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Published on: December 11, 2017
Release kinetics of copeptin in patients undergoing transcoronary ablation of septal hypertrophy
Christoph Liebetrau1, Holger Nef, Sebastian Szardien
1Department of Cardiology, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany. c.liebetrau@kerckhoff-klinik.de
Insights
Copeptin levels rise rapidly after myocardial infarction, peaking at 90 minutes and returning to baseline within 24 hours. This rapid release pattern aids in early acute myocardial infarction diagnosis.
Area of Science:
- Cardiology
- Biomarker Research
Background:
- Establishing copeptin release kinetics in acute myocardial infarction (AMI) has been challenging.
- Transcoronary ablation of septal hypertrophy (TASH) in hypertrophic obstructive cardiomyopathy serves as a model for AMI.
Purpose of the Study:
- To analyze the release kinetics of copeptin following TASH.
- To evaluate copeptin as an early biomarker for myocardial infarction.
Main Methods:
- 21 patients undergoing TASH were studied.
- Serum copeptin levels were measured at multiple time points pre- and post-TASH (up to 24 hours).
- Sandwich immunoluminometric assay was used for copeptin quantification.
Main Results:
- Copeptin concentrations significantly increased by 30 minutes post-TASH (P = 0.002).
- Peak copeptin levels were observed 90 minutes after the procedure.
- Copeptin returned to baseline levels within 24 hours.
- Creatine kinase (CK) levels also significantly increased post-TASH (P < 0.001).
Conclusions:
- Early rule-out of suspected AMI is feasible using copeptin levels.
- Copeptin, in conjunction with cardiac troponin T, can improve early AMI diagnosis.
Background:
The release kinetics of copeptin in patients with acute myocardial infarction (AMI) have been difficult to establish.
Methods:
We analyzed the release kinetics of copeptin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH) as a model of AMI. We included 21 consecutive patients who underwent TASH. Blood samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and at 2, 4, 8, and 24 h after TASH. Serum copeptin was quantified by a sandwich immunoluminometric assay.
Results:
All patients had copeptin concentrations below the 99th percentile at baseline. The median copeptin concentration was significantly increased at 30 min [16.0 pmol/L; interquartile range (IQR), 13.4-20.2 pmol/L], compared with the median baseline concentration (6.6 pmol/L; IQR, 5.3-8.3 pmol/L; P = 0.002). The copeptin concentration peaked 90 min after induction of myocardial infarction and returned to baseline concentrations (median, 8.2 pmol/L; IQR, 6.3-10.1) after 24 h, compared with the above baseline values (P = 0.06). Serum creatine kinase (CK) activities were significantly increased above baseline values by 1 day after TASH [median maximal postprocedural CK activity, 935.0 U/L (IQR, 545.5-1115.0 U/L); median baseline CK activity, 80.0 U/L (IQR, 63.5-109.0 U/L); P < 0.001].
Conclusions:
Our results provide additional evidence that early rule-out of suspected AMI is possible by using the copeptin concentration in combination with cardiac troponin T.
