Cardiac troponins in suspected acute coronary syndrome: a meta-analysis of published trials.

We performed a meta-analysis of published trials to determine the predictive value of cardiac troponin I (cTnI) and T (cTnT) levels for adverse events (death and myocardial infarction) in acute coronary syndrome without ST elevation (ACS). The accumulated odds ratio (OR) for adverse events (30 days) in ACS with elevated cTnI (n = 5,759) and cTnT (n = 5,483) was 4.9 (95% confidence interval, CI, 3.9-6.2) and 4.6 (95% CI 3.8-5.5), respectively. Trials that mandated timed serum sampling (6 or more hours after symptom onset) had an improved predictive value for elevated cTnI (n = 2,807, OR 8.8; 95% CI 5.9-13.2) and cTnT (n = 1,990, OR 8.5; 95% CI 5.9-12.5). In conclusion, cTnI and cTnT provide similar information in ACS. The risk of adverse events is 4-fold higher in patients with suspected ACS and elevated serum cTn. For patients with an elevated timed (6-hour) sample the risk is over 8-fold higher.     

Prognostic value of troponins in patients with non-ST-segment elevation acute coronary syndromes and chronic kidney disease

BACKGROUND: The prognostic value of cardiac troponins (cTn) in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) and chronic kidney disease (CKD) is debated. HYPOTHESIS: We tested the performance of cTnI and cTnT for risk stratification in patients with CKD and evaluated the prognostic significance of cTnI and cTnT elevations by their magnitude across the range of CKD severity. METHODS: We examined correlations among cTn elevation, CKD, and in-hospital mortality in 31,586 high-risk patients with NSTE ACS included in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress ADverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines initiative (CRUSADE). Cardiac tropinins I and T levels were categorized as ratios of each site's upper limit of normal (ULN) for myocardial necrosis: normal (cTn ratio < or =1 x ULN), mild (cTn ratio > 1-3 x ULN), and major (cTn ratio > 3 x ULN) elevation. Estimated glomerular filtration rate (eGFR) was calculated using the abbreviated Modification of Diet in Renal Disease equation. Stages of CKD were categorized as normal to mild (eGFR > 60 mL/min), moderate (eGFR 30-60 mL/min), or severe (eGFR < 30 mL/min). RESULTS: Mortality increased more steeply across CKD stages (2.0%-12.9%) than across cTn ratio categories (2.7%-5.4%). In normal or mild CKD, mortality was low regardless of cTn elevations. In moderate CKD, mortality increased incrementally with cTnI (3.3% versus 5.4% versus 7.4%) and cTnT (3.7% versus 5.3% versus 7.3%) elevation. Among severe CKD patients, only major cTn elevations further distinguished risk (cTnI: 10.1% versus 9.7% versus 14.6%; cTnT: 7.0% versus 5.7% versus 14.0%). CONCLUSIONS: In patients with CKD, cTnI and cTnT perform equally in differentiating short-term prognosis following NSTE ACS; however, the prognostic impact of cTn is dependent upon the degree of CKD severity.     

Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study.

AIMS: Retrospective studies and post hoc analyses have suggested that mild elevations in the creatine kinase-MB (CK-MB) isoenzyme following percutaneous coronary intervention (PCI) may be associated with an increased risk of death in the long term. However, this finding is still controversial, and the prognostic significance of elevations of more sensitive markers of myocardial damage, such as the cardiac troponins, has not been established. In this multicentre prospective cohort study, we evaluated the influence of post-procedural elevations of CK-MB and troponin I (cTnI) on long-term mortality. METHODS AND RESULTS: The CK-MB and PCI study included 3494 consecutive patients undergoing PCI from February 2000 to October 2000 in 16 Italian tertiary centres. Blood samples were collected at baseline, and at 8-12 and 18-24 h after the procedure, and were analysed in a core biochemistry laboratory. CK-MB elevation was detected in 16% of the patients, and was associated with increased 2-year mortality [7.2 vs. 3.8%; odds ratio (OR): 1.9; 95% confidence interval (CI): 1.3-2.8; P<0.001). The degree of CK-MB elevation (peak CK-MB ratio) independently predicted the risk of death (adjusted OR per unit: 1.04; 95% CI: 1.01-1.07; P=0.009). A cTnI elevation was detected in 44.2% of the cases and was not associated with a significant increase in mortality (4.9 vs. 4.0%; OR: 1.2; 95% CI: 0.9-1.7; P=0.2). CONCLUSION: Post-procedural elevations of CK-MB, but not cTnI, influence 2-year mortality.     

