Abstract 2425: Absence of Auto-Antibodies against Cardiac Troponin I Predicts Improvement of Left Ventricular Function after Acute Myocardial Infarction

Application of antibodies against cardiac troponin I (cTnI-Ab) can induce dilation and dysfunction of the heart in mice. Recently, we demonstrated that immunization with cTnI induces inflammation and fibrosis in myocardium of mice. Others have shown that autoanti-bodies to cTnI are present in patients with acute coronary syndrome. But little is known about the clinical relevance of detected cTnI-Ab. First, anti-cTnI and anti-cTnT antibody titers were measured in sera from 272 patients with dilated- (DCM) and 185 with ischemic- (ICM) cardiomyopathy. Secondly, 108 patients with acute myocardial infarction (AMI) were included for a follow-up study. Heart characteristics were determined by magnetic resonance imaging 4 days and 6 –9 months after AMI. Altogether, in 7,0% of patients with DCM and in 9,2% with ICM an anti-cTnI IgG antibody titer ≥1:160 was measured. In contrast, only in 1,7% of patients with DCM and in 0,5% with ICM an anti-cTnT IgG antibody titer ≥1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titers ≥1:160. TnI-Ab negative patients showed a significant increase in LVEF and stroke volume 6 –9 months after AMI. In contrast, there was no significant increase in LVEF and stroke volume in TnI-Ab positive patients. We demonstrate for the first time that the prevalence of cTnI-Abs in patients with AMI has an impact on the improvement of the LVEF over a study period of 6 –9 months.

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P1735Two-hour algorithm for early diagnosis of acute myocardial infarction using a novel high-sensitivity cardiac troponin I assay

European Heart Journal ◽

10.1093/eurheartj/ehz748.0489 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

T Nestelberger ◽

J Boeddinghaus ◽

J Greenslade ◽

L Cullen ◽

W Parsonage ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Predictive Value ◽

Cardiac Troponin ◽

Troponin I ◽

Validation Cohort ◽

High Sensitivity ◽

Final Diagnosis ◽

Cardiac Troponin I

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

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Faculty Opinions recommendation of One-hour rule-in and rule-out of acute myocardial infarction using high-sensitivity cardiac troponin I.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725420089.793507697 ◽

2015 ◽

Author(s):

Patrick Ray

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiac Troponin ◽

Troponin I ◽

High Sensitivity ◽

Cardiac Troponin I ◽

Rule Out

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Acceptable Analytical Variation May Exceed High-Sensitivity Cardiac Troponin I Cutoffs in Early Rule-Out and Rule-In Acute Myocardial Infarction Algorithms

Clinical Chemistry ◽

10.1373/clinchem.2016.255448 ◽

2016 ◽

Vol 62 (6) ◽

pp. 887-889 ◽

Cited By ~ 36

Author(s):

Peter A Kavsak ◽

Andrew C Don-Wauchope ◽

Stephen A Hill ◽

Andrew Worster

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiac Troponin ◽

Troponin I ◽

High Sensitivity ◽

Cardiac Troponin I ◽

Analytical Variation ◽

Rule Out

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Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

Clinical Chemistry ◽

10.1093/clinchem/40.7.1291 ◽

1994 ◽

Vol 40 (7) ◽

pp. 1291-1295 ◽

Cited By ~ 197

Author(s):

J E Adams ◽

K B Schechtman ◽

Y Landt ◽

J H Ladenson ◽

A S Jaffe

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Creatine Kinase ◽

Cardiac Troponin ◽

Troponin I ◽

Characteristic Curve ◽

Cardiac Injury ◽

Cardiac Troponin I ◽

Creatine Kinase Mb ◽

Coronary Care

Abstract Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.

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