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Haemodynamic and anatomic progression of aortic stenosis
  1. Virginia Nguyen1,2,3,
  2. Claire Cimadevilla1,2,
  3. Candice Estellat4,
  4. Isabelle Codogno1,
  5. Virginie Huart5,
  6. Joelle Benessiano5,
  7. Xavier Duval6,
  8. Philippe Pibarot7,
  9. Marie Annick Clavel8,
  10. Maurice Enriquez-Sarano8,
  11. Alec Vahanian1,2,3,
  12. David Messika-Zeitoun1,2,3
  1. 1Department of Cardiology, Assistance Publique—Hôpitaux de Paris, Bichat Hospital, Paris, France
  2. 2INSERM U698, Bichat Hospital, Paris, France
  3. 3University Paris 7, Paris, France
  4. 4Department of Epidemiology, Biostatistic and Clinical research, Assistance Publique—Hôpitaux de Paris, Bichat Hospital, Paris, France
  5. 5Centre de Ressources Biologique, Assistance Publique—Hôpitaux de Paris, Bichat Hospital, Paris, France
  6. 6Centre d'Investigation Clinique 007, Assistance Publique—Hôpitaux de Paris, Bichat Hospital, Paris, France
  7. 7Department of Medicine, Québec Heart and Lung Institute, Laval University, Québec city, Québec, Canada
  8. 8Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota, USA
  1. Correspondence to Dr David Messika-Zeitoun, AP-HP, Cardiovascular division, Bichat Hospital, 46 rue Henri Huchard, Paris 75018, France; david.messika-zeitoun{at}bch.aphp.fr

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).

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