학술논문
Haemodynamic and anatomic progression of aortic stenosis.
Document Type
Academic Journal
Author
Nguyen V; Department of Cardiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France INSERM U698, Bichat Hospital, Paris, France University Paris 7, Paris, France.; Cimadevilla C; Department of Cardiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France INSERM U698, Bichat Hospital, Paris, France.; Estellat C; Department of Epidemiology, Biostatistic and Clinical research, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France.; Codogno I; Department of Cardiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France.; Huart V; Centre de Ressources Biologique, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France.; Benessiano J; Centre de Ressources Biologique, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France.; Duval X; Centre d'Investigation Clinique 007, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France.; Pibarot P; Department of Medicine, Québec Heart and Lung Institute, Laval University, Québec city, Québec, Canada.; Clavel MA; Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota, USA.; Enriquez-Sarano M; Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota, USA.; Vahanian A; Department of Cardiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France INSERM U698, Bichat Hospital, Paris, France University Paris 7, Paris, France.; Messika-Zeitoun D; Department of Cardiology, Assistance Publique-Hôpitaux de Paris, Bichat Hospital, Paris, France INSERM U698, Bichat Hospital, Paris, France University Paris 7, Paris, France.
Source
Publisher: BMJ Pub. Group Country of Publication: England NLM ID: 9602087 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1468-201X (Electronic) Linking ISSN: 13556037 NLM ISO Abbreviation: Heart Subsets: MEDLINE
Subject
Language
English
Abstract
Background: Aortic valve stenosis (AS) is a progressive disease, but the impact of baseline AS haemodynamic or anatomic severity on AS progression remains unclear.
Methods: In 149 patients (104 mild AS, 36 moderate AS and 9 severe AS) enrolled in 2 ongoing prospective cohorts (COFRASA/GENERAC), we evaluated AS haemodynamic severity at baseline and yearly, thereafter, using echocardiography (mean pressure gradient (MPG)) and AS anatomic severity using CT (degree of aortic valve calcification (AVC)).
Results: After a mean follow-up of 2.9±1.0 years, mean MGP increased from 22±11 to 30±16 mm Hg (+3±3 mm Hg/year), and mean AVC from 1108±891 to 1640±1251 AU (arbitrary units) (+188±176 AU/year). Progression of AS was strongly related to baseline haemodynamic severity (+2±3 mm Hg/year in mild AS, +4±3 mm Hg/year in moderate AS and +5±5 mm Hg/year in severe AS (p=0.01)), and baseline haemodynamic severity was an independent predictor of haemodynamic progression (p=0.0003). Annualised haemodynamic and anatomic progression rates were significantly correlated (r=0.55, p<0.0001), but AVC progression rate was also significantly associated with baseline haemodynamic severity (+141±133 AU/year in mild AS, +279±189 AU/year in moderate AS and +361±293 AU/year in severe AS, p<0.0001), and both baseline MPG and baseline AVC were independent determinants of AVC progression (p<0.0001).
Conclusions: AS progressed faster with increasing haemodynamic or anatomic severity. Our results suggest that a medical strategy aimed at preventing AVC progression may be useful in all subsets of patients with AS including those with severe AS and support the recommended closer follow-up of patients with AS as AS severity increases.
Clinical Trial Registration: COFRASA (clinicalTrial.gov number NCT 00338676) and GENERAC (clinicalTrial.gov number NCT00647088).
(Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)
Methods: In 149 patients (104 mild AS, 36 moderate AS and 9 severe AS) enrolled in 2 ongoing prospective cohorts (COFRASA/GENERAC), we evaluated AS haemodynamic severity at baseline and yearly, thereafter, using echocardiography (mean pressure gradient (MPG)) and AS anatomic severity using CT (degree of aortic valve calcification (AVC)).
Results: After a mean follow-up of 2.9±1.0 years, mean MGP increased from 22±11 to 30±16 mm Hg (+3±3 mm Hg/year), and mean AVC from 1108±891 to 1640±1251 AU (arbitrary units) (+188±176 AU/year). Progression of AS was strongly related to baseline haemodynamic severity (+2±3 mm Hg/year in mild AS, +4±3 mm Hg/year in moderate AS and +5±5 mm Hg/year in severe AS (p=0.01)), and baseline haemodynamic severity was an independent predictor of haemodynamic progression (p=0.0003). Annualised haemodynamic and anatomic progression rates were significantly correlated (r=0.55, p<0.0001), but AVC progression rate was also significantly associated with baseline haemodynamic severity (+141±133 AU/year in mild AS, +279±189 AU/year in moderate AS and +361±293 AU/year in severe AS, p<0.0001), and both baseline MPG and baseline AVC were independent determinants of AVC progression (p<0.0001).
Conclusions: AS progressed faster with increasing haemodynamic or anatomic severity. Our results suggest that a medical strategy aimed at preventing AVC progression may be useful in all subsets of patients with AS including those with severe AS and support the recommended closer follow-up of patients with AS as AS severity increases.
Clinical Trial Registration: COFRASA (clinicalTrial.gov number NCT 00338676) and GENERAC (clinicalTrial.gov number NCT00647088).
(Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)