteria, and ≥70 times as defined by the Society for Cardiovascular Angiography and Interventions (SCAI [2014]) was identified in 33%, 6.6%, and 3.3% of patients, respectively. During 5 years of follow-up, the all-cause mortality rate was 3.4% (n = 132) and the cardiovascular mortality rate was 2.0% (n = 77). Both all-cause mortality and cardiovascular mortality increased with higher peak cTnI, and were independently predicted by a cTnI ≥70 times the URL (adjusted hazard ratio [HR] 2.45, 95% confidence interval [CI] 1.20-5.02 and adjusted HR 3.17, 95% CI 1.31-7.67, respectively; reference, cTnI <1 × URL]. The SCAI (2014) threshold was significantly associated with 5-year cardiovascular mortality (adjusted HR 2.66, 95% CI 1.20-5.89; reference, cTnI, <70 × URL) and all-cause mortality (adjusted HR 2.23, 95% CI 1.16-4.30; reference, cTnI <70 × URL).ConclusionIn patients with normal pre-procedural cTnI who underwent elective PCI, a post-procedural cTnI ≥70 times the URL independently predicted 5-year all-cause and cardiovascular mortality. Therefore, only the SCAI (2014) post-procedural cTnI threshold was independently associated with long-term mortality.
| S-EPMC11002541 | biostudies-literature
Project description:BackgroundWhether individual cardiologist billings are associated with differences in ambulatory care management and clinical outcomes in patients with coronary artery disease (CAD) and heart failure (HF) remains poorly understood.MethodsWe conducted a population-based, retrospective cohort study of cardiologists who treat patients with CAD or HF using administrative claims data in Ontario, Canada. The primary exposure was cardiologist billing quintile. We then stratified median billing amounts into quintiles, from lowest (quintile 1) to highest billing physicians (quintile 5).ResultsThe main outcomes of interest were cardiac diagnostic and therapeutic procedures that occurred within 365 days of the index visit. Our 2 cohorts respectively consisted of 170,959 patients with CAD seen by 1 of 423 cardiologists and 56,262 HF patients seen by 1 of 413 cardiologists. CAD patients of higher-billing cardiologists had higher rates of echocardiograms (adjusted odds ratio [aOR], 1.65; 95% confidence interval [CI], 1.39 to 1.94 for quintile 5 vs quintile 2) and stress tests (aOR, 1.50; 95% CI, 1.28-1.75) at 1 year, with a similar pattern for HF patients of echocardiogram (aOR, 1.40; 95% CI, 1.23-1.59; P < 0.001) and stress test (aOR, 1.32; 95% CI, 1.15-1.51) use. CAD patients of cardiologists in quintile 1 had a higher mortality rate (aOR, 1.16; 95% CI, 1.03-1.31), and HF patients of cardiologists in billing quintile 4 had a lower hospitalization rate at 1 year (OR, 0.94; 95% CI, 0.89-0.99; P = 0.02).ConclusionsCardiac patients seen by the highest-billing cardiologists received more noninvasive cardiac testing compared with lower-billing cardiologists.
| S-EPMC8209405 | biostudies-literature
Project description:BACKGROUND: High-sensitivity cardiac troponin T (hs-cTnT) in serum is a useful marker of acute myocardial injury, yet information is limited in patients with chronic obstructive pulmonary disease. We aimed to explore the association between hs-cTnT levels and cardiac and pulmonary dysfunction in patients with stable chronic obstructive pulmonary disease and at-risk individuals. METHODS: We examined community-dwelling adults with/without chronic obstructive pulmonary disease, with a life-long smoking history, current symptoms of dyspnea during exertion, prolonged coughing, and/or sputum. Serum hs-cTnT concentrations were measured, and subjects underwent pulmonary function tests, high-resolution computed tomography of the chest, an echocardiogram, and a 6-minute walking test. RESULTS: Eighty-six stable patients were identified (mean age 65.5 years; predicted forced expiratory volume in 1 second [FEV1% predicted] 75.0%). Their overall mean hs-cTnT level was 0.008 ng/mL. Logarithmically transformed hs-cTnT levels significantly and positively correlated with age, smoking index, serum high-sensitivity C-reactive protein levels, right ventricle systolic pressure, low attenuation area percentage, and brain natriuretic peptide levels (range r=0.231-0.534, P=0.000 to P=0.042). Further, logarithmically transformed hs-cTnT values significantly and negatively correlated with forced vital capacity, FEV1% predicted, diffusion capacity, arterial oxygen tension, and 6-minute walking distance (range r= -0.482 to -0.377, P=0.000 to P=0.002). Multivariate analyses showed that hs-cTnT values varied independently according to the following three parameters: high-sensitivity C-reactive protein levels (B=0.157, ?=0.450, t=3.571, P=0.001), age (B=0.008, ?=0.352, t=2.789, P=0.009), and right ventricular systolic pressure (B=0.008, ?=0.280, t=2.202, P=0.035). CONCLUSION: Even in patients with stable chronic obstructive pulmonary disease, the serum troponin T concentration was controlled by at least three major factors, ie, systemic inflammation, advancing age, and right cardiac overload.
