Abstract 14077: Use of Cardiac Troponin I to Identify Acute Myocardial Infarction in Patients With Impaired Renal Function

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Beatrice von Jeinsen ◽  
Stergios Tzikas ◽  
Lars Palapies ◽  
Tanja Zeller ◽  
Christoph Bickel ◽  
...  

Introduction: Cardiac troponins are the gold standard to diagnose acute myocardial infarction (AMI). Troponin I (TnI) levels are known to be increased in patients with chronic kidney disease (CKD) irrespective of an AMI. The established diagnostic TnI cut-off to detect AMI is calculated based on a healthy reference population and might not be representative for CKD patients. Hypothesis: The aim of this study was to investigate TnI levels in patients with and without CKD with suspected AMI and to calculate CKD- optimized diagnostic TnI thresholds. Methods: Of 1572 patients enrolled with suspected AMI, 266 patients showed an impaired renal function with estimated glomerular filtration rate (eGFR) of less then 60ml/min and were classified as patients with CKD. N=77 (34%) of patients with CKD and n=278 (24%) without CKD had the final diagnosis AMI. TnI was measured on admission and after 3h. Based on receiver operator characterics curve analyses (AUROC) of the baseline levels CKD optimized TnI threshold were derived. Sensitivity and specifity were calculated for the 99th percentile cut-off (30.0 pg/mL), the optimized cut-off (58.0 pg/mL) and the change in TnI concentration within 3h after admission. Results: Patients with CKD had higher TnI levels then patients without CKD (6.0pg/mL vs. 20.9pg/ml; p<0.001). This difference was more pronounced in patients without AMI (median 9.1 vs. 4.4; p<0.001), whereas the difference diminished in AMI patients (median 337.4 vs. 238.6; p=0.83). In CKD patients TnI remained a strong marker to detect AMI with AUROC of 0.933 compared to 0.969 in patients without CKD. Applying the 99th percentile threshold it was associated with a relevant loss of specificity in CKD patients with 80% compared to 96% in patients without CKD. This poor specificity could be regained by use of a higher CKD-optimized threshold or use of the change in TnI concentration within 3h leading to specificities of 90% and 96%, respectively. Conclusions: Patients presenting with suspected AMI and CKD have higher TnI levels on admission compared to patients without CKD leading to a low specificity detecting AMI in CKD patients. Using an CKD-optimized TnI cut-off level on admission or using the change in TnI concentration within 3h is able to regain this lost specificity.

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Tri Prasetyorini ◽  
Rizka Noviyanti ◽  
Putu Puja Permata Kasih ◽  
Diah Lestari

Acute Myocardial Infarction (AMI) is a manifestation of acute myocardial ischemia and is generally caused by the rupture of atherosclerosis and thrombus in the coronary blood vessels. Rupture causes an inflammatory process that leukocytes which acts as a marker of inflammation increases. Heart muscle damage that occurs also resulted in levels of troponin I as one of the markers of increased cardiac examination. Based on that research aims to determine the correlation between the levels of troponin I and the number of leukocytes in patients with suspected AMI.This research method is analytical observation with a data sample of 100 patients with suspected AMI diagnosis by doctors as well as examine the levels of troponin I and the number of leukocytes in dr. Abdulmadjid Chasbullah Bekasi. The correlation between the levels of troponin I and leukocyte counts were analyzed using Spearman's test. Data studied consisted of 52 people (52%) men and 48 (48%) of women. By age group, age range 46-65 years become the largest age group into patients with suspected AMI is 55 people (55%). Obtained 34 (34%) of patients with suspected AMI who had higher levels of troponin I and normal leukocyte count, and 39 (39%) of patients with suspected AMI who had troponin I levels and elevated leukocyte count. On Spearman’s test seen the correlation between levels of troponin I with the total of leukocytes in patients with suspected AMI (p = 0.000 and r = 0.50). This shows an increase in troponin I, which runs parallel with the increase in the total of leukocytes. Suggested for further research to see the difference increased levels of troponin I and the total of leukocytes between 3-5 hours and 14-18 hours after myocardial injury


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Bang ◽  
C Hansen ◽  
K Glerup Lauridsen ◽  
C Alcaraz Frederiksen ◽  
M Schmidt ◽  
...  

