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Gary S Francis - One of the best experts on this subject based on the ideXlab platform.
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cardiac Troponins and chronic kidney disease
Kidney International, 2006Co-Authors: A S Kanderian, Gary S FrancisAbstract:The prevalence of coronary artery disease in patients with chronic kidney disease (CKD) is high, and acute myocardial infarction contributes significantly to the steep mortality rate in this population. Diagnosing an acute coronary syndrome in these patients is often difficult though essential. Traditional diagnostic tools such as symptoms and electrocardiographic manifestations are not entirely helpful in patients with CKD, and physicians are often left to rely on laboratory analysis of biomarkers such as cardiac troponin. However, troponin levels are increased in patients with renal failure in the absence of clinical myocardial ischemia, making their interpretation problematic. Several theories have been proposed for the mechanism of elevated troponin levels in CKD. Irrespective of our uncertainty regarding mechanism, studies have shown that there is a strong prognostic implication of elevated troponin levels; and that it is predictive of increased risk of mortality and cardiovascular events. Troponin levels rise over 6-8 h in the setting of acute myocardial injury; hence, it is imperative to obtain these levels sequentially in patients with CKD in whom a clinical cardiac event is suspected. A distinct rise and fall in the levels over baseline strongly support the diagnosis of acute myocardial necrosis. Despite uncertainties regarding increased Troponins in patients with CKD, their value remains clear.
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cardiac Troponins in renal insufficiency review and clinical implications
Journal of the American College of Cardiology, 2002Co-Authors: Benjamin J Freda, W Wilson H Tang, Frederick Van Lente, Franklin W Peacock, Gary S FrancisAbstract:Patients with renal insufficiency may have increased serum Troponins even in the absence of clinically suspected acute myocardial ischemia. While cardiovascular disease is the most common cause of death in patients with renal failure, we are just beginning to understand the clinical meaning of serum troponin elevations. Serum troponin T is increased more frequently than troponin I in patients with renal failure, leading clinicians to question its specificity for the diagnosis of myocardial infarction. Many large-scale trials demonstrating the utility of serum Troponins in predicting adverse events and in guiding therapy and intervention in acute coronary syndromes have excluded patients with renal failure. Despite persistent uncertainty about the mechanism of elevated serum Troponins in patients with reduced renal function, data from smaller groups of renal failure patients have suggested that troponin elevations are associated with added risk, including an increase in mortality. It is possible that increases in serum troponin from baseline in patients with renal insufficiency admitted to hospital with acute coronary syndrome may signify myocardial necrosis. Further studies are needed to clarify this hypothesis.
Petr Jarolim - One of the best experts on this subject based on the ideXlab platform.
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high sensitivity cardiac troponin assays in the clinical laboratories
Clinical Chemistry and Laboratory Medicine, 2015Co-Authors: Petr JarolimAbstract:Immunoassays measuring cardiac Troponins I or T have become firmly established as critical tools for diagnosing acute myocardial infarction. While most contemporary assays provide adequate diagnostic per- formance, the increased sensitivity and precision of the new, high sensitivity assays that have already been introduced into clinical practice, provide the potential to further shorten intervals between blood draws or the time needed to detect the first significant troponin eleva- tion. In addition to the relatively modest benefits at the diagnostic end, the high sensitivity assays and the inves- tigational ultrasensitive cardiac troponin assays offer improvements for predicting major adverse cardiovas- cular events, development of heart failure or transition to end-stage kidney disease. These novel high sensitivity assays can measure troponin concentrations in 50% - 100% of healthy individuals and therefore allow for the distribution of troponin values within a healthy cohort to be measured, patient ' s baseline troponin levels to be monitored, and clinicians to be alerted of deteriorating cardiorenal conditions. We envisage that the high sensi- tivity assays will become important tools for predicting each patient ' s risk of future adverse events and for guid- ing and monitoring corresponding adjustments of pre- ventative therapeutic interventions.
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Cardiac Troponins and High-sensitivity Cardiac Troponin Assays
Clinics in laboratory medicine, 2014Co-Authors: Michael J. Conrad, Petr JarolimAbstract:Measurement of circulating cardiac Troponins I and T has become integral to the diagnosis of myocardial infarction. This article discusses the structure and function of the troponin complex and the release of cardiac troponin molecules from the injured cardiomyocyte into the circulation. An overview of current cardiac troponin assays and their classification according to sensitivity is presented. The diagnostic criteria, role, and usefulness of cardiac troponin for myocardial infarction are discussed. In addition, several examples are given of the usefulness of high-sensitivity cardiac troponin assays for short-term and long-term prediction of adverse events.
