Objectives: To investigate left atrial (LA) function as a reservoir, a
s a conduit and as a booster pump in essential hypertension (EH). LA v
olumes were echocardiographically measured in 28 untreated hypertensiv
e patients and in 20 control subjects. Background: LA makes a large co
ntribution in left ventricular filling, especially in patients with im
paired diastolic function. LA function is fundamental in left ventricu
lar filling in hypertensive patients as hypertension results in left v
entricular diastolic dysfunction. Methods: Diagnosis of EH (blood pres
sure >140/90 mm Hg) was based on three repeated readings of blood pres
sure (BP). Patients with myocardial infarction, cardiomyopathy, valvul
ar or congenital heart disease were excluded. Doppler diastolic early
(E) and late (A) velocity of mitral inflow were measured. The followin
g indexes were calculated: left ventricular mass index (LVMI) using th
e Penn convention; left ventricular stroke volume (LVSV); LA reservoir
volume (LARV=LA maximal volume at mitral valve opening minus minimal
volume); LA conduit volume (LACV=LVSV-LARV). Atrial systolic function
was assessed by calculating the active emptying fraction (volume at on
set of atrial systole minus minimal volume/volume at onset of atrial s
ystole, the E/A ratio and the LA ejection force (0.5 rho A(2) MOA, whe
re rho=the density of blood, MOA=mitral orifice area from the paraster
nal short axis view). Measurements were obtained in all hypertensive p
atients before and after 16 weeks administration of either enalapril (
10 or 20 mg) or enalapril +/- chlorthalidone (20/25 mg) once a day. Re
sults: After 16 weeks of treatment, BP was reduced significantly (from
172/110 to 137/86 mm Hg, P<0.001). LVMI decreased significantly as we
ll (from 141 to 123 g/m(2)) although it was higher compared to control
s (94 g/m(2), P<0.001). LARV decreased significantly (from 35.4 to 29.
3 cm(3), P<0.05) while LACV increased significantly (from 43.8 to 51.3
cm(3), P<0.05). LA active emptying fraction and E/A ratio did not cha
nge. LA ejection force decreased significantly (from 20.9 to 18.1 kdyn
es, P<0.05) but it was greater than controls (16.7 kdynes, P<0.01). Th
ere was a positive relationship of LVMI to LARV (P<0.01) in controls (
r=0.77) which held true in hypertensive patients, before (r=0.72) and
after treatment (r=0.69). There was a negative relationship of LVMI to
LACV (P<0.01) in controls (r=-0.65), and in hypertensive patients unt
reated (r=-0.74) and after treatment (r=-0.72). Conclusions: Our resul
ts showed that in hypertensive patients, LA reservoir function increas
es and LA conduit function decreases, while LA ejection force increase
s. Antihypertensive treatment with enalapril and/or thiazide, induces
normalisation of the LA function in parallel to left ventricular hyper
trophy regression.