title: Treatment of acromegaly improves myocardial abnormalities.
abstract: BACKGROUND
  Treatment for acromegaly decreases left ventricular (LV) mass, but it is not clear whether diastolic dysfunction is also reversible. With Doppler echocardiography, before and after effective therapy, we assessed the LV morphology and function of patients with acromegaly who were free of complications.
  
  
  METHODS
  In 15 patients with active acromegaly (age range, 33.4 +/- 9.3 years), we compared LV Doppler echocardiographic indices, before and after transsphenoidal surgery or radiotherapy or before and after both procedures, noting a significant drop in plasma levels of growth hormone (<2.0 ng/mL after oral glucose tolerance testing). Patients did not have arterial hypertension, diabetes mellitus, thyroid dysfunction, or coronary artery disease. Occasionally, in this series, patients had no symptoms of heart failure, and patients who underwent treatment with somatostatin analog drugs were not included because they did not have a significant hormonal drop. The follow-up period after hormonal control was 2.7 +/- 1.7 years. We also studied 15 healthy control subjects matched for age, sex, and body surface area.
  
  
  RESULTS
  Patients with acromegaly compared with healthy control subjects had increased LV mass index, relative wall thickness, and deteriorated diastolic function. After therapy, most of the abnormalities improved: LV mass index (104 +/- 21 g/m(2) x 87 +/- 21 g/m(2); P <.01), LV relative wall thickness (0.40 +/- 0.06 x 0.35 +/- 0.04; P <.01), proto/telediastolic transmitral peak flow velocity ratio (1.17 +/- 0.33 x 1.49 +/- 0.34; P <.001), and isovolumetric relaxation period (126 +/- 18 ms x 113 +/- 13 ms; P <.05).
  
  
  CONCLUSIONS
  Treatment of acromegaly in patients without clinical heart failure improves both LV morphology and diastolic function. Avoidance of progression to more advanced forms of acromegalic cardiomyopathy should be possible.
authors.affiliation: Heart Institute (InCor) and Endocrine Unit, University of Sao Paulo Medical School, Sao Paulo, Brazil. dclcaio@incor.usp.br
authors.forename: Caio B
authors.initials: CB
authors.lastname: Vianna
authors.forename: Marcelo L C
authors.initials: ML
authors.lastname: Vieira
authors.forename: Charles
authors.initials: C
authors.lastname: Mady
authors.forename: Bernardo
authors.initials: B
authors.lastname: Liberman
authors.forename: Anai E S
authors.initials: AE
authors.lastname: Durazzo
authors.forename: Mirta
authors.initials: M
authors.lastname: Knoepfelmacher
authors.forename: Luiz R
authors.initials: LR
authors.lastname: Salgado
authors.forename: Jose A F
authors.initials: JA
authors.lastname: Ramires
mesh_terms: D000172:Acromegaly / Q000097:blood / Q000150:complications / Q000628:therapy*; D000328:Adult; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015150:Echocardiography, Doppler; D005260:Female; D005500:Follow-Up Studies; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000209:etiology / Q000628:therapy
chemical_list: D015415:Biomarkers; D013006:Growth Hormone