Key result
Higher dietary sodium strongly linked to impaired LV diastolic filling in young hypertensive men.
Why the study?
Dietary sodium intake modulates left ventricular hypertrophy in established essential hypertension, but its relationship with left ventricular structural or functional changes in early essential hypertension was unclear.
Does dietary sodium intake correlate with impaired left ventricular diastolic filling in young men with early essential hypertension?
Observational (n=89)
Does dietary sodium intake correlate with impaired left ventricular diastolic filling in young men with early essential hypertension?
Higher dietary sodium intake is independently associated with impaired left ventricular diastolic filling in young men with early, untreated essential hypertension.
Answers are grounded in this paper and cite their sources.
Sodium intake may associate with early LV changes in mild hypertension; leaves open whether restriction prevents remodeling.
AIMS: Dietary sodium intake modulates left ventricular hypertrophy in established essential hypertension independent of blood pressure level. We conducted this study to elucidate the relationship between sodium intake and left ventricular structural or functional changes in early essential hypertension. METHODS: Forty-four young male patients (age 25.9 +/- 2.6 years) with mild essential hypertension that had never been treated and 45 normotensive male control subjects of similar age were examined. Dietary sodium intake was measured from 24 h urinary sodium excretion, blood pressure from 24 h ambulatory monitoring (SpaceLabs 90207), left ventricular structure from 2-D guided M-mode echocardiography, and diastolic filling of the left ventricle (as the main compound of diastolic function in a young population) by pulse-wave Doppler sonography. RESULTS: In hypertensive patients, daily sodium excretion correlated with the ratio of late (A) to early (E) maximum velocity (A/E; r = + 0.27, P = 0.07), velocity time integrals (A/E; r = + 0.54, P < 0.001) as well as atrial contribution, as a percent of left ventricular filling (VH ATCO; r = + 0.52, P < 0.001) independent of heart rate, whereas the opposite correlations were observed in normotensive (all P < 0.001). Stepwise multiple regression analysis confirmed these results. Sodium excretion emerged as the strongest independent determinant of impaired diastolic filling in hypertensive patients (velocity time integrals A/E: R(2) = 0.49, beta = 0.57, P = 0.0001; VH ATCO: R(2) = 0.48, beta = + 0.56, P < 0.0001; Vmax A/E: ns). In normotensive subjects, sodium excretion was a similar strong, but inverse determinant of diastolic filling (velocity time integrals A/E: R(2) = 0.40, beta = -0.43, P = 0.0028). Heart rate was a strong determinant of diastolic filling in hypertensive patients (beta = +0.55, P = 0.0002) and in normotensive subjects (beta = + 0.34, P = 0.011). Left ventricular mass and end-diastolic volume index were not related to diastolic filling in either group. CONCLUSION: In early essential hypertension, sodium excretion is correlated with impaired left ventricular diastolic filling independent of left ventricular mass. The renin-angiotensin-aldosterone-aldosterone system might be a mediator of the observed correlation.
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M Langenfeld (1998) conducted an observational in Early essential hypertension (n=89). Dietary sodium intake vs. Normotensive controls was evaluated on Impaired left ventricular diastolic filling (velocity time integrals A/E) (beta = 0.57, p=0.0001). In young men with early essential hypertension, dietary sodium excretion was strongly correlated with impaired left ventricular diastolic filling (beta = 0.57, P = 0.0001).
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