Importance of low concentrations of cardiac troponins.
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Female↗
Biomedical subjects
Allan S Jaffe
Publications and source records attributed to Allan S Jaffe.
Clinical importance of cardiac troponin release and cardiac abnormalities in patients with supratentorial cerebral hemorrhages.
OBJECTIVE: To determine the Incidence of cardiac troponin T (cTnT) elevation, electrocardiographic (ECG) changes, and arrhythmias in supratentorial intracerebral hemorrhage (ICH) and their association with early mortality. PATIENTS AND METHODS: Patients with supratentorial ICHs admitted to Mayo Clinic, Rochester, Minn, from March 1998 to October 2003 were studied. We excluded moribund patients with ICHs who died within 12 hours of hospital admission. Cardiac troponin T levels measured on admission and day 2 were determined by a third-generation enzyme-linked immunosorbent assay. Continuous ECG monitoring was performed In all patients. Computed tomographic scans were graded and correlated with abnormal cardiac variables. RESULTS: Peak levels of cTnT were elevated at 0.035 to 1.2 microg/L (mean +/- SD, 0.27 +/- 0.38 microg/L) in 10 (20%) of 49 patients and were not associated with changes in creatine kinase MB fraction or ECG results. The cTnT levels did not correlate with location or side of hemorrhage or mortality at 30 days. Seventy (64%) of 110 patients displayed ECG abnormalities. The ECG changes did not correlate with the location or side of ICH, hydrocephalus, midline shift, or extension to the ventricles. CONCLUSION: The cTnT elevations in survivors of acute ICH are frequent but without confirmatory ECG changes that suggest mild myocardial injury. One-month mortality is not influenced by such cTnT elevations. In addition, ECG abnormalities are common but likely benign in patients with supratentorial ICH who survive the initial insult.
Adult↗
Troponin: the biomarker of choice for the detection of cardiac injury.
It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the "cornerstone" of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease.
Biomarkers↗
The Pilot Randomized Study of Nesiritide Versus Dobutamine in Heart Failure (PRESERVD-HF).
Acute heart failure syndromes (AHFS) are related to several diseases affecting not only the heart but also the kidneys and blood vessels. Emerging evidence indicates that myocardial injury may also play a role in the pathophysiology of AHFS, as suggested by increased levels of markers of injury, such as cardiac troponin (cTn). Although cTn is a known prognostic marker, the release of cTn during hospitalization has not been evaluated prospectively with serial measures. We prospectively evaluated patterns of cTn release by conducting serial measures of cTnI and cTnT in patients hospitalized for AHFS. This study enrolled 51 patients with AHFS who were admitted with worsening heart failure (HF) and a history of coronary artery disease (CAD) in whom an acute coronary event was not suspected. Levels of cTnI and cTnT were measured at 8, 32, 56, and 80 hours after study entry. At baseline, 73.9% of patients had detectable cTnI, and 43.5% had detectable cTnT levels. The median concentrations of cTnI and cTnT were unchanged from 0 to 32 hours, increased from 32 to 56 hours, then either plateaued (cTnT) or decreased to baseline (cTnI). Of the 26 patients who had no detectable cTn levels at baseline, 2 (7.7%) developed detectable cTnT and 5 (41.7%) developed detectable cTnI release during hospitalization. Detectable levels of cTn at baseline were related to short-term clinical events. In this study of patients with CAD in whom an acute coronary event was not suspected, most had detectable levels of cTn present at admission, and some patients developed cTn release during hospitalization. Because cTn release may be a marker for myocardial injury, this study raises the possibility that injury occurred in most patients admitted with AHFS. Therefore, the goal of therapy for AHFS should be not only to improve symptoms and hemodynamics but also to salvage myocardium. Accordingly, therapies for AHFS that are aimed at improving hemodynamics may affect long-term prognosis by either injuring or salvaging myocardium.
Adrenergic beta-Agonists↗
Lower rather than higher levels of B-type natriuretic peptides (NT-pro-BNP and BNP) predict short-term mortality in end-stage heart failure patients treated with nesiritide.
Elevated plasma natriuretic peptides in heart failure (HF) usually indicate a poor outcome and low levels a compensated state. In advanced chronic HF, however, low levels may reflect an impaired neurohormonal response. To assess this hypothesis, this study analyzed whether N-terminal-pro-B-type natriuretic peptide (NT-pro-BNP) and B-type natriuretic peptide (BNP) levels were related to mortality in 40 patients treated for decompensated chronic HF. Cardiovascular mortality during follow-up (10 +/- 1 months) was 40%. BNP levels were lower in patients who died (487 +/- 60 vs 836 +/- 99 pg/ml, p <0.02), as were NT-pro-BNP levels (9,507 +/- 1,178 vs 17,611 +/- 4,338 pg/ml, p <0.05). These data support the hypothesis that patients with end-stage HF and poor short-term survival have lower natriuretic peptide levels than those who survive. These findings suggest that the natriuretic peptide system can no longer contribute adequately to neurohormonal compensation and that paradoxically low peptide levels are an adverse prognostic marker in advanced HF.