Vascular surgery patients: perioperative and long-term risk according to the ACC/AHA guidelines, the additive role of post-operative troponin elevation.

AIMS: The objectives of this study are to evaluate the prognostic role of pre-operative stratification in patients undergoing elective major vascular surgery, the timing of adverse outcomes, and the predictive role of troponin (cTn). METHODS AND RESULTS: Consecutive vascular surgery candidates (n=391) were prospectively stratified and treated according to the ACC/AHA guidelines. The patients were categorized into three groups: (1) with coronary revascularization in the past 5 years, (2) with intermediate clinical risk predictors, and (3) with minor or no clinical risk predictors. cTnI was measured post-operatively. By 18 months, 18.7% of subjects had experienced death or acute myocardial infarction (MI) (by the ACC/ESC criteria). The hazard ratio (HR) was 5.21 (95% CI=2.60-10.43; P<0.0001) in group 1 and 2.58 (95% CI=1.27-4.38; P=0.004) in group 2 when compared with group 3. Most events occurred within 30 days. Elevations of cTnI were associated with adverse outcomes even after multivariable adjustment at long-term (adjusted overall HR=4.73, 95% CI=2.92-7.65; P<0.0001) and at 30 days (adjusted HR=5.52, 95% CI=3.23-9.42; P<0.0001). CONCLUSION: After pre-operative stratification, patients undergoing elective major vascular surgery remain at high risk of MI and death. Events occur mainly early after surgery. cTnI elevations are frequent and independently associated with increased risk. These findings suggest the need for a major re-evaluation of our approach to these patients.     

Predictors of major postoperative cardiac complications in a surgical ICU.

INTRODUCTION: Cardiovascular complications are associated with increased mortality and morbidity during the postoperative period, resulting in longer hospital stay and higher treatment costs. OBJECTIVES: The aim of this study was to identify predictors of major postoperative cardiac complications. METHODS: 187 patients undergoing noncardiac surgery, admitted to a surgical intensive care unit (ICU) between November 2004 and April 2005. Variables recorded were age, gender, American Society of Anesthesiologists (ASA) physical status, type and magnitude of surgery, mortality, ICU and hospital length of stay (LOS), Simplified Acute Physiology Score II (SAPS II), cardiac troponin I (cTnI) at postoperative day 0, 1, 2 and 3, history of hypertension, hyperlipidemia, Revised Cardiac Risk Index (RCRI) score, major cardiac events (MCE): acute myocardial infarction (AMI), pulmonary edema (PE), ventricular fibrillation (VF) or primary cardiac arrest (PCA). Correlations between variables and MCE were made by univariate analysis by simple logistic regression with odds ratio (OR) and 95% confidence interval (95% CI). RESULTS: Total of 14 MCE: 9 AMI, 1 VF, 4 PE. Significant risk factors for MCE were high-risk surgery (OR 8.26, 95% CI 1.76-38.85, p = 0.008), RCRI > or = 2 (OR 4.0, 95% CI 1.22-13.16, p = 0.022), admission cTnI (OR 1.46, 95% CI 1.07-1.99, p = 0.018); day 1 cTnI (OR 1.75, 95% CI 1.27-2.41, p = 0.001); day 2 cTnI (OR 2.23, 95% CI 1.24-3.98, p = 0.007), SAPS II (OR 1.08, 95% CI 1.04-1.12, p < 0.001). Patients with MCE had longer ICU LOS (19.1 +/- 19.3 days against 3.4 +/- 4.9) (OR 1.15, 95% CI 1.08-1.22, p < 0.001) and higher ICU mortality (21.4% versus 4.6%) (OR 5.63, 95% CI 1.31-24.23, p = 0.02) in the ICU. CONCLUSIONS: High-risk surgery, RCRI > or = 2, cTnI levels and SAPS II were predictors of postoperative MCE. Patients with MCE had longer ICU stay and higher mortality rate.     

