Characteristics and usefulness of unintended premature ventricular contraction during invasive assessment of aortic stenosis.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 08 2020
Historique:
received: 16 01 2020
accepted: 18 02 2020
pubmed: 24 3 2020
medline: 15 5 2021
entrez: 24 3 2020
Statut: ppublish

Résumé

Postextrasystolic potentiation (PESP)-associated augmentation in left ventricular-aorta pressure gradient (LVAoG) observed after incidental premature ventricular contraction (PVC) during resting echocardiography is similar to dobutamine stress echocardiography (DSE)-associated augmentation in LVAoG in patients with low-flow, low-gradient (LF-LG) aortic stenosis (AS). What is not known is whether a similar relationship exists when unintended PVC causes PESP during cardiac catheterization in patients with AS. We retrospectively reviewed all catheterizations performed for patients with at least moderate AS who had LVAoG assessment. Univariate and multivariate analyses were conducted to determine the predictors of pre- and post-PVC mean LVAoG ≥ 40 mmHg. Between September 2015 to September 2017, of 140 individuals undergoing cardiac catheterization, 34 met study criteria. Mean pre-PVC gradient was 38.9 ± 22.8 mmHg. All patients exhibited PESP-associated augmentation of LVAoG by an average of 28 ± 12%. In multivariate analysis, the only significant predictor of post-PVC mean LVAoG ≥ 40 mmHg was preserved LV function (OR 6.81; 95% CI 1.41-32.82, p = 0.02). Inability to generate ≥ 40 mmHg of mean LVAoG post-PVC had 100% specificity for nonsevere AS in our observational cohort. Unintended but interpretable PVCs occurred in one in four patients with AS undergoing cardiac catheterization with measurable hemodynamics. All of our patients with PVCs, regardless of underlying LVEF, exhibited PESP-associated augmentation of LVAoG. Our exploratory analysis suggests that inability to generate ≥40 mmHg of mean LVAoG post-PVC is highly specific for nonsevere AS.

Sections du résumé

BACKGROUND
Postextrasystolic potentiation (PESP)-associated augmentation in left ventricular-aorta pressure gradient (LVAoG) observed after incidental premature ventricular contraction (PVC) during resting echocardiography is similar to dobutamine stress echocardiography (DSE)-associated augmentation in LVAoG in patients with low-flow, low-gradient (LF-LG) aortic stenosis (AS). What is not known is whether a similar relationship exists when unintended PVC causes PESP during cardiac catheterization in patients with AS.
METHODS
We retrospectively reviewed all catheterizations performed for patients with at least moderate AS who had LVAoG assessment. Univariate and multivariate analyses were conducted to determine the predictors of pre- and post-PVC mean LVAoG ≥ 40 mmHg.
RESULTS
Between September 2015 to September 2017, of 140 individuals undergoing cardiac catheterization, 34 met study criteria. Mean pre-PVC gradient was 38.9 ± 22.8 mmHg. All patients exhibited PESP-associated augmentation of LVAoG by an average of 28 ± 12%. In multivariate analysis, the only significant predictor of post-PVC mean LVAoG ≥ 40 mmHg was preserved LV function (OR 6.81; 95% CI 1.41-32.82, p = 0.02). Inability to generate ≥ 40 mmHg of mean LVAoG post-PVC had 100% specificity for nonsevere AS in our observational cohort.
CONCLUSIONS
Unintended but interpretable PVCs occurred in one in four patients with AS undergoing cardiac catheterization with measurable hemodynamics. All of our patients with PVCs, regardless of underlying LVEF, exhibited PESP-associated augmentation of LVAoG. Our exploratory analysis suggests that inability to generate ≥40 mmHg of mean LVAoG post-PVC is highly specific for nonsevere AS.

Identifiants

pubmed: 32201098
pii: S0167-5273(20)30202-3
doi: 10.1016/j.ijcard.2020.02.053
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

35-38

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest No grants, contracts, and other forms of financial support were provided for this project. The authors have no conflicts of interest to note.

Auteurs

Payam Dehghani (P)

Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: payamde@gmail.com.

Zachary Singer (Z)

College of Medicine, University of Saskatchewan, Regina, Canada. Electronic address: zack.singer1@gmail.com.

Jamie Morrison (J)

Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: jaime.morrison10@gmail.com.

Jeffery Booker (J)

Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: booker.jeff@gmail.com.

Andrea Lavoie (A)

Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: ajlavoie@gmail.com.

Rodney Zimmermann (R)

Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: rodney.zimmermann@saskhealthauthority.ca.

Paul Basran (P)

Royal University Hospital, University of Saskatchewan, Saskatoon, Canada. Electronic address: rsbasran@sasktel.net.

John G Webb (JG)

St Paul's Hospital, University of British Columbia, Vancouver, Canada. Electronic address: webb@providencehealth.bc.ca.

Asim N Cheema (AN)

St. Michael's Hospital, University of Toronto, Toronto, Canada. Electronic address: cheemaa@smh.ca.

Phillippe Pibarot (P)

Institut Universitaire de Cardiologie et de Pneumologie, Université Laval, Québec, Canada. Electronic address: philippe.pibarot@med.ulaval.ca.

Marie-Annick Clavel (MA)

Institut Universitaire de Cardiologie et de Pneumologie, Université Laval, Québec, Canada. Electronic address: marie-annick.clavel@criucpq.ulaval.ca.

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