Aged↗
Elevated donor troponin levels are associated with a lower frequency of allograft vasculopathy.
BACKGROUND: Cardiac allograft vasculopathy (CAV) is considered a major cause of morbidity and mortality in transplant recipients and may reflect immune-mediated endothelial injury in response to the donor heart. Elevated troponin levels in the donor serum might provide a marker for this phenomenon; therefore, we evaluated the relationship of donor troponin levels to the development of CAV. METHODS: A retrospective analysis of troponin levels was undertaken from cardiac donor patients, and transplant recipients were monitored for the development of vasculopathy by angiography (N = 171). RESULTS: Angiographically significant CAV developed in 6% of transplantation patients and troponin levels were inversely related to the severity of CAV. CONCLUSIONS: Elevated donor troponin levels are not associated with the development of CAV but rather with a significantly reduced long-term risk of developing CAV, suggesting a possible protective effect of donor released protein.
Adult↗
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.
Adrenergic beta-Antagonists↗
Excess weight at time of presentation of myocardial infarction is associated with lower initial mortality risks but higher long-term risks including recurrent re-infarction and cardiac death.
OBJECTIVES: To evaluate the influence of elevated body mass index (BMI) on short- and long-term survival following acute myocardial infarction (AMI). BACKGROUND: Recent studies suggest an obesity survival paradox in individuals undergoing percutaneous coronary intervention with better 30-day and 1-year outcomes in obese relative to normal weight patients. We tested a similar obesity paradox hypothesis following acute myocardial infarction. METHODS: Short- and long-term all-cause mortality, and risk of recurrent AMI were evaluated according to BMI status in 894 consecutive survivors of AMI <80 years of age admitted to the Mayo Clinic Coronary Care Unit between January 1, 1988 and April 16, 2001. Normal weight, overweight and obesity were defined as BMI <25, 25-29.9, and >30 kg/m(2), respectively. RESULTS: Overall mortality following hospital discharge was significantly lower in overweight and obese patients and was mostly attributable to lower 6-month mortality (adjusted HR = 0.47, P = 0.01 for BMI >25 kg/m(2)) relative to normal weight patients, while long-term mortality among 6-month survivors was similar in all 3 groups. The risk of recurrent AMI was higher in patients with BMI >25 kg/m(2) (adjusted HR = 2.30, P = 0.01). Overweight and obese patients were significantly more likely to die from cardiac rather than non-cardiac causes (P < 0.01). CONCLUSIONS: Following AMI, overweight and obese individuals although paradoxically protected from short-term death have a long-term mortality risk that is similar to normal weight individuals. Younger age at the time of initial infarction and fewer non-cardiovascular comorbidities presumably explain the short-lived obesity survival paradox following myocardial infarction.
Aged↗
Low heart rate variability and the effect of depression on post-myocardial infarction mortality.
BACKGROUND: Depression is associated with an increased risk for mortality after acute myocardial infarction (MI). The purpose of this study was to determine whether low heart rate variability (HRV) mediates the effect of depression on mortality. METHODS: Twenty-four-hour ambulatory electrocardiograms were obtained from 311 depressed patients with a recent acute MI who were enrolled in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial and from 367 nondepressed patients who met the ENRICHD medical inclusion criteria. Standard HRV indexes were extracted from the recordings. RESULTS: The log of very low-frequency (LnVLF) power, an index of HRV derived from power spectral analysis of the electrocardiogram signal (0.0033-0.04 Hz [in milliseconds squared]), was lower in the depressed than in the nondepressed patients (P<.001). There were 47 deaths (6.1%) during a 30-month follow-up. After adjusting for potential confounders, the depressed patients remained at higher risk for all-cause mortality compared with the nondepressed patients (hazard ratio, 2.8; 95% confidence interval [CI], 1.4-5.4; P<.003). When LnVLF power was entered into the model, the hazard ratio for depression dropped to 2.1 (95% CI, 1.1-4.2; P = .03). The proportion of the risk for depression attributable to LnVLF power was 0.27 (95% CI, 0.23-0.31; P<.001). CONCLUSIONS: Low HRV partially mediates the effect of depression on survival after acute MI. This finding helps to clarify the physiological mechanisms underlying depression's role as a risk factor for mortality in patients with coronary heart disease. It also raises the possibility that treatments that improve both depression and HRV might also improve survival in these patients.
Circadian Rhythm↗
Reduced risks of death and CHF are associated with statin therapy administered acutely within the first 24 h of AMI.