| S-EPMC4330031 | biostudies-literature
Project description:Object: Patients with aneurysmal subarachnoid hemorrhage (aSAH) have an increased incidence of cardiac events and short-term unfavorable neurological outcomes during the acute phase of bleeding. We studied whether troponin I elevation after ictus can predict future major adverse cardiac events (MACEs) and long-term neurological outcomes after 2 years. Methods: Consecutive aSAH patients within 3 days of bleeding were eligible for review from a prospective observational cohort (ClinicalTrials.gov Identifier: NCT04785976). Potential predictors of future MACEs and unfavorable long-term neurological outcomes were calculated by Cox and logistic regression analyses. Additional Kaplan-Meier curves were performed. Results: A total of 213 patients were enrolled with an average follow-up duration of 34.3 months. Individuals were divided into two groups: elevated cTnI group and unelevated cTnI group. By the last available follow-up, 20 patients had died, with an overall all-cause mortality rate of 9.4% and an annual all-cause mortality rate of 3.8%. Patients with elevated cTnI had a significantly higher risk of future MACEs (10.6 vs. 2.1%, p = 0.024, and 95% CI: 1.256-23.875) and unfavorable neurological outcomes at discharge, 3-month, 1-, 2-years, and last follow-up (p = 0.001, p < 0.001, p = 0.001, p < 0.001, and p < 0.001, respectively). In the Cox analysis for future MACE, elevated cTnI was the only independent predictor (HR = 5.980; 95% CI: 1.428-25.407, and p = 0.014). In the multivariable logistic analysis for unfavorable neurological outcomes, peak cTnI was significant (OR = 2.951; 95% CI: 1.376-6.323; p = 0.005). Kaplan-Meier analysis indicated that the elevated cTnI was correlated with future MACE (log-rank test, p = 0.007) and subsequent death (log-rank test, p = 0.004). Conclusion: cTnI elevation after aSAH could predict future MACEs and unfavorable neurological outcomes.
| S-EPMC8200557 | biostudies-literature
Project description:PurposeTo investigate the association of cardiac Troponin T (cTnT) with prognosis in critically ill patients without myocardial infarction.MethodsAdult patients admitted to the intensive care units (ICUs) of the Beth Israel Deaconess Medical Center between 2008 and 2019 who were free of myocardial infarction with a length of ICU stay ≥24 hours and available cTnT records within 24 hours before and after ICU admission were included. The association between cTnT on ICU admission and hospital mortality was evaluated by multivariable logistic regression analysis. The discrimination capacity of cTnT on ICU admission for predicting hospital mortality was examined by receiver operating characteristic (ROC) analysis.ResultsA total of 2960 patients were included. Elevated cTnT (>0.01 ng/mL) was observed in 2730 (92.23%) patients with a higher hospital mortality compared to normal cTnT (11.21% versus 7.39%, P=0.075). There was no statistically significant association between elevated cTnT on ICU admission and hospital mortality (adjusted odds ratio 1.50, 95% confidence interval (CI) 0.88-2.57). Poor discrimination capacity was found for cTnT on ICU admission to predict hospital mortality (area under the ROC curve 0.48, 95% CI 0.44-0.53).ConclusioncTnT on ICU admission has limited prognostic value in critically ill patients without myocardial infarction.
| S-EPMC8235952 | biostudies-literature
Project description:BACKGROUND:In most patients with stable coronary artery disease, plasma cardiac troponin T levels are below the limit of detection for the conventional assay. The distribution and determinants of very low circulating troponin T levels, as well as their association with cardiovascular events, in such patients are unknown. METHODS:We used a new, high-sensitivity assay to determine the concentration of cardiac troponin T in plasma samples from 3679 patients with stable coronary artery disease and preserved left ventricular function. Results of the assay were analyzed in relation to the incidence of cardiovascular events during a median follow-up period of 5.2 years. RESULTS:With the highly sensitive assay, concentrations of cardiac troponin T were at or above the limit of detection (0.001 microg per liter) in 3593 patients (97.7%) and at or above the 99th percentile for apparently healthy subjects (0.0133 microg per liter) in 407 patients (11.1%). After adjustment for other independent prognostic indicators, there was a strong and graded increase in the cumulative incidence of cardiovascular death (adjusted hazard ratio per unit increase in the natural logarithm of the troponin T level, 2.09; 95% confidence interval [CI], 1.60 to 2.74; P<0.001) and of heart failure (adjusted hazard ratio, 2.20; 95% CI, 1.66 to 2.90; P<0.001) in this study group. Increased risk associated with higher levels of troponin T was evident well below the limit of detection of conventional cardiac troponin T assays and below the 99th percentile of values in a healthy population. There was no association between troponin T levels as measured with the highly sensitive assay and the incidence of myocardial infarction (adjusted hazard ratio, 1.16; 95% CI, 0.97 to 1.40; P=0.11). CONCLUSIONS:After adjustment for other independent prognostic indicators, cardiac troponin T concentrations as measured with a highly sensitive assay were significantly associated with the incidence of cardiovascular death and heart failure but not with myocardial infarction in patients with stable coronary artery disease.
