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(Circulation. 2002;106:227.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Copenhagen County University Hospital (K.W., M.H.O.), Glostrup, Denmark; Weill Medical College of Cornell University (K.W., V. Palmieri, R.B.D.), New York, NY; Haukeland Hospital (E.G.), Bergen, Norway; VA Medical Center (V. Papademetriou), Washington, DC; Helsinki University Central Hospital (M.S.N.), Helsinki, Finland; Ullevål University Hospital (G.S.), Oslo, Norway; University of Massachusetts Medical Center (G.P.A.), Worcester, Mass; and Sahlgrenska University Hospital-Östra (B.D.), Göteborg, Sweden.
Correspondence to Dr Kristian Wachtell, Laboratory of Cardiology, Department of Medicine, Copenhagen County University Hospital, Glostrup, DK-2600 Glostrup, Denmark. E-mail kristian{at}wachtell.net
Background We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear.
Methods and Results Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174±21 to 147±19 over 95±11 to 82±10 mm Hg and LV mass from 234±56 to 194±50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4±2.0% to 16.8±2.1% and stress-corrected midwall FS increased from 97±13 to 105±12% (all P<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (ß=-0.211), RWT (ß=-0.334, all P<0.001), and diastolic BP (ß=-0.088, P<0.05) and directly related to SV (ß=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (ß=-0.153) and RWT (ß=-0.562) and directly with changes in SV (ß=0.145) and systolic BP (ß=0.s221, all P<0.001) with control for blinded therapy.
Conclusions Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.
Key Words: echocardiography electrocardiography hypertrophy heart failure hypertension
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