Serum copeptin might improve risk stratification and management of aortic valve stenosis: a review of pathophysiological insights and practical implications

Abstract

Over recent decades, the prevalence of aortic valve stenosis (AVS) has been constantly increasing possibly owing to the aging of general population. Severe AVS as determined by an aortic valve area (AVA) of <1 cm² has been regarded as a serious clinical condition potentially associated with a variety of adverse outcomes, including sudden cardiac death (SCD). However, patients with severe AVS (in the absence of overt high-risk features) are usually evaluated and managed exclusively based on symptomatology or imperfect prognostic tools including exercise testing and biomarkers, with a potential risk of mismanagement, suggesting the need for further objective risk stratifiers in this setting. Within this context, copeptin (C-terminal pro-vasopressin), a novel neurohormone widely considered as the surrogate marker of the arginine-vasopressin (AVP) system, may potentially serve as a reliable prognostic and therapeutic guide (e.g. timing of aortic valvular intervention) in patients with severe AVS largely based on its hemodynamic, fibrogenic as well as autonomic implications in these patients. Accordingly, the present paper aims to discuss clinical and pathophysiological implications of copeptin in the setting of AVS along with a summary of biomarkers and other prognostic tools used in this setting.

Keywords: aortic valve stenosis; copeptin; prognostic implication; prognostic tool; therapeutic implication.

Figure 1.

Potential therapeutic algorithm for the management of severe AVS based on copeptin guidance (a proposed scheme that is largely based on pathophysiological implications and the authors’ perspective, and hence, warrants clinical studies to be used as a routine management algorithm). AVA, aortic valve area; AVS, aortic valve stenosis; LVEF, low left ventricular ejection; TAVI, transcatheter aortic valve implantation. *LVEF < 50%, hypotension at rest or exercise, very high transaortic gradient (max jet velocity ⩾ 5 m/sec), severe valvular calcification, rapid progression in jet velocity (0.3 m/s/y).^,, **Surgical or percutaneous TAVI. ***Dyspnea, orthopnea, angina, syncope, dizziness. β Should include clinical visits at regular intervals. The whole algorithm (with copeptin measurement) should be repeated at each visit to timely detect copeptin rise and other clinical changes, and to make the clinical decision accordingly.