Payam Dehghani1, Zachary Singer2, Jamie Morrison3, Jeffery Booker4, Andrea Lavoie5, Rodney Zimmermann6, Paul Basran7, John G Webb8, Asim N Cheema9, Phillippe Pibarot10, Marie-Annick Clavel11. 1. Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: payamde@gmail.com. 2. College of Medicine, University of Saskatchewan, Regina, Canada. Electronic address: zack.singer1@gmail.com. 3. Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: jaime.morrison10@gmail.com. 4. Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: booker.jeff@gmail.com. 5. Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: ajlavoie@gmail.com. 6. Prairie Vascular Research Network, University of Saskatchewan, Regina, Canada. Electronic address: rodney.zimmermann@saskhealthauthority.ca. 7. Royal University Hospital, University of Saskatchewan, Saskatoon, Canada. Electronic address: rsbasran@sasktel.net. 8. St Paul's Hospital, University of British Columbia, Vancouver, Canada. Electronic address: webb@providencehealth.bc.ca. 9. St. Michael's Hospital, University of Toronto, Toronto, Canada. Electronic address: cheemaa@smh.ca. 10. Institut Universitaire de Cardiologie et de Pneumologie, Université Laval, Québec, Canada. Electronic address: philippe.pibarot@med.ulaval.ca. 11. Institut Universitaire de Cardiologie et de Pneumologie, Université Laval, Québec, Canada. Electronic address: marie-annick.clavel@criucpq.ulaval.ca.
Abstract
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.
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.
Authors: Daniel A Gomes; Rita Reis Santos; Pedro Freitas; Mariana Sousa Paiva; João Abecasis; Maria Salomé Carvalho; Frank A Flachskampf; Maria João Andrade Journal: Clin Res Cardiol Date: 2022-09-10 Impact factor: 6.138