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earlier detection of myocardial injury in a preliminary evaluation using a new troponin i assay with improved sensitivity
American Journal of Clinical Pathology, 2007Co-Authors: Stacy E F Melanson, David A Morrow, Petr JarolimAbstract:Cardiac Troponins are important biochemical markers for defining the presence of myocardial injury. However, limitations in troponin testing exist, including the relatively late increase in troponin after onset of ischemia. We therefore evaluated a more sensitive troponin assay for detection of myocardial injury in “early presenters.” Discarded serial specimens were obtained from 103 patients who had a negative cardiac troponin I (cTnI) result followed by a positive cTnI result. Results were obtained using our current cTnI method and a new more sensitive assay, TnI-Ultra (Siemens Medical Solutions, Diagnostics Division,
Elizabeth Selvin - One of the best experts on this subject based on the ideXlab platform.
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high sensitivity cardiac Troponins for mortality risk stratification in middle aged adults with kidney dysfunction
Journal of the American College of Cardiology, 2020Co-Authors: Olive Tang, Kunihiro Matsushita, Josef Coresh, Ron C Hoogeveen, Christie M Ballantyne, Morgan E Grams, Elizabeth SelvinAbstract:High-sensitivity troponin I (hs-cTnI) and T (hs-cTnT) are associated with cardiovascular (CVD) and mortality risk. Both Troponins are elevated in the setting of chronic kidney disease. We assessed the association of hs-cTnI and hs-cTnT with mortality in adults with and without chronic kidney disease
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performance of high sensitivity cardiac troponin assays to reflect comorbidity burden and improve mortality risk stratification in older adults with diabetes
Diabetes Care, 2020Co-Authors: Olive Tang, Natalie Daya, Kunihiro Matsushita, Josef Coresh, Richey A Sharrett, Ron C Hoogeveen, Gwen B Windham, Christie M Ballantyne, Elizabeth SelvinAbstract:OBJECTIVE Incorporation of comorbidity burden to inform diabetes management in older adults remains challenging. High-sensitivity cardiac Troponins are objective, quantifiable biomarkers that may improve risk monitoring in older adults. We assessed the associations of elevations in high-sensitivity cardiac troponin I (hs-cTnI) and T (hs-cTnT) with comorbidities and improvements in mortality risk stratification. RESEARCH DESIGN AND METHODS We used logistic regression to examine associations of comorbidities with elevations in either troponin (≥85th percentile) among 1,835 participants in the Atherosclerosis Risk in Communities (ARIC) Study with diabetes (ages 67–89 years, 43% male, 31% black) at visit 5 (2011–2013). We used Cox models to compare associations of high cardiac Troponins with mortality across comorbidity levels. RESULTS Elevations in either troponin (≥9.4 ng/L for hs-cTnI, ≥25 ng/L for hs-cTnT) were associated with prevalent coronary heart disease, heart failure, chronic kidney disease, pulmonary disease, hypoglycemia, hypertension, dementia, and frailty. Over a median follow-up of 6.2 years (418 deaths), both high hs-cTnI and high hs-cTnT further stratified mortality risk beyond comorbidity levels; those with a high hs-cTnI or hs-cTnT and high comorbidity were at highest mortality risk. Even among those with low comorbidity, a high hs-cTnI (hazard ratio [HR] 3.0 [95% CI 1.7, 5.4]) or hs-cTnT (HR 3.3 [95% CI 1.8, 6.2]) was associated with elevated mortality. CONCLUSIONS Many comorbidities were reflected by both hs-cTnI and hs-cTnT; elevations in either of the Troponins were associated with higher mortality risk beyond comorbidity burden. High-sensitivity cardiac Troponins may identify older adults at high mortality risk and be useful in guiding clinical care of older adults with diabetes.
Daych Chongnarungsin - One of the best experts on this subject based on the ideXlab platform.