Minor myocardial damage detected by troponin T is a powerful predictor of long-term prognosis in patients with acute decompensated heart failure

BACKGROUND: The progression of chronic heart failure (CHF) is characterized by frequent exacerbation requiring hospitalization and high mortality. Clinical deterioration is triggered by many factors that could promote ongoing myocytes injury. We sought to determine whether a specific marker of cardiac injury, troponin T (cTnT), is associated with prognosis in acute decompensated heart failure (ADHF). METHODS: One hundred and eighty-four consecutive patients with ADHF were enrolled in the absence of an acute coronary syndrome. A cTnT value> or =0.1 ng/ml in samples drawn at 6, 12 or 24 h after hospital admission was considered abnormal. RESULTS: Increased levels of cTnT were found in 58 patients (31.5%, group 1). There were no significant differences between group 1 and patients with cTnT<0.1 ng/ml (group 2) in terms of demographic and clinical characteristics, although ischemic etiology was more prevalent in group 1 (51.7% vs. 31.7%, p=0.009). During follow-up, the mortality in groups 1 and 2 was 31% and 17.5% (p=0.038, OR=2.13, 95% CI: 1.03-4.69), respectively. The 3-year free-CHF readmission survival in group 1 and 2 was 25% and 53% (log rank test p=0.015). In a Cox proportional hazard model, poor tissue perfusion (HR=2.46, 95% CI=1.31-4.6), previous infarction (HR=1.99, 95% CI=1.02-3.9) and cTnT> or =0.1 ng/ml (HR=1.74, 95% CI=1.05-2.9) emerged as the independent predictors of long-term outcome. CONCLUSIONS: One third of patients with decompensated CHF had elevated levels of cTnT. Troponin T was an independent long-term prognostic marker of morbidity and mortality and it suggests a role of biochemical risk stratification in this setting.     

Biomarker-based risk assessment model in acute pulmonary embolism.

AIMS: Despite growing interest in biomarkers application for risk evaluation in acute pulmonary embolism (APE), no decision-making levels have been defined. METHODS AND RESULTS: We developed a biomarker-based risk stratification in 100 consecutive, normotensive on admission, APE patients (35 males, 65 females, 62+/-18 years). On admission serum NT-proBNP and cardiac troponin T (cTnT) levels were assessed and echocardiography was performed. All-cause 40-day mortality was 15% and APE mortality was 8%. In univariable analysis, cTnT>0.07 microg/L predicted all-cause mortality, hazard ratio (HR) 9.2 (95% CI: 3.3-26.1, P<0.0001), and APE mortality, HR 18.1 (95% CI: 3.6-90.2, P=0.0004); similarly, NT-proBNP>7600 ng/L predicted all-cause and APE mortalities [HR 6.7 (95% CI: 2.4-19.0, P=0.0003) and 7.3 (95% CI: 1.7-30.6, P=0.007)]. NT-proBNP<600 ng/L indicated uncomplicated outcome. Multivariable analysis revealed that cTnT>0.07 microg/L was the most significant independent predictor, whereas NT-proBNP and systemic systolic blood pressure measured on admission and echocardiographic parameters were non-significant. APE mortality in patients with NT-proBNP> or =600 ng/L and cTnT> or =0.07 microg/L reached 33%. NT-proBNP<600 ng/L indicated group without deaths. APE mortality for patients with NT-proBNP> or =600 ng/L and cTnT<0.07 microg/L was 3.7%. Incorporation of echocardiographic data did not improve group selection. CONCLUSION: Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT> or =0.07 microg/L and NT-proBNP> or =600 ng/L are at high risk of APE mortality, whereas NTproBNP<600 ng/L indicates excellent prognosis.     

Troponin elevations after electroconvulsive therapy: the need for caution

Background

Electroconvulsive therapy is used to treat patients with severe or resistant depression. Troponin elevations are associated with an adverse prognosis, and it is well known that central nervous system insults can cause biochemical evidence of cardiac injury. No study previously has studied this with electroconvulsive therapy.

Methods

Patients scheduled for electroconvulsive therapy were enrolled. Clinical information, an electrocardiogram, and a baseline sample for cardiac troponin I and T (cTnI and cTnT) were obtained. Electroconvulsive therapy was done with standard techniques. Subsequently, electrocardiograms and additional samples were obtained. cTnT was measured with the Roche assay and cTnI with the Dade Stratus equipment. Values above the 99th percentile were considered abnormal.

Results

Seventy patients completed the study. Four patients had elevated levels of cTn before treatment. In 3 patients, the elevations persisted. Four additional patients developed elevated cTn levels during electroconvulsive therapy. Two of the patients with cTn elevations died. No other events occurred during follow-up.

