scholarly journals Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction

2006 ◽  
Vol 99 (10) ◽  
pp. 1141-1147 ◽  
Author(s):  
Lene H. Madsen ◽  
Geir Christensen ◽  
Terje Lund ◽  
Victor L. Serebruany ◽  
Chris B. Granger ◽  
...  
2021 ◽  
Author(s):  
Sajad Khiali ◽  
Parvin Sarbakhsh ◽  
Sina Mashayekhi ◽  
Elham Mohamadrezapour ◽  
Samaneh Dousti ◽  
...  

Purpose: Given the potential anti-ischemic effects of allopurinol, we aimed to assess whether allopurinol administration may reduce myocardial injury following non-ST elevation myocardial infarction (NSTEMI). Methods: A randomized clinical trial (RCT) was conducted on 100 individuals with NSTEMI. The intervention group (n=50) received 600 mg oral allopurinol at the time of diagnosis of NSTEMI, followed by 300 mg every day for two next days and the standard treatment of NSTEMI, while the control group (n=50) received only the standard treatment. Serum concentrations of cardiac troponin I (cTnI) were measured at baseline, and 8, 16, 24, and 32 hours after the treatment. Results: The baseline demographic and clinical data of the patients were not statistically different between the intervention and control groups (all P > 0.05). The comparing estimated marginal mean ± standard error for cardiac troponin I (cTnI) levels revealed no significant difference between the study groups (2.93 ± .27, 2.25 ± .27; P=0.082). The linear mixed model results showed that the interaction of time and group was not statistically different (P=0.751). Moreover, there was a decreasing trend over time for cTnI in both groups (P=0.039). Conclusion: The present pilot RCT did not support the potential cardio-protective benefits of allopurinol administration on decreasing myocardial injury following NSTEMI.


Author(s):  
F.R. Marpaung ◽  
Sidarti Soehita SFHS ◽  
Yogiarto Yogiarto ◽  
Yusri Yusri

Acute coronary syndrome (ACS) is caused by atherosclerotic plaque rupture and microembolization which lead to decreased oxygensupply into the myocardium. Generally, ACS includes an unstable angina (UA), non ST elevation myocardial infarction (NSTEMI) andST elevation myocardial infarction. ACS may lead to ST elevation Myocardial Infarction (STEMI) and finally a sudden death. Cardiactroponin is used routinely for diagnosing acute coronary syndrome (ACS); however, troponin is not elevated in the initial hours ofACS—precluding their usefulness in the early diagnosis. The aim of this study is to determine the diagnostic value of h-FABP Rapid testin relation to Cardiac Troponin I in NSTEMI. Seventy five patients with ACS were enrolled in this study. All patients presented symptomswithin six hours of the onset and suffered typical chest pain. Blood samples were obtained for rapid test h-FABP (cardiodetect) andTroponin I (tropospot). The h-FABP showed a 93.5% sensitivity, 95% CI: 81.1–98.3 and 82.8% specificity, 95% CI: 63.5–93.5, PositivePredictive Value 89.6%, 95% CI: 76.6–96.1, Negative Predictive Value 88.9%, 95% CI: 69.7–97.1, respectively in the first six hours.Troponin I had a 60.9% sensitivity, 95% CI: 45.4–74.5 and 96.6% specificity, 95% CI: 80.4–99.8, Positive Predictive Value 96.6%,95% CI: 80.4–99.8, Negative Predictive Value 60.9%, 95% CI: 45.4–74.5, respectively in the first six hours. Based on this study resulton patients with Non ST Elevation Myocardial Infarction (NSTEMI), it is suggested to determine the h-FABP as well. For this purpose,point-of-care h-FABP test can be utilized, as it has the advantage of highly sensitivity and specificity, beside it can carry on a bedsidetesting and show a rapid test results as well.


1992 ◽  
Vol 38 (11) ◽  
pp. 2203-2214 ◽  
Author(s):  
G S Bodor ◽  
S Porter ◽  
Y Landt ◽  
J H Ladenson

Abstract To improve the specificity of biochemical markers of myocardial infarction (MI), we have developed a double monoclonal "sandwich" enzyme immunoassay to measure cardiac troponin-I (cTnI) in serum. We produced eight IgG monoclonal antibodies against human cardiac troponin-I (cTnI) and tested them against human and animal (canine, bovine, and rabbit) troponins. Five antibodies were cardiac-specific; none of the antibodies were species-specific. Two of the five cTnI-specific monoclonal antibodies were utilized in an immunoassay. Standards were made by adding purified human cTnI to affinity-stripped cTnI-free human sera to cover the range 0-100 micrograms/L for cTnI. The dose-response curve was nonlinear but reproducible. Total assay imprecision (CV) varied between 11% and 21%. The upper limit of the reference range (nonparametric 95% interval) was established as 3.1 micrograms/L by measuring cTnI concentration in sera of 159 hospitalized patients without evidence of cardiac disease. Purified human skeletal TnI up to 10,000 micrograms/L did not affect the assay (calculated cross-reactivity < 0.1%). Diagnostic sensitivities of creatine kinase MB isoenzyme (CK-MB) and cTnI were evaluated retrospectively in 49 consecutive patients with proven MI. In the 30 patients for whom sufficient information was available to establish an accurate time course, CK-MB was more sensitive during the first 4 h after the onset of chest pain, but thereafter the sensitivities were similar up to 48 h. However, cTnI is more cardiac-specific than is CK-MB and remains increased longer than does CK-MB.


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