title: Midwall myocardial shortening in athletic left ventricular hypertrophy.
abstract: BACKGROUND
  Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown.
  
  
  METHODS
  Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects.
  
  
  RESULTS
  Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2).
  
  
  CONCLUSIONS
  Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.
authors.affiliation: Department of Cardiology, St Mary's Hospital, Praed Street, Paddington, London W2 1NY, UK. j.mayet@ic.ac.uk
authors.forename: Jamil
authors.initials: J
authors.lastname: Mayet
authors.forename: Ben
authors.initials: B
authors.lastname: Ariff
authors.forename: Balvinder
authors.initials: B
authors.lastname: Wasan
authors.forename: Neil
authors.initials: N
authors.lastname: Chapman
authors.forename: Manjit
authors.initials: M
authors.lastname: Shahi
authors.forename: Roxy
authors.initials: R
authors.lastname: Senior
authors.forename: Rodney A
authors.initials: RA
authors.lastname: Foale
authors.forename: Simon A McG
authors.initials: SA
authors.lastname: Thom
mesh_terms: D000328:Adult; D004452:Echocardiography; D004699:Endocardium / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000473:pathology*; D005082:Physical Exertion / Q000502:physiology; D011237:Predictive Value of Tests; D018570:Risk Assessment; D013177:Sports; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*