Conclusions

Elevations of cTn occurred in 11.5% of patients treated with electroconvulsive therapy. Some of the elevations preceded therapy and some occurred during treatment. Given the adverse prognostic importance of cTn elevations in general, in addition to additional studies, an increased degree of medical scrutiny may be appropriate for this group of patients and for those receiving electroconvulsive therapy. © 2011 Elsevier Inc. All rights reserved.     

Marathon Running as a Cause of Troponin Elevation: A Systematic Review and Meta‐Analysis

Background: Cardiac troponin (cTn) has high sensitivity and specificity for myocardial injury in acute coronary syndrome. Our objective was to review the published literature regarding the incidence of cTn elevations in marathon runners. Methods: Systematic review and meta‐analysis of observational studies published before September 2009. We included studies of patients who had completed a marathon and had serum cTn levels within 24 hours. The primary outcome was the odds ratio for conversion of a normal pre‐marathon cTn to an elevated post‐marathon cTn. Secondary outcomes included the pooled prevalence of cTn elevation and comparison of the odds ratio for post‐marathon elevation of cTnI versus cTnT. Results: Sixteen studies of 939 participants met criteria for inclusion. The mean age was 39 ± 4 years and patients were 74 ± 14% male. There were 6 pre‐marathon cTn elevations and 579 post‐race elevations. The pooled odds ratio for converting from a normal pre‐race to an elevated post‐race cTn was 51.84 (95% CI 16–168, I²= 66%, P < 0.001). The pooled incidence of a post‐marathon cTn elevation was 51% (95% CI 33–69, I²= 98%, P < 0.001) of all runners. For the primary outcome there was no significant publication bias. Age and gender were not associated, but publication date and assay sensitivity was associated with cTn elevation. cTnI was less commonly elevated versus cTnT. Conclusions: The available data demonstrate that cTn levels are frequently elevated after a marathon with unclear cardiovascular significance. This elevation of cTn appears to be consistent among a diverse patient population. (J Interven Cardiol 2010;23:443–450)     

Do cardiac troponins provide prognostic insight in hemodialysis patients?

BACKGROUND: The diagnosis of myocardial necrosis in patients with chronic renal failure is often difficult because biochemical markers of cardiac damage such as creatine kinase MB (CKMB) and cardiac troponin T (cTnT) may be spuriously elevated. Recent small studies also report unexplained elevations in cardiac troponin I (cTnI) in chronic renal failure patients undergoing hemodialysis. The relative incidence of elevated cardiac troponins in this population and their relationship to clinical events remain unknown. OBJECTIVE: To determine the incidence and prognostic significance of asymptomatic elevations of cTnT and cTnI in patients undergoing hemodialysis for chronic renal failure. DESIGN: Prospective cohort study. SETTING: University tertiary care teaching hospital. PATIENTS: One hundred thirteen patients over 21 years of age undergoing onsite hemodialysis were enrolled between December 1997 and February 1998. MEASUREMENTS: All-cause and cardiovascular mortality, hospitalization for acute myocardial infarction, unstable angina or congestive heart failure, new onset sustained arrhythmia or need for unscheduled emergency hemodialysis due to volume overload at 30 days and six months. RESULTS: The incidence of abnormal results for cTnT, cTnI and CKMB were 42%, 15% and 4%, respectively. Independent predictors of mortality at six months were median age greater than 63 years (odds ratio 14.3, 95% CI 1.5 to 130.3, P=0.019) and positive cTnT (odds ratio 13.6, 95% CI 2.5 to 73.2, P=0.002). Diabetics were more likely to have positive cTnI and cTnT results than nondiabetics (P<0.001 and P=0.023, respectively). CONCLUSIONS: cTnT is commonly elevated in patients with chronic renal failure even in the absence of acute coronary syndromes. cTnT may be an important independent prognostic marker in patients on hemodialysis for chronic renal failure. While less common, elevations of cTnI are more frequent than CKMB elevations. The basis of these cardiac troponin elevations is unclear. These findings may represent, in part, a subclinical myocardial injury, an inflammatory response to chronic renal failure or a chronically volume overloaded state.     