Abstract Introduction Current ESC guidelines have introduced a 0h/1h algorithm for accelerated rule-in or rule-out of acute myocardial infarction (MI) when using assay specific high-sensitive cardiac troponin I (hs-cTnI). Several studies have investigated the diagnostic performance and safety of this approach using different hs-cTnI assays. However, little is known of the diagnostic performance of a 0h/30min algorithm. Purpose To evaluate the diagnostic accuracy of early rule-in or rule-out of MI after 30 minutes by applying assay specific hs-cTnI cut-off values from a recently validated 0h/1h algorithm. Methods We prospectively enrolled chest pain patients suggestive of MI admitted to the Emergency Department. Patients underwent serial hs-cTnI measurements at admission (0 hour) and after 3 hours according to clinical practice. In addition, hs-cTnI measurements were performed after 30 minutes. The assay specific cut-off values from the 0h/1h algorithm were applied to the 30 minute cohort (figure 1). Final diagnosis was adjudicated independently by two physicians. Results In total, 943 patients were included. MI was the final diagnosis in 67 (7.1%) patients. Overall, absolute hs-cTnI values after 30 minutes were significantly higher in the MI group than in the non-MI group (19.2 (Q1:Q3) 2.7–75.3) ng/L versus 0.1 (0.2–0.7) ng/L, p<0.001). When applying the assay-specific hs-cTnI cut-off valuesfor the 0h/1h algorithmto the 30 minute patient cohort, 52.4% of patients were classified as rule-out with a negative predictive value of 100% (95% CI: 99.2–100). In total, 8.5% were classified as rule-in with a positive predictive value of 83.8% (95% CI: 74.2–90.3). Sensitivity was 100% (95% CI: 94.6–100) and specificity was 97.4% (95% CI: 95.7–98.6). Overall, 39.1% were assigned to the observational zone with a 3.5% prevalence of MI. Conclusions The use of assay specific hs-cTnI measurement at admission (0h) and 30 min later can be used to safely rule-out MI. This indicates that it might be safe to develop a 0h/30min algorithm and hereby reduce time to diagnosis even further. NCT03634384. Acknowledgement/Funding Randers Regional Hospital, A.P Møller Foundation, Boserup Foundation, Korning Foundation, Højmosegård Grant, Siemens Healthcare (TNIH assays), etc.


2010 ◽  
Vol 13 (1) ◽  
pp. 18-22 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Romano Arcieri ◽  
Maria Quarto ◽  
Gianluca Pendenza ◽  
Chiara Lanzillo ◽  
...  

2019 ◽  
Vol 65 (11) ◽  
pp. 1437-1447 ◽  
Author(s):  
Thomas Nestelberger ◽  
Jasper Boeddinghaus ◽  
Jaimi Greenslade ◽  
William A Parsonage ◽  
Martin Than ◽  
...  

