(Circulation. 2001;103:678.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From Clinica Medica, Ospedale S. Gerardo, Monza, II Università di Milano, Milan, Italy (G.M.); Clinica Medica I, IRCCS San Matteo, Università di Pavia, Pavia, Italy (S.P.); Cattedra Medicina Interna, Università di Brescia, Brescia, Italy (M.L.M., E.A.-R.); Cattedra Medicina Interna, Clinica Medica I, Università "Federico II," Napoli, Italy (B.T.); Centro Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy (C.C., L.S.); and the Division of Cardiology, University of Massachusetts, Worcester, Mass (G.P.A.).
Correspondence to Professor Giuseppe Mancia, Clinica Medica, Università di Milano, Ospedale S.Gerardo, via Donizetti, Monza (Milano), Italy. E-mail sperlini{at}unipv.it
BackgroundIt 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.
Methods and ResultsMidwall 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/cm2, P<0.05) were associated with a marked reduction in LV mass index (from 159±30 to 133±26 g/m2, 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.
ConclusionsRegression 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.
Key Words: echocardiography hemodynamics hypertrophy myocardial contraction systole
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