title: Familial predisposition of left ventricular hypertrophy.
abstract: OBJECTIVE
  The study evaluated the contribution of familial predisposition to the risk of left ventricular hypertrophy (LVH).
  
  
  BACKGROUND
  Left ventricular hypertrophy is a multifactorial condition that serves as an important predictor of cardiovascular mortality. At present it is unclear whether familial predisposition contributes to the manifestation of LVH. Thus, we determined whether siblings of subjects with LVH are at increased risk to present with an elevation of LV mass or an abnormal LV geometry.
  
  
  METHODS
  Echocardiographic and anthropometric measurements were performed in 2,293 individuals who participated in the echocardiographic substudies of population-based MONICA Augsburg surveys. In addition, a total of 319 siblings of survey participants with echocardiographic evidence of LVH were evaluated. The risk of these siblings to present with LVH or abnormal LV geometry was estimated by comparison with 636 subjects matched for gender and age that were selected from the entire echocardiography study base.
  
  
  RESULTS
  Blood pressure, body mass index, age, and gender (i.e., known determinants of LV mass) were comparable in LVH-siblings and the matched comparison group. However, septal and posterior wall thicknesses, relative wall thickness as well as LV mass index were significantly elevated in LVH-siblings (p < 0.001, each) whereas LV dimensions did not differ. Likewise, the prevalence of LVH was raised in LVH-siblings, as was the relative risk of LVH after adjustment for confounders (p < 0.05). More specifically, LVH-siblings displayed increased prevalences of concentric remodeling and concentric LVH (p < 0.05) but not of eccentric LVH.
  
  
  CONCLUSIONS
  Familial predisposition appears to contribute to increased LV wall thickness, to the development of LV hypertrophy and abnormal LV geometry.
authors.affiliation: Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Germany. heribert.schunkert@klinik.uni-regensburg.de
authors.forename: H
authors.initials: H
authors.lastname: Schunkert
authors.forename: U
authors.initials: U
authors.lastname: Bröckel
authors.forename: C
authors.initials: C
authors.lastname: Hengstenberg
authors.forename: A
authors.initials: A
authors.lastname: Luchner
authors.forename: M W
authors.initials: MW
authors.lastname: Muscholl
authors.forename: K
authors.initials: K
authors.lastname: Kurzidim
authors.forename: B
authors.initials: B
authors.lastname: Kuch
authors.forename: A
authors.initials: A
authors.lastname: Döring
authors.forename: G A
authors.initials: GA
authors.lastname: Riegger
authors.forename: H W
authors.initials: HW
authors.lastname: Hense
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D002306:Cardiac Volume / Q000235:genetics; D004452:Echocardiography; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D020257:Ventricular Remodeling / Q000235:genetics