title: Reversibility of left ventricular mechanical dysfunction in patients with hypertensive heart disease.
abstract: OBJECTIVE
  Prior studies indicate that hypertension is associated with mechanical systolic dysfunction, even in the presence of a normal ejection fraction, but whether this cardiac dysfunction may be ameliorated by antihypertensive treatment is unknown.
  
  
  METHODS
  To test the hypothesis that mechanical systolic dysfunction in hypertension may respond to blood pressure-lowering therapy, we studied 182 patients with uncontrolled hypertension who underwent a 24-week trial of intensive versus standard antihypertensive therapy (titrated to a goal SBP <130 versus <140 mmHg) and had both baseline and follow-up echocardiography. We examined changes in left ventricular systolic function, reflected by systolic global longitudinal strain (GLS), in the entire cohort and in the subset of patients with systolic dysfunction at baseline (defined as GLS >-15%).
  
  
  RESULTS
  Despite all patients having a preserved left ventricular ejection fraction (≥50%), almost a third (32%) had mechanical systolic dysfunction at baseline. In the total sample, GLS significantly improved in response to antihypertensive therapy (-16.8 ± 3.8 to -18.7 ± 3.4%; P < 0.0001), and this improvement was especially evident in patients with baseline dysfunction (13.1 ± 2.2 to -17.0 ± 2.9%; P < 0.0001). Improvement in GLS was associated with lower BMI (P = 0.015) and was greater in women than in men (P = 0.003). Although uncorrelated with blood pressure change, GLS improvement was related to having received high doses of antihypertensive therapy during the study (P = 0.040).
  
  
  CONCLUSIONS
  In patients with hypertensive heart disease and normal left ventricular ejection fraction, abnormalities in left ventricular mechanical systolic function can be ameliorated in the setting of targeted antihypertensive treatment.
authors.affiliation: aFrom the Cardiovascular Division, Brigham and Women's Hospital, Harvard University, Boston, Massachusetts bNovartis, East Hanover, New Jersey cState University of New York at Buffalo, Buffalo, New York dUniversity of Alabama, Birmingham, Alabama eUniversity of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Susan
authors.initials: S
authors.lastname: Cheng
authors.forename: Amil M
authors.initials: AM
authors.lastname: Shah
authors.forename: Juan Pablo
authors.initials: JP
authors.lastname: Albisu
authors.forename: Akshay S
authors.initials: AS
authors.lastname: Desai
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Hilkert
authors.forename: Joseph
authors.initials: J
authors.lastname: Izzo
authors.forename: Suzanne
authors.initials: S
authors.lastname: Oparil
authors.forename: Bertram
authors.initials: B
authors.lastname: Pitt
authors.forename: Scott D
authors.initials: SD
authors.lastname: Solomon
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D004452:Echocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D016032:Randomized Controlled Trials as Topic; D013318:Stroke Volume / Q000502:physiology; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*
chemical_list: D000959:Antihypertensive Agents