Prognostic value of preoperative cardiac troponin I in patients with non-ST-segment elevation acute coronary syndromes undergoing coronary artery bypass surgery

STUDY OBJECTIVES: Elevated levels of cardiac troponin I (cTnI) have been associated with adverse short-term and long-term outcomes in acute coronary syndrome (ACS) patients and in patients who underwent coronary artery bypass grafting (CABG); however, the prognostic implications of preoperative cTnI determination have not been investigated so far. DESIGN AND SETTING: Retrospective study in a department of cardiothoracic surgery of a university hospital. PATIENTS AND METHODS: A possible correlation between preoperative cTnI levels and major adverse cardiac events (MACE) and in-hospital mortality in CABG patients with non-ST-segment elevation ACS (NSTE-ACS) was investigated. cTnI was determined in 1,978 of 3,124 consecutive CABG patients. Among these, 1,592 patients had preoperative cTnI levels < 0.1 ng/mL and therefore served as control subjects (group 1), 265 patients had NSTE-ACS with cTnI levels from 0.11 to 1.5 ng/mL (group 2), and 121 patients had NSTE-ACS with cTnI levels > 1.5 ng/mL (group 3). cTnI levels, clinical data, MACE, and in-hospital mortality were recorded prospectively. Logistic regression and receiver operating characteristic analyses were applied to determine prognostic cutoff values of cTnI. RESULTS: Perioperative myocardial infarction was found in 5.8% of the patients in group 1, 8.3% of the patients in group 2 (odds ratio [OR], 1.5; 95% confidence interval [CI], 0.9 to 2.5), and 18.2% patients in group 3 (OR, 3.6; 95% CI, 2.1 to 6.2; p < 0.0001, Cochran-Armitage trend test). Low cardiac output syndrome occurred in 1.5% of patients in group 1, 4.2% of patients in group 2 (OR, 2.8; 95% CI, 1.3 to 6.1), and 10.9% patients in group 3 (OR, 6.5; 95% CI, 2.9 to 14.4; p < 0.0001). In-hospital mortality was 1.5% in group 1, 3.0% in group 2 (OR, 2.0; 95% CI, 0.8 to 4.8), but 6.6% in group 3 (OR, 4.6; 95% CI, 1.9 to 11.1; p < 0.0001). Univariate and multivariate logistic regression analyses identified cTnI as the strongest preoperative predictor for MACE and in-hospital mortality, respectively. CONCLUSIONS: Preoperative cTnI measurement before CABG appears as a powerful and independent determinant of short-term surgical risk in patients with NSTE-ACS.     

Prediction of cerebrovascular event risk following myocardial infarction

IntroductionPatients with coronary artery disease (CAD) are at increased risk of stroke. The aim of this study was to analyze the prognostic accuracy of selected clinical and laboratory variables in stroke risk prediction following discharge after myocardial infarction (MI).MethodsWe analyzed 404 consecutive patients (aged 68.1±13.7 years; 63.4% male; 37.4% with diabetes) without previous stroke who were discharged in sinus rhythm after being admitted for MI. The following data were collected: cardiovascular risk factors, admission blood glucose (BG), HbA1c, creatinine, peak troponin levels; glomerular filtration rate (GFR) by the MDRD formula; maximum Killip class; GRACE score for in-hospital and 6-month mortality; and extent of CAD. Patients were followed for two years and each variable was tested as a possible predictor of cerebrovascular events (stroke or transient ischemic attack [TIA]).ResultsDuring follow-up, 27 patients were admitted for stroke or TIA. The presence of diabetes, hypertension, dyslipidemia and previously known CAD, type of MI (STEMI vs NSTEMI) and extent of CAD did not predict cerebrovascular risk. The following variables were associated with higher stroke risk: GFR <60 ml/min/m² (p=0.029, OR 2.65, 95% CI 1.07-6.55); maximum Killip class >1 (p=0.025, OR 2.71, 95% CI 1.10-6.69); GRACE in-hospital mortality >180 (p=0.001, OR 4.09, 95% CI 1.64-10.22); admission BG >140 mg/dl (p=0.001, OR 5.74, 95% CI 1.87-17.58); GRACE 6-month mortality >150 (p=0.001, OR 4.50, 95% CI 1.80-6.27); and peak troponin >42 ng/ml (p=0.032, OR 2.64, 95% CI 1.06-6.59). Logistic regression analysis produced a model with the predictors GRACE 6-month mortality >150 (OR 3.26; p=0.014) and admission BG >7.7 mmol/l (OR 4.09; p=0.017) that fi tted the data well (Hosmer-Lemeshow: p=0.916).Discussion/conclusionsIn patients with MI, variables known to be predictors of in-hospital mortality, including admission BG, renal function, acute heart failure and GRACE score, were found to be useful predictors of stroke during 2-year follow-up. While both GRACE score for 6-month mortality >150 and admission BG >7.7 mmol/l were independent predictors of stroke, CV risk factors, previously known CAD, and extent of CAD assessed by coronary angiography did not improve stroke risk prediction. This study highlights the need for even more aggressive secondary prevention in patients most at risk.     