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combined d dimer and cardiac Troponins for pulmonary embolism in renal insufficiency
The American Journal of Medicine, 2014Co-Authors: Charat Thongprayoon, Wisit Cheungpasitporn, Daych ChongnarungsinAbstract:We thank Lindner et al for their interesting research study, “D-dimer to Rule Out Pulmonary Embolism in Renal Insufficiency” in the April 2014 issue of the Journal. The authors demonstrated the high sensitivity of D-dimer for exclusion of pulmonary embolism. Unfortunately, its specificity decreased significantly with impaired renal insufficiency. We would propose the addition of cardiac enzymes (troponin I or T) to D-dimer in the study model to provide higher specificity in the diagnosis of pulmonary embolism in patients with chronic kidney disease. Although renal impairment is a condition associated with elevated D-dimer and troponin concentrations, serum Troponins are high in 30% to 50% of patients with moderate to extensive pulmonary embolism with a significant increase in mortality. Elevated troponin T is also significantly associated with an increased risk of cardiovascular disease mortality in patients with chronic kidney disease.
Evangelos Giannitsis - One of the best experts on this subject based on the ideXlab platform.
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Troponins established and novel indications in the management of cardiovascular disease
Heart, 2018Co-Authors: Evangelos Giannitsis, Hugo A KatusAbstract:### Learning objectives ### Cardiac Troponins Cardiac Troponins (cTn) are components of the thin filament of the sarcomere of striated muscle regulating excitation–contraction coupling in the heart.1 2 Owing to their superior sensitivity and cardiac tissue specificity compared with cardiac enzymes or creatine kinase-MB mass, cardiac troponin T or I (cTn) are now considered the preferred biomarkers for the diagnosis of myocardial injury.3 4 Reasons for elevated cTn with or without kinetic changes are numerous and sometimes multifactorial while in some cases a reason cannot be identified despite intensive diagnostic work-up.4 Use of high-sensitivity (hs) troponin assays allow more accurate and earlier detection of myocardial infarction (MI).5–7 Higher analytical sensitivity increases the number of patients with analytically true positive cTn result due to non-ST-elevation MI but also due to numerous acute or chronic diseases in the absence of overt ischaemic heart disease. Use of hsTn has also enabled to determine a 99th percentile value of a healthy reference population and to demonstrate lower reference values for women than for men.5 8 For diagnosis, prognosis and management of acute coronary syndrome (ACS), cTn should—with few exceptions—be measured serially …
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differential diagnosis of elevated Troponins
Heart, 2006Co-Authors: Susanne Korff, Hugo A Katus, Evangelos GiannitsisAbstract:In the year 2000, the European Society of Cardiology and the American College of Cardiology Committee jointly redefined myocardial infarction (MI) by an elevation of cardiac troponin T (cTnT) or I (cTnI) in conjunction with clinical evidence of myocardial ischaemia.1 Since then, cTnT and cTnI have replaced creatine kinase-MB (CK-MB) as the preferred biochemical markers for the diagnosis of MI. The decision for including cardiac Troponins (cTn) in the diagnostic pathway was made because of the high sensitivity of cTn for detection of even small amounts of myocardial necrosis. An elevation of cTn indicates the presence of, but not the underlying reason for, myocardial injury. Hence, besides acute myocardial infarction (AMI), there is a myriad of potential diseases with troponin release, including acute pulmonary embolism, heart failure, myocarditis, and end stage renal disease. But regardless of what the release mechanism into the blood from cardiac myocytes is, elevated cTnT and cTnI almost always imply a poor prognosis. This article attempts to highlight the differential diagnosis of elevated cTn according to the various aetiologies of myocyte damage (table 1). View this table: Table 1 Causes of elevated Troponins, prevalence, and underlying mechanism The troponin complex consists of three subunits—troponin C, troponin I, and troponin T—and is located on the myofibrillar thin (actin) filament of striated (skeletal and cardiac) muscle (fig 1). The cardiac isoforms troponin T and I are only expressed in cardiac muscle. Hence, cardiac troponin T (cTnT) and I (cTnI) are more specific than creatine kinase (CK) values for myocardial injury and, because of their high sensitivity, they may even be elevated when CK-MB concentrations are not. The cTn complex regulates excitation–contraction coupling in the heart. Cardiac troponin C (cTnC), a calcium (Ca2+) binding 18-kD-protein, regulates the activation of the actin filaments. cTnI (∼23 kD) inhibits contraction in the absence of Ca …