BACKGROUND: Reports have demonstrated an association between statin therapy during the first day of hospitalization for acute myocardial infarction (AMI) and reduced mortality. There are little data about whether early statin therapy reduces risk of CHF and alters timing of death. METHODS: We identified 3226 consecutive patients with AMI from 1993 through 2000 and divided them into early statin therapy (statins were administered within the initial 24 h of hospitalization, n=220) and non-statin therapy groups (n=3006). We compared mortality risks, rates of CHF development and measures of peak CK and CK-MB values between the groups. RESULTS: In-hospital mortality was lower in the early statin therapy group (2.7%) compared to the non-statin therapy group (9.2%), p=0.001. We observed no differences in the median time to death (statin group 132 h vs. non-statin group 72 h), p=0.3. Patients with very early statin treatment had lower peak CK (624 ng/ml) and CK-MB (46 ng/ml) values compared to non-statin patients (848 ng/ml and 84 ng/ml), p<0.01. Patients in the early statin group had lower risks of developing CHF during hospitalization (10.2 %) compared to the non-statin group (25.7%), p<0.001. CONCLUSION: Very early administration of statin therapy during the first day of hospitalization for AMI was associated with lower in-hospital mortality, lower rates of developing CHF and reduced peak biomarker release. These data support a benefit from early statin therapy in AMI and support the need for prospective studies which test whether very early statin therapy might also reduce infarct size.
Aged↗
Practical implementation of the guidelines for unstable angina/non-ST-segment elevation myocardial infarction in the emergency department: a scientific statement from the American Heart Association Council on Clinical Cardiology (Subcommittee on Acute Cardiac Care), Council on Cardiovascular Nursing, and Quality of Care and Outcomes Research Interdisciplinary Working Group, in Collaboration With the Society of Chest Pain Centers.
In the United States each year, >5.3 million patients present to emergency departments with chest discomfort and related symptoms. Ultimately, >1.4 million individuals are hospitalized for unstable angina and non-ST-segment elevation myocardial infarction. For emergency physicians and cardiologists alike, these patients represent an enormous challenge to accurately diagnose and appropriately treat. This update of the 2002 American College of Cardiology/American Heart Association Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction (UA/NSTEMI) provides an evidence-based approach to the diagnosis and treatment of these patients in the emergency department, in-hospital, and after hospital discharge. Despite publication of the guidelines several years ago, many patients with UA/NSTEMI still do not receive guidelines-indicated therapy.
Angina Pectoris↗
Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome.
BACKGROUND: Evaluation of patients who present to the hospital with a complaint of chest pain or other signs or symptoms suggestive of acute coronary syndrome (ACS) is time-consuming, expensive, and problematic. Recent investigations have indicated that increases in biomarkers upstream from biomarkers of necrosis (cardiac troponins I and T), such as inflammatory cytokines, cellular adhesion molecules, acute-phase reactants, plaque destabilization and rupture biomarkers, biomarkers of ischemia, and biomarkers of myocardial stretch may provide earlier assessment of overall patient risk and aid in identifying patients with higher risk of an adverse event. APPROACH AND CONTENT: The purpose of this review is to provide an overview of the pathophysiology and clinical and analytical characteristics of several biomarkers that may have potential clinical utility to identify ACS patients. These biomarkers (myeloperoxidase, metalloproteinase-9, soluble CD40 ligand, pregnancy-associated plasma protein A, choline, ischemia-modified albumin, unbound free fatty acids, glycogen phosphorylase isoenzyme BB, and placental growth factor) have demonstrated promise and need to be more thoroughly evaluated for commercial development for implementation into routine clinical and laboratory practice. SUMMARY: Specifications that have been addressed for cardiac troponins and natriuretic peptides will need to be addressed with the same scrutiny for the biomarkers discussed in this review. They include validating analytical imprecision and detection limits, calibrator characterization, assay specificity and standardization, pre-analytical issues, and appropriate reference interval studies. Crossing boundaries from research to clinical application will require replication in multiple settings and experimental evidence supporting a pathophysiologic role and, ideally, interventional trials demonstrating that monitoring single or multiple biomarkers improves outcomes.
Acute Disease↗
Effects of antidepressant medication on morbidity and mortality in depressed patients after myocardial infarction.
