Impact of dietary sodium intake on left ventricular diastolic filling in early essential hypertension

Abstract

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. ResultsIn hypertensive patients, daily sodium excretion correlated with the ratio of late (A) to early (E) maximum velocity (Vmax AlE; r= +0'27, P=0'07), velocity time integrals (AlE; r= +0,54, P<O'OOI) as well as atrial contribution, as a percent of left ventricular filling (VH A TCO; r= +0'52, P<O'OOI) independent of heart rate, whereas the opposite correlations were observed in normotensives (all IntroductionDietary salt intake is known to profoundly influence the structure of the left ventricle in hypertensive heart disease. Previous clinical and intervention studies examining patients with established essential hypertension have identified dietary sodium intake as a determinant of left ventricular hypertrophy independent of the level of hypertensive blood pressure[1-4 I . Although the impact Heart rate was a strong determinant of diastolic filling in hypertensive patients (p= +0,55, P=0'0002) and in normotensive subjects (p= +0,34, P=O·OII). Left ventricular mass and enddiastolic volume index were not related to diastolic filling in either group. ConclusionIn early essential hypertension, sodium excretion is correlated with impaired left ventricular diastolic filling independent of left ventricular mass. The reninangiotensin-aldosterone system might be a mediator of the observed correlation. (Eur Heart J 1998; 19: 951-958) Key Words: Essential hypertension, sodium, diastolic filling.of salt intake on left ventricular hypertrophy was reconfirmed in established essential hypertension, little is known about the relationship between sodium intake and left ventricular structure at the onset of hypertensive heart disease.Diastolic dysfunction of the left ventricle is found in the absence[51 or the presence[6 1 of left ventricular hypertrophy in patients with essential hypertension. It has been reported that a substantial proportion of patients with essential hypertension have evidence of impaired diastolic function without signs of left ventricular hypertrophy[7l. Other studies showed that the diastolic function of the left ventricle declines, from normotensive subjects to patients with essential hypertension without left ventricular hypertrophy to those with left ventricular hyp...

Aldosterone to renin ratio as a determinant of exercise blood pressure response in hypertensive patients

“…The presence of impaired systolic function would blunt BP rise, 9 whereas diastolic dysfunction may be associated with an exaggerated BP rise during exercise, 19 but with more advanced degree of diastolic dysfunction, the cardiac stroke volume during exercise fails to increase adequately and this limits BP rise. 9 As aldosterone impairs vascular endothelial function, 14 it would not be surprising that it would also cause left ventricular diastolic dysfunction where there is an excess aldosterone activity, 20 which may interact adversely with dietary salt 21 in producing this functional cardiac abnormality. The key to understanding the pathogenesis of hypertension may be to unravel the mechanism(s) behind this inappropriate aldosterone secretion as represented by a raised ARR.…”

Sodium Intake and Cardiovascular Disease

“…Some studies, by design, included only individuals who met specific BP criteria (12,24,28,37,65,67,79,84,92). Other studies performed stratified analyses based on BP cut-off points (54,55).…”

“…Initially evaluated to examine the relationship with BP, these analyses revisit the National Health and Nutrition Examination Survey (NHANES) data (44,45) and intervention studies, such as the Trials of Hypertension Prevention (TOHP) Phase I (TOHP I) and Phase II (TOHP II) (21) and the Trial of Nonpharmacological Interventions in the Elderly (TONE) (8). This review encompasses 17 observational studies that address the association between sodium intake and CVD (37,44,45,52,68,(84)(85)(86)(87), including measures of cardiac dysfunction (12,24,28,29,54,55,67,79). Although there are currently no randomized clinical trials of CVD morbidity and mortality in relation to sodium intake, two intervention studies evaluate sodium's effects on the vasculature (36,80), three studies evaluate sodium and measures of cardiac dysfunction (34,51,90), and four studies explore longitudinal outcomes for individuals having taken part in an intervention study (8,21,65,92,94).…”

Endogenous lithium clearance: a diagnostic method of assessing sodium sensitivity in hypertension. Methodological and clinical implications

“…In their pioneering study of a Chinese population, Avolio et al [15] demonstrated that increased consumption of salt (13.3 g NaCl/day vs. 7.3 g NaCl/day) was associated with significantly higher stiffness of the aortal wall measured using the pulse wave velocity method, regardless of the age and BP of the subjects. Other authors have also demonstrated a BP-independent influence of sodium on left ventricular hypertrophy [16] and impaired contractility of the left ventricle [17].…”