和肽素联合肌钙蛋白I评估老年急性心肌梗死患者预后的价值

目的:研究和肽素(COP)及肌钙蛋白I(cTnI)对老年急性心肌梗死(AMI)患者预后评估的价值。方法:纳入北京医院急诊科2016年8月至2018年8月收治的81例老年AMI患者作为研究对象,收集来诊首次血清标本,测定COP和cTnI并完善其他相关检查,随访6个月评估各因素与死亡风险的关联程度,并比较各指标对预后的评估...     

Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction.

AIMS: Peri-procedural non-Q-wave myocardial infarction is a frequent and prognostically important complication of percutaneous coronary intervention (PCI). It has been postulated that statins may reduce the rate of myocardial injury after PCI. METHODS AND RESULTS: Four hundred and fifty-one patients scheduled for elective PCI and not on statins were randomly assigned to either no treatment or to statin treatment. Statin administration was started at least 3 days before the procedure.Incidence of peri-procedural myocardial injury was assessed by analysis of creatinine kinase myocardial isoenzyme (CK-MB: upper limit of normal [ULN] 3.5 ng/ml) and cardiac troponin I (cTn I, ULN 0.10 ng/ml) before, 6 and 12 h after the intervention. A large non-Q-wave myocardial infarction was defined as a CK-MB elevation >5 times ULN alone or associated with chest pain or ST segment or T wave abnormalities. Median CK-MB peak after PCI was 1.70 (interquartile ranges 1.10-3.70) ng/ml in the Statin group and 2.20 (1.30-5.60) ng/ml in the Control group (p=0.015). Median peak of cTnI after PCI was 0.13 (0.05-0.45) ng/ml in the Statin group and 0.21 (0.06-0.85) ng/ml in the Control group (p=0.033). The incidence of a large non-Q-wave myocardial infarction was 8.0% in the Statin group and 15.6% in the Control group (p=0.012: OR=0.47; 95% CI=0.26-0.86). The incidence of cTnI elevation >5 times ULN was 23.5% in the Statin group and 32% in the Control group (p=0.043: OR=0.65; 95% CI=0.42-0.98). By logistic regression analysis, the independent predictors of CK-MB elevation >5 times ULN after PCI were intra-procedural angiographic complications (OR=9.36; 95% CI=3.06-28.64; p<0.001), statin pre-treatment (OR=0.33; 95% CI=0.13-0.86; p=0.023) and age >65 years (OR=2.58; 95% CI=1.09-6.11; p=0.031). CONCLUSIONS: Pre-procedural statin therapy reduces the incidence of large non-Q-wave myocardial infarction after PCI.     

Evaluation of B-type natriuretic peptide for risk assessment in unstable angina/non-ST-elevation myocardial infarction: B-type natriuretic peptide and prognosis in TACTICS-TIMI 18

OBJECTIVES: This study was designed to evaluate B-type natriuretic peptide (BNP) for risk assessment and clinical decision making over a range of cut points, alone and with cardiac troponin I (cTnI), in patients with non-ST-elevation acute coronary syndromes (ACS). BACKGROUND: B-type natriuretic peptide holds promise for risk stratification. Additional evidence regarding optimal decision limits, use in combination with troponin, and use in targeting therapy is needed before acceptance into clinical use for ACS. METHODS: We evaluated BNP at baseline in 1,676 patients with non-ST-elevation ACS randomized to early invasive versus conservative management. RESULTS: Patients with elevated BNP (>80 pg/ml; n = 320) were at higher risk of death at seven days (2.5% vs. 0.7%, p = 0.006) and six months (8.4% vs. 1.8%, p < 0.0001). The association between BNP and mortality at six months (adjusted odds ratio [OR] 3.3; 95% confidence interval [CI] 1.7 to 6.3) was independent of important clinical predictors, including cTnI and congestive heart failure (CHF). Patients with elevated BNP had a fivefold higher risk of developing new CHF by 30 days (5.9% vs. 1.0%, p < 0.0001). B-type natriuretic peptide added prognostic information to cTnI, discriminating patients at higher mortality risk among those with negative (OR 6.9; 95% CI 1.9 to 25.8) and positive (OR 4.1; 95% CI 1.9 to 9.0) baseline cTnI results. No difference was observed in the effect of invasive versus conservative management when stratified by baseline levels of BNP (p(interaction) > or = 0.6). CONCLUSIONS: Elevated BNP (>80 pg/ml) at presentation identifies patients with non-ST-elevation ACS who are at higher risk of death and CHF and adds incremental information to cTnI. Additional work is needed to identify therapies that may reduce the risk associated with increased BNP.     

