scholarly journals Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle

1997 ◽  
Vol 43 (6) ◽  
pp. 976-982 ◽  
Author(s):  
Mary D McLaurin ◽  
Fred S Apple ◽  
Ellen M Voss ◽  
Charles A Herzog ◽  
Scott W Sharkey
Keyword(s):  
Skeletal Muscle ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cardiac Troponin ◽  
First Generation ◽  
Troponin T ◽  
Ischemic Heart ◽  
Cardiac Troponin T ◽  
Dialysis Patients ◽  
Acute Ischemic Heart Disease

Abstract Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.

scholarly journals Predictors of High-Sensitivity Cardiac Troponin T Elevation in Patients with Acute Paroxysmal Supraventricular Tachycardia and Ischemic Heart Disease

2017 ◽  
Vol 44 (5) ◽  
pp. 306-311 ◽  
Author(s):  
Mehdi Sayadnik ◽  
Akbar Shafiee ◽  
Yaser Jenab ◽  
Arash Jalali ◽  
Saeed Sadeghian
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Supraventricular Tachycardia ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
Ischemic Heart ◽  
Paroxysmal Supraventricular Tachycardia ◽  
Cardiac Troponin T ◽  
Enzyme Elevation

We studied the predictors and patterns of high-sensitivity cardiac troponin T (hs-cTnT) elevation in patients with paroxysmal supraventricular tachycardia (PSVT) in the presence and absence of ischemic heart disease. During calendar year 2013, we enrolled 70 of 72 consecutive adult patients with PSVT who presented at our center within 4 hours after the onset of tachycardia. On the basis of increased hs-cTnT at either of 2 initial measurements, we divided patients into groups (hs-cTnT–positive and hs-cTnT–negative), to study the predictors of enzyme elevation. We then divided the hs-cTnT–positive patients into 2 groups—those with and those without ischemic heart disease—and compared hs-cTnT changes. We observed hs-cTnT elevation in 52 of the 70 patients (74.3%). The hs-cTnT–positive patients were significantly older (P=0.008) and had a significantly higher duration of tachycardia (P=0.01). Older age, the presence of chest pain, lower diastolic blood pressure, and longer duration of tachycardia increased the odds of enzyme elevation. Among patients with elevated hs-cTnT levels, the baseline and maximal hs-cTnT levels were significantly higher in ischemic patients (P=0.01 and P=0.003, respectively). The increase in hs-cTnT seemed to be higher and longer in ischemic patients, although this was not statistically significant (P=0.908). Finally, hs-cTnT did not decrease to baseline levels within 48 hours in either group. We found that hs-cTnT levels increased in all our patients with PSVT, more so in those with ischemic heart disease.

Elevation of cardiac troponin T in patients with decompensated heart failure can predict the presence of ischemic heart disease

2004 ◽  
Vol 10 (5) ◽  
pp. S158
Author(s):  
Himura Yoshihiro ◽  
Tamaki Youdou ◽  
Miake Makoto ◽  
Motooka Makoto ◽  
Izumi Toshiaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Decompensated Heart Failure ◽  
Ischemic Heart ◽  
Cardiac Troponin T

scholarly journals Elevated levels of cardiac troponin T in patients with permanent atrial fibrillation without ischemic heart disease

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P4083-P4083
Author(s):  
S. R. Ulimoen ◽  
S. Enger ◽  
J. Norseth ◽  
A. H. Pripp ◽  
M. Abdelnoor ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Ischemic Heart ◽  
Cardiac Troponin T ◽  
Permanent Atrial Fibrillation

scholarly journals Increased cardiac troponin T and endothelin-1 concentrations in dialysis patients may indicate heart disease

1999 ◽  
Vol 14 (8) ◽  
pp. 1948-1955 ◽  
Author(s):  
Christian Löwbeer ◽  
Astrid Ottosson-Seeberger ◽  
Sven A. Gustafsson ◽  
Rolf Norrman ◽  
Johan Hulting ◽  
...  
Keyword(s):  
Heart Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Dialysis Patients ◽  
Endothelin 1

scholarly journals Multicenter evaluation of a second-generation assay for cardiac troponin T