BACKGROUND: Depression after myocardial infarction (MI) is associated with higher morbidity and mortality. Although antidepressants are effective in reducing depression, their use in patients with cardiovascular disease remains controversial. OBJECTIVE: To undertake a secondary analysis to determine the effects of using antidepressants on morbidity and mortality in post-MI patients who participated in the Enhancing Recovery in Coronary Heart Disease study. DESIGN: Observational secondary analysis. SETTING: Eight academic sites. PATIENTS: The Enhancing Recovery in Coronary Heart Disease clinical trial randomized 2481 depressed and/or socially isolated patients from October 1, 1996, to October 31, 1999. Depression was diagnosed using a structured clinical interview. This analysis was conducted on the 1834 patients enrolled with depression (849 women and 985 men). INTERVENTION: Use of antidepressant medication. MAIN OUTCOME MEASURES: Event-free survival was defined as the absence of death or recurrent MI. All-cause mortality was also examined. To relate exposure to antidepressants to subsequent morbidity and mortality, the data were analyzed using a time-dependent covariate model. RESULTS: During a mean follow-up of 29 months, 457 fatal and nonfatal cardiovascular events occurred. The risk of death or recurrent MI was significantly lower in patients taking selective serotonin reuptake inhibitors (adjusted hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.38-0.84), as were the risk of all-cause mortality (adjusted HR, 0.59; 95% CI, 0.37-0.96) and recurrent MI (adjusted HR, 0.53; 95% CI, 0.32-0.90), compared with patients who did not use selective serotonin reuptake inhibitors. For patients taking non-selective serotonin reuptake inhibitor antidepressants, the comparable HRs (95% CIs) were 0.72 (0.44-1.18), 0.64 (0.34-1.22), and 0.73 (0.38-1.38) for risk of death or recurrent MI, all-cause mortality, or recurrent MI, respectively, compared with nonusers. CONCLUSIONS: Use of selective serotonin reuptake inhibitors in depressed patients who experience an acute MI might reduce subsequent cardiovascular morbidity and mortality. A controlled trial is needed to examine this important issue.
Antidepressive Agents↗
Practical implementation of the Guidelines for Unstable Angina/Non-ST-Segment Elevation Myocardial Infarction in the emergency department.
In the United States each year, >5.3 million patients present to emergency departments with chest discomfort and related symptoms. Ultimately, >1.4 million individuals are hospitalized for unstable angina and non-ST-segment elevation myocardial infarction. For emergency physicians and cardiologists alike, these patients represent an enormous challenge to accurately diagnose and appropriately treat. This update of the 2002 American College of Cardiology/American Heart Association Guidelines for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction (UA/NSTEMI) provides an evidence-based approach to the diagnosis and treatment of these patients in the emergency department, in-hospital, and after hospital discharge. Despite publication of the guidelines several years ago, many patients with UA/NSTEMI still do not receive guidelines-indicated therapy.
Angina, Unstable↗
Use of biomarkers in the emergency department and chest pain unit.
The use of biomarkers of cardiac injury in the emergency department (ED) and observation unit settings has several nuances that are different and, therefore, worthy of its own set of use guidelines. The markers that are used, however, are the same. The primary marker of choice continues to be cardiac troponin (Tn). Other markers that have been used because of the need in the ED for rapid triage have been myoglobin and fatty acid binding protein. In addition, some centers still prefer less sensitive and less specific markers such as creatine kinase myocardial band (CK-MB). More recently, a push has occurred to develop markers of ischemia, such as ischemia modified albumin (IMA),to determine which patients have ischemia, even in the absence of cardiac injury. As troponin assays become more sensitive and method for use becomes better understood, the use of these other markers are being relegated to lesser and lesser roles. Markers of ischemia are useful, but at present, despite some enthusiasm, are not ready for routine use. Before describing the recommendations for clinical use of biomarkers in the ED, a basic understanding of some of the science and measurement issues related to these analytes is helpful.
Acute Disease↗
Can creatine kinase MB levels predict mortality after cardiac surgery?
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Journal Article↗
Quality specifications for B-type natriuretic peptide assays.
BACKGROUND: The objective of this report is to improve the quality of immunochemical measurements of B-type natriuretic peptide (BNP) and its N-terminal propeptide (NT-proBNP). The recommendations proposed are intended for use by manufacturers of commercial assays, by clinical laboratories using those assays, by clinical trial groups and research investigators, and by regulatory agencies, such as the United States Food and Drug Administration. METHODS: A group of cardiac biomarker experts reviewed and abstracted the scientific literature to provide recommendations pertaining to the quality specifications for BNP/NT-proBNP assays. RESULTS: The evidence-based recommendations encourage manufacturers to endorse and consistently follow the proposed recommendations; encourage that all package inserts for BNP/NT-proBNP immunoassays include uniform information on assay design, preanalytical performance characteristics, analytical performance characteristics, and clinical performance; and encourage regulatory agencies to adopt a minimal and uniform set of criteria for manufacturers to provide when seeking clearance for new and/or improved assays. CONCLUSIONS: These recommendations address the use of BNP and NT-proBNP as cardiac biomarkers and not their physiologic and/or pathophysiologic relevance.
Biomarkers↗
Validation of the 99th percentile cutoff independent of assay imprecision (CV) for cardiac troponin monitoring for ruling out myocardial infarction.
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Diagnosis, Differential↗