Author + information
- Received December 15, 2017
- Revision received March 18, 2018
- Accepted April 17, 2018
- Published online July 9, 2018.
- Erwan Salaun, MDa,b,
- Haïfa Mahjoub, MD, PhDa,
- Abdellaziz Dahou, MD, PhDa,
- Patrick Mathieu, MD, MSca,
- Éric Larose, MD, MSca,
- Jean-Pierre Després, PhDa,
- Josep Rodés-Cabau, MDa,
- Benoit J. Arsenault, PhDa,
- Rishi Puri, MBBS, PhDc,
- Marie-Annick Clavel, DVM, PhDa and
- Philippe Pibarot, DVM, PhDa,∗ (, )@universitelaval@PPibarot
- aInstitut Universitaire de Cardiologie et de Pneumologie de Québec/Québec Heart & Lung Institute, Laval University, Quebec City, Québec, Canada
- bCentre de Résonance Magnétique Biologique et Médicale (CRMBM), UMR 7339, Centre National de la Recherche Scientifique, Aix-Marseille Université, Marseille, France
- cCleveland Clinic Coordinating Center for Clinical Research (C5R), Cleveland, Ohio
- ↵∗Address for correspondence:
Dr. Philippe Pibarot, Laval University, Institut Universitaire de Cardiologie et de Pneumologie de Québec, 2725 Chemin Sainte-Foy #A2075, Québec, G1V-4G5 Québec, Canada.
Background Dysmetabolic profile has been associated with native aortic valve stenosis. However, there are limited data on the effects of an atherogenic milieu and its potential implications on the structural and hemodynamic deterioration of aortic bioprosthetic valves.
Objectives This prospective longitudinal study sought to determine the predictors and impact on outcomes of hemodynamic valve deterioration (HVD) of surgically implanted aortic bioprostheses.
Methods A total of 137 patients with an aortic bioprosthesis implanted for a median time of 6.7 (interquartile range: 5.1 to 9.1) years prospectively underwent a first (baseline) assessment with complete Doppler echocardiography, quantitation of bioprosthesis leaflet calcification by multidetector computed tomography (CT), and a fasting blood sample to assess cardiometabolic risk profile. All patients underwent a second (follow-up) Doppler echocardiography examination at 3 (interquartile range: 2.9 to 3.3) years post-baseline visit. HVD was defined by an annualized change in mean transprosthetic gradient ≥3 mm Hg/year and/or worsening or transprosthetic regurgitation by ≥1/3 class. The primary endpoint was a nonhierarchical composite of death from any cause or aortic reintervention procedure (redo surgical valve replacement or transcatheter valve-in-valve implantation) for bioprosthesis failure.
Results Thirty-four patients (25.6%) had leaflet calcification on baseline CT, and 18 patients (13.1%) developed an HVD between baseline and follow-up echocardiography. Fifty-two patients (38.0%) met the primary endpoint during subsequent follow-up after the second echocardiographic examination. Leaflet calcification (hazard ratio [HR]: 2.58; 95% confidence interval [CI]: 1.35 to 4.82; p = 0.005) and HVD (HR: 5.12; 95% CI: 2.57 to 9.71; p < 0.001) were independent predictors of the primary endpoint. Leaflet calcification, insulin resistance (homeostatic model assessment index ≥2.7), lipoprotein-associated phospholipase A2 activity (Lp-PLA2 per 0.1 nmol/min/ml increase), and high level of proprotein convertase subtilisin/kexin 9 (PCSK9) (≥305 ng/ml) were associated with the development of HVD after adjusting for age, sex, and time interval since aortic valve replacement.
Conclusions HVD identified by Doppler echocardiography is independently associated with a marked increase in the risk of valve reintervention or mortality in patients with a surgical aortic bioprosthesis. A dysmetabolic profile characterized by elevated plasma Lp-PLA2, PCSK9, and homeostatic model assessment index was associated with increased risk of HVD. The presence of leaflet calcification as detected by CT was a strong predictor of HVD, providing incremental risk-predictive capacity.
Dr. Pibarot has received research grants from Edwards Lifesciences and Medtronic for echocardiography core lab analyses in transcatheter aortic valve replacement. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Blase Carabello, MD, served as Guest Editor for this paper.
- Received December 15, 2017.
- Revision received March 18, 2018.
- Accepted April 17, 2018.
- 2018 American College of Cardiology Foundation
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