1997 ◽  
Vol 43 (10) ◽  
pp. 1877-1884 ◽  
Author(s):  
Hannsjörg Baum ◽  
Siegmund Braun ◽  
Willie Gerhardt ◽  
Georges Gilson ◽  
Gerd Hafner ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Troponin ◽  
First Generation ◽  
Second Generation ◽  
Troponin T ◽  
Myocardial Damage ◽  
Cross Reactivity ◽  
Cardiac Troponin T ◽  
Marathon Runners ◽  
Assay Time

Abstract We report on the evaluation of the second-generation assay for cardiac troponin T (cTnT) on the Enzymun®system. This new assay is completely specific for the cardiac isoform of TnT, utilizing two cardiospecific monoclonal antibodies. The assay time is reduced to 45 min. The interassay precision shows a median CV of 5.5%; 20% interassay CV was found between 0.05 and 0.1 μg/L. The cardiosensitivity of the second-generation cTnT assay in patients with ischemic myocardial injury appears equivalent when compared with the first-generation assay. We found no falsely positive results in patients with skeletal muscle damage including multitraumas, surgery patients, and marathon runners who showed highly increased values with the unspecific first-generation assay. In Duchenne disease cTnT was still increased, but to a much lower extent. cTnT remains increased in renal failure, but to a lesser degree than with the first-generation assay. The cause of this increase remains unclear. Although a cross-reactivity of skeletal muscle TnT in the second-generation assay could be excluded by our findings, minor myocardial damage or expression of the cardiac isoform of TnT in regenerating muscles cannot be ruled out in those cases with apparently falsely increased cTnT values. The second-generation cTnT assay is a step forward in the combination of cardiosensitivity and cardiospecificity in biochemical markers for diagnosis of heart disease.

Abstract 16708: Cathelicidin Related Antimicrobial Peptide Treated Bone Marrow Derived Mononuclear Cells Improves Cardiac Function in a Mouse Model of Acute Myocardial Infarction: Potential Therapeutic Targets in Ischemic Heart Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuri M Klyachkin ◽  
Prabhakara R Nagareddy ◽  
Ahmed Asfour ◽  
Shaojing Ye ◽  
Erhe Gao ◽  
...  
Keyword(s):  
Heart Disease ◽  
Cardiac Function ◽  
Ischemic Heart Disease ◽  
Infarct Size ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
In Vivo Studies ◽  
Boyden Chamber ◽  
Acute Ischemic Heart Disease

Introduction: Limited stem cell retention following intracoronary administration for ischemic heart disease has reduced the clinical efficacy of this novel therapy. Cathelicidins have been shown to prime BMMNC migration towards low gradients of SDF-1 suggesting a potential role in BMMNC retention. We sought to assess the safety and efficacy of BMMNC pre-treatment with CRAMP for treatment of acute ischemic heart disease. METHODS: BMMNCs isolated from GFP mice were incubated with recombinant CRAMP (2.5 μg/ml) or placebo for 1 hour followed by chemotaxis studies towards low levels of SDF-1 (2 ng/ml) using a Boyden chamber in vitro. During the in vivo studies, mice were randomized into 3 groups: AMI followed by injection of phosphate buffered saline (PBS), BMMNCs alone, or BMMNCs incubated with CRAMP. Scar size, survival and retention of injected BMNNCs were examined by immunohistochemistry at 5 weeks. Left ventricular function was measured by echocardiography at baseline, 48 hours, and 5 weeks after MI. Changes in infarct size between 5 days and 5 weeks after AMI was assessed by cardiac MRI utilizing delayed gadolinium enhancement. RESULTS: Treatment of BMNNCs with CRAMP enhanced their migration towards low, yet physiological, levels of SDF-1 (Fig 1A). In vivo, a greater proportion of cell survival and retention was observed in the BMNNC+CRAMP group than in the BMNNC-alone group (Fig 1B) and this was associated with higher percentage of BrdU positive cells (Fig 1C). Moreover, BMNNC+CRAMP administration led to significantly better survival, improvement of cardiac function (Fig 1D-H) and reduction in infarct size compared with other control groups (Fig 1I). CONCLUSIONS: Cathelicidins enhance BMMNC retention after intramyocardial administration for acute ischemic heart disease resulting in enhanced recovery. Therapies employing this strategy may represent an effective method for improving cardiac recovery and survival rate after AMI in human studies.

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