Abstract BACKGROUND We aimed to derive and externally validate a 0/2-h algorithm using the high-sensitivity cardiac troponin I (hs-cTnI)-Access assay. METHODS We enrolled patients presenting to the emergency department with symptoms suggestive of acute myocardial infarction (AMI) in 2 prospective diagnostic studies using central adjudication. Two independent cardiologists adjudicated the final diagnosis, including all available medical information including cardiac imaging. hs-cTnI-Access concentrations were measured at presentation and after 2 h in a blinded fashion. RESULTS AMI was the adjudicated final diagnosis in 164 of 1131 (14.5%) patients in the derivation cohort. Rule-out by the hs-cTnI-Access 0/2-h algorithm was defined as 0-h hs-cTnI-Access concentration &lt;4 ng/L in patients with an onset of chest pain &gt;3 h (direct rule-out) or a 0-h hs-cTnI-Access concentration &lt;5 ng/L and an absolute change within 2 h &lt;5 ng/L in all other patients. Derived thresholds for rule-in were a 0-h hs-cTnI-Access concentration ≥50 ng/L (direct rule-in) or an absolute change within 2 h ≥20 ng/L. In the derivation cohort, these cutoffs ruled out 55% of patients with a negative predictive value (NPV) of 99.8% (95% CI, 99.3–100) and sensitivity of 99.4% (95% CI, 96.5–99.9), and ruled in 30% of patients with a positive predictive value (PPV) of 73% (95% CI, 66.1–79). In the validation cohort, AMI was the adjudicated final diagnosis in 88 of 1280 (6.9%) patients. These cutoffs ruled out 77.9% of patients with an NPV of 99.8% (95% CI, 99.3–100) and sensitivity of 97.7% (95% CI, 92.0–99.7), and ruled in 5.8% of patients with a PPV of 77% (95% CI, 65.8–86) in the validation cohort. CONCLUSIONS Safety and efficacy of the l hs-cTnI-Access 0/2-h algorithm for triage toward rule-out or rule-in of AMI are very high. TRIAL REGISTRATION APACE, NCT00470587; ADAPT, ACTRN1261100106994; IMPACT, ACTRN12611000206921.


2013 ◽  
Vol 20 (6) ◽  
pp. 672-678 ◽  
Author(s):  
Tomasz Podolecki ◽  
Radosław Lenarczyk ◽  
Jacek Kowalczyk ◽  
Andrzej Świątkowski ◽  
Piotr Chodór ◽  
...  

1970 ◽  
Vol 8 (3) ◽  
pp. 57-63
Author(s):  
Md Sahabuddin Joarder ◽  
Md Jafarullah ◽  
Ahmed Moinuddin

Introduction: Cardiac troponin-I (cTnI) is known to have the highest specificity and analytic sensitivity for detection of myocardial injury; it is used both as diagnostic and prognostic marker. This study was aimed to confirm this idea. Subjects & methods: This prospective observational study included 60 patients of 40 to 65 years age range diagnosed as acute myocardial infarction. The mean ages were 50±8 years and 53±8 years in Q -wave AMI and non Q-wave AMI respectively. Male and female patients included were 86.7% and 13.3%; BMI was 25.3±1.5. Results: Study showed troponin-I 7.53±0.086 ng/ml in Q wave and in non Q-wave AMI was 6.38±0.64 ng/ml after 24 hours of attack of AMI without any significant difference between two groups (P>0.05). The mean troponin-I within 9 hours of attack, were 1.60±0.80 ng/ml and 2.7±1.4 ng/ml in stable and unstable group respectively and the difference found statistically significant (P<0.05). The mean troponin-I between 9-24 hours of attack were 2.90±1.20 ng/ml and 4.90±3.20 ng/ml in stable and unstable group respectively and the difference found statistically significant (P<0.01). The mean troponin-I in unstable group after 24 hours was 9.20±4.30 ng/ml which was more than between 9-24 hours and the difference was significant (P>0.001). In clinicopathological outcome evaluation 37 patients had troponin-I level >1.5 ng/ml in which 29 patients developed unstability and 8 patients were stable. Conclusion: Serum cTnI is better and more characteristic biomarker for risk prediction and prognosis evaluation in AMI patients. Key words: Cardiac Troponin-I, acute myocardial infarction, risk stratification.   DOI: 10.3329/bjms.v8i3.3984 Bangladesh Journal of Medical Sciences Vol.8(3) 2009 p57-63


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Nestelberger ◽  
J Boeddinghaus ◽  
J Greenslade ◽  
L Cullen ◽  
W Parsonage ◽  
...  

