title: Influence of dynamic obstruction and hypertrophy location on diastolic function in hypertrophic cardiomyopathy.
abstract: BACKGROUND
  Hypertrophic cardiomyopathy (HCM) is a disease with marked genetic and phenotypic heterogeneity. It is well known that obstructive septal forms of this disease entail worse clinical outcome compared with nonobstructive septal and apical forms. The objective of this study was to analyze the differences in left ventricular diastolic function in different subgroups of HCMs and to assess the influence of the location of myocardial hypertrophy and the presence of dynamic obstruction on impairment of diastolic function and its correlation with the clinical status.
  
  
  METHODS
  We studied 86 patients with HCM; 27 with the obstructive asymmetric septal type (OAS), 37 with the nonobstructive asymmetric septal type (NOAS) and 22 with apical hypertrophic cardiomyopathy (ApHCM). Patients underwent conventional and tissue Doppler echocardiography and were assessed applying the latest recommendations regarding diastolic dysfunction. Cardiac magnetic resonance was used to study the various morphologic subtypes and quantify left ventricular mass (LVM).
  
  
  RESULTS
  The early diastolic annular velocity (e') was significantly lower in OAS with a median of 5 cm/s compared with NOAS with 7 cm/s and ApHCM with 7.5 cm/s (P = 0.0002), and the E/e' ratio was 8.5 in ApHCM, 10 in NOAS and 14 in OAS (P = 0.0001); no significant differences were found in LVM or maximal wall thickness.
  
  
  CONCLUSIONS
  In HCM, the location of left ventricular hypertrophy and the presence of dynamic obstruction affect the degree of diastolic dysfunction; impairment is greater in patients with the OAS type, and markedly less in patients with apical involvement.
authors.affiliation: aCardiac Imaging Department, Instituto Cardiovascular de Buenos Aires, Buenos Aires, Argentina bCenter for Computational Imaging and Simulation Technologies in Biomedicine, Universitat Pompeu Fabra cCetir Sant Jordi dCentro Cardiovascular Sant Jordi eInstitució Catalana de Recerca i Estudis Avançats, Barcelona, Spain.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Avegliano
authors.forename: J Pablo
authors.initials: JP
authors.lastname: Costabel
authors.forename: Marina
authors.initials: M
authors.lastname: Huguet
authors.forename: Jorge
authors.initials: J
authors.lastname: Thierer
authors.forename: Marcelo
authors.initials: M
authors.lastname: Trivi
authors.forename: Tobon-Gomez
authors.initials: TG
authors.lastname: Catalina
authors.forename: Mario
authors.initials: M
authors.lastname: Petit
authors.forename: Bart
authors.initials: B
authors.lastname: Bijnens
authors.forename: Alejandro
authors.initials: A
authors.lastname: Frangi
authors.forename: Ricardo
authors.initials: R
authors.lastname: Ronderos
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity / Q000502:physiology; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology*; D015150:Echocardiography, Doppler / Q000379:methods; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D011446:Prospective Studies; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D016277:Ventricular Function, Left / Q000502:physiology; D014694:Ventricular Outflow Obstruction / Q000209:etiology*; D055815:Young Adult