Abstract

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.

Highlights

  • Elevation of AVP and copeptin can be observed in a variety of pathophysiological conditions e.g. type 2 diabetes[7,8], pneumonia[9], acute pancreatitis[10,11], sepsis[12,13] and cardiac stress and injury[14,15,16,17]

  • To determine whether the heart contributes to the release of copeptin into the bloodstream in humans, we measured copeptin levels in patients suffering an acute myocardial infarction (AMI) and in patients without AMI

  • Levels of cardiac troponin T (cTnT), as established biomarker representing myocardial ischemia, as well as copeptin were determined in samples from the aorta (AO) and the coronary venous sinus (CVS) in patients with (n = 15) and without (n = 14) the diagnosis AMI

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Summary

Introduction

Elevation of AVP and copeptin can be observed in a variety of pathophysiological conditions e.g. type 2 diabetes[7,8], pneumonia[9], acute pancreatitis[10,11], sepsis[12,13] and cardiac stress and injury[14,15,16,17]. Besides the established biomarkers for cardiac injury like cardiac troponins, copeptin levels might provide additional information regarding circulatory stress levels and hemodynamic instability. Copeptin has shown to provide amendatory diagnostic information for early discrimination of e.g. acute myocardial infraction (AMI) in combination with cardiac troponins in most published studies[14,15,16,17]. This study implies a potential release of copeptin from the heart into the circulation. We analyzed a potential release from the heart by measuring the concentration of copeptin using a transcoronary gradient model (TCG) in patients with AMI

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