Abstract Background We aimed to derive and externally validate a 0/2h-algorithm using the novel high-sensitivity cardiac troponin I (hs-cTnI-Access) assay. Methods We enrolled patients presenting to the emergency department with symptoms suggestive of acute myocardial infarction (AMI) in two prospective chest pain trials. Two independent cardiologists adjudicated the final diagnosis including all available medical information including cardiac imaging. Hs-cTnI concentrations were measured at presentation and after 2h. Primary diagnostic endpoint was the derivation and validation of an hs-cTnI-Access specific 0/2h-algorithm. Primary prognostic endpoint was overall survival of patients after 30- and 720-days of follow-up. Results AMI was the adjudicated final diagnosis in 164/1131 (14.5%) patients in the derivation and in 88/1280 (6.9%) patients in the validation cohort. Median hs-cTnI Access concentrations at presentation were significantly higher in patients with AMI as compared to patients with non-AMI in both cohorts (104 ng/L versus 3.4 ng/L and 29 ng/L vs. 2.3 ng/L, p-value both <0.001) Applying the derived hs-cTnI-Access 0/2h-algorithm (Figure 1A) to the validation cohort (Figure 1B), 77.9% of patients were ruled-out (sensitivity 97.7% [95% CI, 92–99.7], negative predictive value [NPV] 99.8% [95% CI, 99.3–100]), and 5.8% of patients were ruled-in (specificity 98.6% [95% CI, 97.7–99.2], positive predictive value [PPV] 77% [95% CI, 65.8–86]). Among 1617 patients ruled-out for AMI in both cohorts together, 3 (0.2%) patients with AMI have been missed, of whom 2 patients had type 2 myocardial infarction (both with tachyarrhythmia). Patients ruled-out by the 0/2h-algorithm had a survival rate of 98.4% and 99.9% after two years or one year of follow up in both cohorts, respectively. Figure 1 Conclusions Diagnostic performance of the hs-cTnI Access 0/2h-algorithm for triage of AMI is excellent with high safety for rule-out and high accuracy for rule-in. Acknowledgement/Funding European Union, Swiss National Foundation, University Hospital Basel, University Basel


2015 ◽  
Vol 61 (6) ◽  
pp. 870-876 ◽  
Author(s):  
Craig B Wilen ◽  
Jeffrey J Szymanski ◽  
Steven Hung ◽  
Anand Rajan ◽  
Paul M Lavigne ◽  
...  

Abstract BACKGROUND Myocardial infarction is characterized by an increase of cardiac troponin I (cTnI) above the 99th percentile of a reference population. Our hospital switched from 1 contemporary cTnI assay to another and observed a doubling of cTnI results above the assays' respective 99th percentile cutoffs. We investigated the potential impact on inpatient management and outcomes. METHODS We performed a retrospective cohort study of 45 498 individuals with ≥1 cTnI result between January 2013 and June 2014. The Dimension cTnI assay was used in 2013; the Abbott Architect cTnI assay was used in 2014. RESULTS Before switching cTnI assays, 19.2% (4742/30 872) of patients had at least 1 of the first 3 cTnIs above the 99th percentile (0.07 μg/L). After switching to the Architect cTnI assay, 31.4% (4034/14 626) of patients had at least 1 cTnI above the 99th percentile (0.03 μg/L). This increase was due to the difference in the assays' 99th percentile cutoffs. Having an increased cTnI reported on the Architect assay that would not have been reported as such on the Dimension assay (0.03–0.06 μg/L) correlated with increased inpatient mortality, length of stay, non–ST elevation myocardial infarction diagnosis, therapeutic heparin use, and percutaneous coronary intervention, relative to individuals with cTnI &lt;0.03 μg/L. CONCLUSIONS The changes observed in patient outcomes and management were likely due to the increased sensitivity and lower 99th percentile cutoff of the Architect assay. It is important to recognize the potential impact that differences in sensitivity and assay configuration may have on patient management.


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