Cardiac troponins T and I in patients with end-stage renal disease: the relation with left ventricular mass and their prognostic value

BACKGROUND: Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial. HYPOTHESIS: The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and left ventricular mass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively. METHODS: We included 129 patients with ESRD (71 men, age 44 +/- 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, and transthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years. RESULTS: The cTnT concentration was > 0.03-0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p = 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were 25 (19.4%) deaths during follow-up. Multivariable analysis showed that elevation of cTnT and cTnI did not emerge as an independent predictor for death. Serum albumin level (p < 0.001) was the strongest predictor of mortality, followed by age (p = 0.002) and LVMI (p = 0.005). CONCLUSIONS: Cardiac troponin T and I related significantly to the LVMI. The increased serum concentration of cardiac troponins probably originates from the heart; however, they are not independent predictors for prognosis.     

Impact of admission hyperglycemia and diabetes mellitus on short- and long-term mortality after acute myocardial infarction in the coronary intervention era

The influence of admission hyperglycemia and diabetes on short- and long-term mortality of patients with acute myocardial infarction (AMI) in the percutaneous coronary intervention (PCI) era was investigated. From 1996 to 2003, a total of 802 consecutive patients with AMI underwent coronary angiography. Primary PCI was performed in 724 patients (90%). Three-year mortality curves were constructed using the Kaplan-Meier method. Cox proportional hazard regression was used to identify independent predictors of 30-day mortality and mortality from 30 days to 3 years. There were 261 patients with admission hyperglycemia (admission glucose>or=11.1 mmol/L) and 212 patients with diabetes. Admission hyperglycemia was associated with a significantly higher 30-day mortality rate (8.4% vs 2.4%, p<0.001). However, there was no significant difference in 30-day mortality rates between diabetic and nondiabetic patients (5.7% vs 3.9%, p=0.29). Conversely, diabetes significantly increased mortality from 30 days to 3 years (10.0% vs 5.5%, p=0.03), but admission hyperglycemia did not (8.4% vs 5.9%, p=0.19). Multivariate analysis showed that hyperglycemia was an independent predictor of 30-day mortality (odds ratio [OR] 1.71, 95% confidence interval [CI] 1.13 to 2.61, p=0.01), but diabetes was not (OR 0.84, 95% CI 0.55 to 1.27, p=0.42). Diabetes was independently associated with mortality from 30 days to 3 years (OR 1.43, 95% CI 1.02 to 1.97, p=0.04), but hyperglycemia had a neutral effect (OR 0.98, 95% CI 0.70 to 1.36, p=0.92). In conclusion, in the PCI era, admission hyperglycemia was associated with short-term mortality, whereas diabetes increased long-term mortality after convalescence in patients with AMI. Admission hyperglycemia and diabetes should be treated as 2 distinct disease states.     

Troponin I and T levels in renal failure patients without acute coronary syndrome: a systematic review of the literature

BACKGROUND: Debate surrounds the interpretation of troponin assays for the diagnosis and prognosis of cardiac disease in patients with renal failure. OBJECTIVES: To systematically review the diagnostic and prognostic test characteristics of quantitative serum cardiac troponin I (cTnI) and T (cTnT) in renal failure patients without acute coronary syndrome (ACS) symptoms. METHODS: English-language literature was identified through searching MEDLINE from 1966 to August 2003 and reviewing reference lists. Studies were excluded if they did not meet research objectives, had fewer than 10 patients or focused primarily on nonrenal patients. Of 119 potential studies, 39 articles with over 349 patients with chronic kidney disease (CKD) and 3899 hemodialysis patients were selected for abstraction. RESULTS: Among CKD and hemodialysis patients without ACS symptoms, cTnI had a mean specificity of 97% (95% CI 93% to 99%) and 96% (95% CI 94% to 98%), respectively, using the myocardial infarction cut-off threshold. The mean specificity of cTnT compared less favourably at 85% (95% CI 75% to 93%) and 71% (95% CI 64% to 77%) for CKD and hemodialysis patients, respectively. In hemodialysis patients without ACS symptoms, positive and negative likelihood ratios for all-cause mortality over 12 to 24 months for cTnT were 4.5 (95% CI 2.9 to 7.1) and 0.6 (95% CI 0.4 to 0.8), and for cTnI were 1.6 (95% CI 0.9 to 2.9) and 1.0 (95% CI 0.9 to 1.1), respectively. CONCLUSIONS: In CKD and hemodialysis patients without ACS symptoms, troponin I, at the myocardial infarction cut-off threshold, is unlikely to be falsely elevated. Among hemodialysis patients without ACS symptoms, a positive troponin T helps predict all-cause mortality.     

Hospitalizaciones y mortalidad por COVID-19 en pacientes con enfermedades inflamatorias reumáticas en Andalucía

ObjectiveTo describe whether rheumatic inflammatory diseases (RID) are associated with a higher risk of hospitalization and/or mortality from COVID-19 and identify the factors associated with hospitalization and mortality in RID and COVID-19 in different Hospitals in Andalusia.MethodsDesign: Multicentre observational case-control study. Patients: RID and COVID-19 from different centres in Andalusia. Controls: patients without RIS matched by sex, age and CRP-COVID.Protocol A list of patients with PCR for COVID-19 was requested from the microbiology service from March 14 to April 14, 2020. The patients who had RID were identified and then consecutively a paired control for each case.Variables The main outcome variable was hospital admission and mortality from COVID-19.Statistical analysis Bivariate followed by binary logistic regression models (DV: mortality/hospital admission).ResultsOne hundred and fifty-six patients were included, 78 with RID and COVID-19 and 78 without RID with COVID-19. The patients did not present characteristics of COVID-19 disease different from the general population, nor did they present higher hospital admission or mortality. The factor associated with mortality in patients with RID was advanced age (OR [95% CI], 1.1 [1.0-1.2]; p = 0.025), while the factors associated with hospitalization were advanced age (OR [95% CI], 1.1 [1.0-1.1]; p = 0.007) and hypertension (OR [95% CI], 3.9 [1.5-6.7]; p = 0.003).ConclusionMortality and hospital admission due to COVID-19 do not seem to increase in RID. Advanced age was associated with mortality in RID and, in addition, HTN was associated with hospital admission.     

Determinants of the length of mechanical ventilation in patients with COPD in the intensive care unit

BACKGROUND: About 10% of the patients with chronic obstructive pulmonary disease (COPD) are at high risk for prolonged mechanical ventilation (MV >21 days), and mortality ranges from 55 to 78% in these patients. OBJECTIVE: To determine the potential risk factors for MV over periods of 1, 2 and 3 weeks in patients with COPD. PATIENTS AND METHOD: The characteristics of patients during the stable period of their disease, on admission to the intensive care unit (ICU) and during the ICU stay were recorded prospectively and analyzed retrospectively for this study. t test, chi(2) test and logistic regression analysis were used for statistical analysis. RESULTS: 86 patients with COPD requiring MV were included in the study. 73, 33, and 13% of the patients required MV longer than 1, 2 and 3 weeks, respectively. There were no significant relationships between the duration of MV and bronchiectasis or the presence of community-acquired pneumonia on admission, baseline pulmonary function test results or blood gas parameters on admission. Development of ventilator-associated pneumonia (VAP; odds ratio, OR: 6; 95% confidence interval, CI: 2-23, p = 0.011) and sepsis (OR: 10; 95% CI: 2-54, p = 0.007) were independent predictors for MV >7 days. VAP was still a risk factor for MV >15 days with an OR of 14 (95% CI: 3-66, p = 0.001). On the other hand MV >21 days was primarily determined by increasing age (OR: 1.2; 95% CI: 1-1.3, p = 0.042), severity of the disease on admission measured by APACHE II score (OR: 1.4; 95% CI: 1-1.7, p = 0.002) and albumin levels (OR: 0.10, 95% CI: 0.01-0.54, p = 0.007). CONCLUSION: Advanced age, severity of disease on admission and development of VAP during ICU stay are the main determinants of MV duration in patients with COPD.