title: Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of chamber geometry.
abstract: BACKGROUND
  It is still unclear whether substantial regression of hypertensive left ventricular hypertrophy (LVH) and normalization of chamber geometry are associated with improved left ventricular (LV) myocardial function.
  
  
  RESULTS
  Midwall mechanics were evaluated in 152 patients undergoing 1 year of effective antihypertensive treatment. Two-dimensionally directed M-mode echocardiography was performed as follows: (1) after a 4-week placebo "run-in" period, (2) after 1 year of treatment with 20 mg/d lisinopril (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3) after a final 1-month placebo period to allow blood pressure (24-hour average ambulatory monitoring) to return to pretreatment levels. Treatment-induced reductions in blood pressure (from 149+/-16/95+/-11 to 131+/-12/83+/-10 mm Hg, P:<0.05) and circumferential end-systolic wall stress (from 84+/-22 to 72+/-19 g/cm(2), P:<0.05) were associated with a marked reduction in LV mass index (from 159+/-30 to 133+/-26 g/m(2), P:<0.05). LVH regression was accompanied by an increase in midwall fractional shortening (from 19.7+/-2.7% to 20.9+/-2.7%, P:<0.05) and by a decrease in relative wall thickness (from 48.2+/-7.7% to 44.1+/-6.7%, P:<0.05). The improvement in midwall function associated with afterload reduction and substantial LVH regression persisted after antihypertensive therapy withdrawal and restoration of the hypertensive state. Despite a significant increase in end-systolic wall stress, further LV chamber remodeling did not occur. The preservation of relative wall thickness was associated with a persistent improvement in midwall systolic function.
  
  
  CONCLUSIONS
  Regression of concentric LVH is associated with an improvement of midwall systolic function, which is more dependent on the normalization of LV geometry than on the reduction in LV systolic stress.
authors.affiliation: Clinica Medica I,IRCCS San Matteo, Università di Pavia, Pavia, Italy. sperlini@unipv.it
authors.forename: S
authors.initials: S
authors.lastname: Perlini
authors.forename: M L
authors.initials: ML
authors.lastname: Muiesan
authors.forename: C
authors.initials: C
authors.lastname: Cuspidi
authors.forename: L
authors.initials: L
authors.lastname: Sampieri
authors.forename: B
authors.initials: B
authors.lastname: Trimarco
authors.forename: G P
authors.initials: GP
authors.lastname: Aurigemma
authors.forename: E
authors.initials: E
authors.lastname: Agabiti-Rosei
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000009:adverse effects; D001794:Blood Pressure; D005260:Female; D006334:Heart Function Tests; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D020257:Ventricular Remodeling
chemical_list: D000959:Antihypertensive Agents