Key result
Acute myocardial infarction was not associated with a significant transcoronary gradient of copeptin compared to non-AMI patients (-0.07 vs -0.18 pmol/L, p=0.78), indicating no direct cardiac release.
Why the study?
Is copeptin directly released from the human heart during acute myocardial infarction?
Cross-Sectional (n=29)
Single-blind (laboratory staff blinded to patient characteristics)
No
Is copeptin directly released from the human heart during acute myocardial infarction?
This study evaluates whether the cardiovascular biomarker copeptin is directly released from the human heart during acute myocardial infarction.
Answers are grounded in this paper and cite their sources.
No direct cardiac copeptin release in AMI; leaves open its extracardiac sources and biomarker specificity.
Copeptin is the C-terminal end of pre-provasopressin released equimolar to vasopressin into circulation and recently discussed as promising cardiovascular biomarker amendatory to established markers such as troponins. Vasopressin is a cytokine synthesized in the hypothalamus. A direct release of copeptin from the heart into the circulation is implied by data from a rat model showing a cardiac origin in hearts put under cardiovascular wall stress. Therefore, evaluation of a potential release of copeptin from the human heart in acute myocardial infarction (AMI) has been done.
No takes yet. Share an insight, caveat, or question.
Boeckel et al. (2016) conducted a cross-sectional in Acute Myocardial Infarction (n=29). Acute Myocardial Infarction vs. Non-AMI patients was evaluated on Transcoronary gradient (TCG) of copeptin (p=0.78). Acute myocardial infarction was not associated with a significant transcoronary gradient of copeptin compared to non-AMI patients (-0.07 vs -0.18 pmol/L, p=0.78), indicating no direct cardiac release.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: