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Plasma homocysteine and calcific aortic valve disease
  1. G M Novaro1,
  2. H D Aronow2,
  3. E Mayer-Sabik3,
  4. B P Griffin3
  1. 1Department of Cardiology, Cleveland Clinic Florida, Weston, Florida, USA
  2. 2Division of Cardiovascular Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
  3. 3Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA
  1. Correspondence to:
    Dr Gian M Novaro
    Department of Cardiology, Desk A23, Cleveland Clinic Florida, 2950 Cleveland Clinic Boulevard, Weston, FL 33331, USA;

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Calcific aortic valve disease and coronary atherosclerotic disease both demonstrate histological features of endothelial disruption and subendothelial accumulation of lipid, lipoprotein, and inflammatory cells.1 These entities also share acknowledged risk factors,2 including hypercholesterolaemia, hypertension, and diabetes mellitus, believed to cause disease at least partly via endothelial injury. Data suggest that raised homocysteine concentrations, also associated with endothelial damage,3 may be an independent risk factor for coronary artery disease.4 Whether raised homocysteine is a risk factor for calcific aortic valve disease is unknown. We hypothesised that increasing homocysteine concentrations might predict the prevalence of calcific aortic valve disease, specifically aortic sclerosis and aortic stenosis, in a group of patients undergoing cardiac surgery.


We retrospectively analysed 76 patients with a mean (SD) age of 66 (13) years, (65% male) who underwent cardiac surgery at the Cleveland Clinic Foundation with intraoperative transoesophageal echocardiography. The patients were originally recruited for a prospective study assessing the relation between plasma homocysteine and aortic atheroma. Exclusion criteria were chronic renal failure, …

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