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Endogenous stress response in Tako-Tsubo cardiomyopathy and acute myocardial infarction
Julia Meissner1, Holger Nef, Joelyn Darga
1Department of Internal Medicine, University Hospital Basel, Basel, Switzerland.
Insights
Copeptin levels, a marker of stress, are significantly lower in patients with Tako-Tsubo cardiomyopathy (TTC) than in those with acute myocardial infarction (AMI). This finding suggests copeptin can help differentiate between these conditions non-invasively.
Area of Science:
- Cardiology
- Biomarkers
- Cardiovascular Disease
Background:
- Tako-Tsubo cardiomyopathy (TTC) and acute myocardial infarction (AMI) share similar clinical presentations.
- Distinguishing TTC from AMI typically requires invasive coronary angiography.
- A non-invasive method for differentiation is highly desirable.
Purpose of the Study:
- To investigate the endogenous stress response in patients with TTC and AMI.
- To assess the utility of plasma copeptin levels in differentiating TTC from AMI.
- To explore copeptin as a potential non-invasive biomarker.
Main Methods:
- Compared plasma copeptin levels in 21 TTC patients and 21 matched AMI patients.
- Measured copeptin levels at initial presentation.
- Analyzed copeptin levels against cardiac troponin T for diagnostic accuracy.
Main Results:
- Copeptin levels were significantly lower in TTC patients (median 4.8 pM) compared to AMI patients (median 25.6 pM).
- Copeptin demonstrated higher diagnostic accuracy (AUC 0.782) than cardiac troponin T (AUC 0.549) for differentiating TTC.
- An optimal copeptin cut-off of 7.8 pM showed 67% sensitivity and 86% specificity.
Conclusions:
- The endogenous stress response differs between TTC and AMI, as indicated by copeptin levels.
- Copeptin shows potential as a valuable non-invasive biomarker for differentiating TTC from AMI.
- Further research may establish copeptin's role in routine clinical practice.
Background:
As the clinical, electrocardiographic and laboratory presentation of Tako-Tsubo cardiomyopathy (TTC) and acute myocardial infarction (AMI) is similar, both entities are in general only distinguishable by coronary angiography. The purpose of this study was to examine the endogenous stress response at presentation, quantified by the copeptin level, of patients with TTC and patients with AMI, as copeptin may be useful in the non-invasive differentiation between both diseases.
Methods:
We compared the endogenous stress response at initial presentation, quantified by the plasma copeptin levels, in 21 consecutive patients finally diagnosed with TTC and 21 patients finally diagnosed with AMI matched for sex and time since chest pain onset.
Results:
The prevalence of cardiovascular risk factors and initial cardiac troponin T levels were comparable in TTC and AMI. Copeptin levels were significantly lower in patients with TTC when compared to patients with AMI (median 4·8 [interquartile range, IQR 3·5-13·5] pM vs. 25·6 [IQR 12·1-63·9] pM, P = 0·002). The accuracy for diagnosing TTC as quantified by the area under the receiver operating characteristics curve was significantly higher for copeptin than for cardiac troponin T (0·782 vs. 0·549, P = 0·031). The optimal cut-off value for differentiation between TTC and AMI was found at a copeptin level of 7·8 pM (sensitivity 67% at a specificity of 86%, negative predictive value 72%, positive predictive value 82%).
Conclusions:
The endogenous stress response, quantified by a novel sensitive biomarker, seems to be different in patients with TTC and AMI. Copeptin levels may be helpful in the non-invasive differentiation between TTC and AMI.
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