title: Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension.
abstract: OBJECTIVE
  To elucidate an association between left ventricular geometric adaptation to sustained hypertension and preclinical extracardiac target organ damage in essential hypertension. We also studied the clinical significance of neurohumoral factors for cardiovascular structural changes.
  
  
  METHODS
  One hundred and forty patients with essential hypertension were divided into four subgroups, based on left ventricular mass index and relative wall thickness. With respect to extracardiac target organ damage, we measured the funduscopic grade of retinal changes and serum creatinine levels.
  
  
  RESULTS
  Among the hypertensive patients, only 19 (14%) had a typical concentric hypertrophy (increase in left ventricular mass index and relative wall thickness). Hypertensive patients with concentric hypertrophy had the most advanced funduscopic abnormalities and the greatest renal involvement, and hypertensive patients without left ventricular hypertrophy had the least extracardiac target organ damage. Plasma renin activity and plasma aldosterone concentration were higher in hypertensive patients with than in those without concentric hypertrophy. In a multiple regression model there was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement, independent of office blood pressure.
  
  
  CONCLUSIONS
  These results clearly demonstrate that echocardiographically determined left ventricular mass and geometry stratify extracardiac target organ damage in patients with essential hypertension more closely than office blood pressure. The present study also suggests that, in addition to blood pressure load, the renin-angiotensin-aldosterone system appears to play an important role in myocardial hypertrophy and peripheral vascular damage in hypertension.
authors.affiliation: Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Shigematsu
authors.forename: M
authors.initials: M
authors.lastname: Hamada
authors.forename: M
authors.initials: M
authors.lastname: Mukai
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: T
authors.initials: T
authors.lastname: Sumimoto
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
mesh_terms: D000450:Aldosterone / Q000097:blood; D002395:Catecholamines / Q000652:urine; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012160:Retina / Q000503:physiopathology*; D012189:Retrospective Studies; D012964:Sodium / Q000652:urine
chemical_list: D002395:Catecholamines; D000450:Aldosterone; D002784:Cholesterol; D012964:Sodium; D003404:Creatinine; D012083:Renin