Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study)
M. Zabalgoitia et al., Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study), AM J CARD, 88(5), 2001, pp. 521-525
Citations number
16
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Depressed midwall shortening has been shown to be an independent predictor
of cardiovascular morbid events in hypertensive patients with left ventricu
lar (IV) hypertrophy despite normal endocardial fractional shortening. The
effects of LV mass changes in hypertensive patients on midwall shortening a
re unclear. To deters mine the impact of LV hypertrophy regression on LV sy
stolic function assessed at the endocardium and the midwall level, 508 pati
ents (58% men, 57% Caucasians, mean age 60 +/- 7 years) participating in th
e Hypertension Optimal Treatment study were prospectively studied by serial
echocardiography at baseline, year 1, year 2, and at the end of the study.
The Hypertension Optimal Treatment study was designed to challenge the exi
stence of the J-curve phenomenon in hypertension. This study enrolled men a
nd women between 50 and 80 years of age with mild to moderate hypertension.
Patients were treated with a regimen based on felodipine with the addition
of other antihypertensive drug classes as needed to reduce the diastolic b
lood pressure to a predefined target of less than or equal to 80, less than
or equal to 85, or less than or equal to 90 mm Hg. From baseline to year 1
, year 2, and end of the study, body mass index was unchanged (30.4, 30.1,
30.2, and 30.5 kg/m(2)); however, diastolic blood pressure was significantl
y reduced (99, 83, 80, and 80 mm Hg, p <0.0001), as was systolic blood pres
sure (161, 139, 137, and 134 mm Hg, p <0.0001) and LV mass index (117, 119,
107, and 106 g/m(2), p <0.0001). Over the same period of observation the e
ndocardial fractional shortening did not change significantly (40%, 42%, 43
%, and 44%); however, shortening at the midwall level showed improvement (2
0%, 21%, 22%, and 30%, p <0.001). In conclusion, midwall shortening is a mo
re sensitive index of systolic function in subjects with pressure-overload
hypertrophy, and it identifies high-risk patients who may benefit from a mo
re aggressive antihypertensive program. The disparity between midwall and e
ndocardial shortening suggests reduced myofibril function in patients with
hypertension-induced hypertrophy. (C) 2001 by Excerpta Medica, Inc.