| S-EPMC2997684 | biostudies-literature
Project description:ObjectiveTo assess the distribution of high-sensitivity cardiac troponin T (hs-cTnT) concentrations in stable chronic obstructive pulmonary disease (COPD), and whether hs-cTnT is associated with pulmonary function.DesignProspectively designed, cross-sectional study.SettingOutpatient clinic of Norwegian teaching hospital and community-based setting.ParticipantsSample of 101 stable COPD patients from the hospital's outpatient clinic and 120 individuals derived from a random general population sample.Main outcomesRatio of hs-cTnT in stable COPD patients compared with references from the general population. Change in ratio of hs-cTnT per unit increase of relevant covariables.ResultsThe crude geometric means of circulating hs-cTnT in the cases and the references were 7.75 and 3.01 ng/l, respectively (p < 0.001); that is, a relative ratio of 2.57 (95% CI 2.05 to 3.23). After adjustment for relevant confounders, this ratio was moderately attenuated to 1.65 (1.31-2.08). In the total study cohort, as well as among stable COPD patients, we found a significant positive association between hs-cTnT and interleukin-6 concentrations (p < 0.001) and the presence of pathologic Q waves (p = 0.023). Among stable COPD patients, one quartile increase in forced expiratory volume 1 was associated with a 39% decrease in hs-cTnT and patient category (Global Initiative of Obstructive Lung Disease classification 2011) was positively associated with hs-cTnT (p trend < 0.001) after multivariate adjustment.ConclusionsStable COPD is independently associated with higher hs-cTnT compared with randomly drawn subjects from the general population. In patients with stable COPD, higher hs-cTnT seems to be associated with immune activation and the severity of the disease.
| S-EPMC3595144 | biostudies-literature
Project description:BackgroundCardiac troponin concentrations are used to identify patients who would benefit from urgent revascularization for acute coronary syndromes. We hypothesized that they might be used in patients with stable ischemic heart disease to identify those at high risk for cardiovascular events who might also benefit from prompt coronary revascularization.MethodsWe measured the cardiac troponin T concentration at baseline with a high-sensitivity assay in 2285 patients who had both type 2 diabetes and stable ischemic heart disease and were enrolled in the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes trial. We tested for an association between the troponin T concentration and a composite end point of death from cardiovascular causes, myocardial infarction, or stroke; we then evaluated whether random assignment to prompt revascularization reduced the rate of the composite end point in patients with an abnormal troponin T concentration (≥14 ng per liter) as compared with those with a normal troponin T concentration (<14 ng per liter).ResultsOf the 2285 patients, 2277 (99.6%) had detectable (≥3 ng per liter) troponin T concentrations and 897 (39.3%) had abnormal troponin T concentrations at baseline. The 5-year rate of the composite end point was 27.1% among the patients who had had abnormal troponin T concentrations at baseline, as compared with 12.9% among those who had had normal baseline troponin T concentrations. In models that were adjusted for cardiovascular risk factors, severity of diabetes, electrocardiographic abnormalities, and coronary anatomy, the hazard ratio for the composite end point among patients with abnormal troponin T concentrations was 1.85 (95% confidence interval [CI], 1.48 to 2.32; P<0.001). Among patients with abnormal troponin T concentrations, random assignment to prompt revascularization, as compared with medical therapy alone, did not result in a significant reduction in the rate of the composite end point (hazard ratio, 0.96; 95% CI, 0.74 to 1.25).ConclusionsThe cardiac troponin T concentration was an independent predictor of death from cardiovascular causes, myocardial infarction, or stroke in patients who had both type 2 diabetes and stable ischemic heart disease. An abnormal troponin T value of 14 ng per liter or higher did not identify a subgroup of patients who benefited from random assignment to prompt coronary revascularization. (Funded by the National Institutes of Health and Roche Diagnostics; BARI 2D ClinicalTrials.gov number, NCT00006305.).
| S-EPMC4627639 | biostudies-literature