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Management of asymptomatic severe aortic stenosis: check or all in?

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Harnessing serum copeptin in asymptomatic severe aortic stenosis
KENAN YALTA, ERTAN YETKIN and GOKAY TAYLAN
Published on: 23 April 2021

Published on: 23 April 2021
Harnessing serum copeptin in asymptomatic severe aortic stenosis
- KENAN YALTA, Cardiologist Trakya University
- Other Contributors:
  ERTAN YETKIN, Cardiologist
  
  GOKAY TAYLAN, cardiologist
Kenan YALTA, MD a
Ertan YETKIN, MD b
Gokay TAYLAN, MD a

a,TrakyaUniversity, CardiologyDepartment, Edirne, TURKEY
b Derindere Hospital, Cardiology Department, Istanbul, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

In clinical practice, timing of aortic valve intervention in asymptomatic severe aortic stenosis (ASAS) has been a challenging task particularly in the absence of overt high-risk features (low ejection fraction, etc.) (1,2). The recently published article by Bing R, et al. (1), has discussed current strategies that might help risk-stratification and management of this precarious valvular phenomenon. In this context, we fully agree with the authors that serum biomarkers including natriuretic peptides, as opposed to certain imaging modalities, generally have significant limitations (1). However, serum copeptin (the surrogate marker of arginine-vasopressine (AVP) axis) might serve as a promising guide to prognostication and clinical decision-making for aortic valve intervention in patients with ASAS (2) largely due to pathophysiological implications of AVP axis in these patients:
Firstly; copeptin elevation in patients with ASAS might help ide...
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Kenan YALTA, MD a
Ertan YETKIN, MD b
Gokay TAYLAN, MD a

a,TrakyaUniversity, CardiologyDepartment, Edirne, TURKEY
b Derindere Hospital, Cardiology Department, Istanbul, TURKEY
Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

In clinical practice, timing of aortic valve intervention in asymptomatic severe aortic stenosis (ASAS) has been a challenging task particularly in the absence of overt high-risk features (low ejection fraction, etc.) (1,2). The recently published article by Bing R, et al. (1), has discussed current strategies that might help risk-stratification and management of this precarious valvular phenomenon. In this context, we fully agree with the authors that serum biomarkers including natriuretic peptides, as opposed to certain imaging modalities, generally have significant limitations (1). However, serum copeptin (the surrogate marker of arginine-vasopressine (AVP) axis) might serve as a promising guide to prognostication and clinical decision-making for aortic valve intervention in patients with ASAS (2) largely due to pathophysiological implications of AVP axis in these patients:
Firstly; copeptin elevation in patients with ASAS might help identify a subgroup with a state of subtle systemic hypoperfusion (potentially associated with the failure to increase cardiac output sufficiently under stress) that might lead to unexpected coronary ischemic events and sudden cardiac death (SCD) particularly during exercise (2). Copeptin elevation due to valvular stenosis might also suggest progressive ventricular remodeling and eventual heart failure in the long term as a consequence of enhanced AVP actions on myocardium (2). However, potential confounding factors (dehydration, infections, etc.) should also be sought before associating ASAS with copeptin elevation (2).
Secondly; augmented myocardial baroreceptor reactivity (namely Bezold-Jarish reflex) is well known to be associated with syncopal attacks and, if substantial, SCD in the setting of severe aortic stenosis largely through induction of bradyarrhythmias and peripheral vasodilatation (2). Interestingly, AVP was previously demonstrated to exert a significant stimulatory impact on baroreceptor reactivity (3,4). Therefore, substantial copeptin elevation might help identify ASAS patients who might particularly be prone to excessive Bezold-Jarish reflex (and hence; to SCD risk) on follow-up. (2).
Thirdly; AVP axis has a significant correlation with adrenergic system partly attributable to the central impact of adrenergic substances on AVP release (2). Therefore, copeptin elevation denotes a state of adrenergic hyperactivation that might account for arrhythmias in patients with ASAS, particularly in those with left ventricular hypertrophy (2).
Finally; copeptin elevation in patients with ASAS might also predict rapid progression of transaortic gradient owing to profibrotic effects of augmented AVP actions on aortic valvular tissue (2).
In summary; copeptin elevation might potentially signify a higher risk for adverse events in patients with ASAS due to the hemodynamic, autonomic and fibrogenic implications of enhanced AVP actions (2). Therefore, adjunctive evaluation of serum copeptin at regular intervals might help dynamic risk-stratification, and might further optimize the timing of aortic valve intervention in these patients (2). However, this needs to be tested in large-scale clinical studies.
Conflict of Interest: None

REFERENCES:
1- Bing R, Dweck MR. Management of asymptomatic severe aortic stenosis: check or all in?

Heart Published Online First: 04 November 2020. doi: 10.1136/heartjnl-2020-317160

2- Yalta K, Palabiyik O, Gurdogan M, Gurlertop Y. Serum copeptin might improve risk stratification and management of aortic valve stenosis: a review of pathophysiological insights and practical implications. Ther Adv Cardiovasc Dis. 2019 Jan-Dec;13:1753944719826420. doi: 10.1177/1753944719826420. PMID: 30803406; PMCID: PMC6376527.
3- Roul G, Riehl-Aleil V, Germain P, Bareiss P. Neurohormonal profile before and after beta-blockade in patients with neurocardiogenic syncope. Pacing Clin Electrophysiol. 1999; 22(7): 1020-30.
4- Mosqueda-Garcia R, Furlan R, Tank J, Fernandez-Violante R. The elusive pathophysiology of neurally mediated syncope. Circulation. 2000; 102(23): 2898-906.
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Conflict of Interest:
None declared.
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