Independent Relations of Left Ventricular Structure With the 24-Hour Urinary Excretion of Sodium and Aldosterone

Jin, Yu; Kuznetsova, Tatiana; Maillard, Marc; Richart, Tom; Thijs, Lutgarde; Bochud, Murielle; Herregods, Marie‐Christine; Burnier, Michel; Fagard, Robert; Staessen, Jan A.

doi:10.1161/hypertensionaha.109.130492

Cited by 61 publications

(48 citation statements)

References 37 publications

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“…13,31 These observations would suggest that aldosterone might require a high-salt environment to induce cardiac damage in humans as well, but the clinical evidence is still scanty. 10,14 In a population study of 371 untreated subjects in northern Belgium, Jin et al 32 reported a significant and independent correlation of LV mass with both UNaE and urinary aldosterone. In that study, however, the correlation of LVMI with UNaE was explained by a relationship with LV wall thickness, whereas urinary aldosterone was related with LV inner dimension.…”

Section: Discussionmentioning

confidence: 99%

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

et al. 2016

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Primary aldosteronism is associated with increased left ventricular (LV) mass independently of blood pressure. Previous studies suggest that elevated aldosterone causes cardiac damage only in the presence of an inappropriate salt status. We examined the relevance of dietary salt intake on cardiac changes in patients with primary aldosteronism before and after treatment. Sixty-five patients with tumoral or idiopathic primary aldosteronism were recruited at a University medical center and followed after either surgical (n=30) or medical (n=35) treatment. At baseline and 1 year after treatment, cardiac morphology and functional variables were measured by echocardiography together with duplicate 24-hour urinary sodium collections. At baseline, LV mass index was associated with urinary sodium excretion and plasma aldosterone levels. During follow-up, blood pressure (from 167/102–135/83 mm Hg; P <0.001) and LV mass index (from 50.5±13.0–44.4±8.9 g/m 2.7 ; P <0.001) decreased significantly with nonsignificant changes in LV geometry and functional properties. At the end of follow-up, percentage decrease in LV mass index was significantly greater in patients who had >10% reduction in urinary sodium excretion (15.0±12.5%) than in the remaining patients (5.5±9.3%; P <0.001). Changes in LV mass index induced by both surgical and medical treatment were directly and independently correlated with changes in blood pressure (β=0.419; P =0.009) and urinary sodium excretion (β=0.334; P =0.012) observed at follow-up. These findings strongly support the hypothesis that dietary salt intake has a crucial role in aldosterone-related LV changes and could contribute to cardiac damage in patients with primary aldosteronism.

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Section: Discussionmentioning

confidence: 99%

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

et al. 2016

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“…20 In humans, evidence that dietary sodium impacts the effects of aldosterone is sparse. In a cross-sectional study conducted in 317 untreated subjects, Jin et al 17 observed that LVM increased with sodium intake (estimated as 24-hour natriuresis) and was positively associated with urinary aldosterone (a better estimate of tissue exposure to aldosterone than plasma aldosterone). Such an observation is similar to findings obtained at baseline in the present cohort.…”

Section: Du Cailar Et Al Left Ventricular Mass Sodium and Aldosteronementioning

confidence: 99%

“…10 -12 Furthermore, several studies conducted in hypertensive patients or in unselected populations observed a positive association between LVM and the circulating level of plasma aldosterone concentration (PAC), [13][14][15] as well as urinary aldosterone excretion. 16,17 Studies performed in animal models indicated that the pressor, proinflammatory, and profibrotic effects of exogenous aldosterone are observed in the presence of a high sodium intake and may be prevented by dietary sodium restriction. 18 -20 The effect of chronic reduction of dietary sodium on LVM has been rarely evaluated, and the respective influence of the decrease in BP and change in dietary sodium could not be clarified.…”

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confidence: 99%

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

et al. 2010

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Abstract-In essential hypertension, the regression of left ventricular hypertrophy is an important goal of treatment. In addition to treatment-associated changes in blood pressure (BP), the roles of other determinants of left ventricular hypertrophy regression, including dietary sodium intake, deserve investigation. In the present study, the change in echographic left ventricular mass index (LVMI) was assessed in 182 patients with never-treated essential hypertension at baseline and after 3 years of treatment by angiotensin converting enzyme inhibitors or angiotensin II receptor antagonists given at recommended doses and associated with other antihypertensive agents. Treatment was associated with satisfactory control of BP (Ͻ140/90 mm Hg) in 64% of patients, and left ventricular hypertrophy prevalence decreased from 56% to 39%. Twenty-four-hour urinary sodium was positively related to LVMI at baseline and at the end of the study, independently of age, sex, and systolic BP. Supine plasma aldosterone concentration was correlated with LVMI only at baseline but not in multivariate analysis. In response to treatment, the percentage of change in LVMI was positively correlated with the absolute changes in systolic BP, urinary sodium, and plasma aldosterone concentration, independently of baseline LVMI. The population was divided into 3 tertiles according to final values of gender-specific urinary sodium. When, within each urinary sodium tertile, patients were divided into those with plasma aldosterone concentration below and above the median (11.6 ng/dL), LVMI progressively increased across sodium tertiles only in patients with high plasma aldosterone concentration. Systolic BP was similar across all of the groups. In conclusion, aldosterone requires the presence of high dietary salt for the expression of its unfavorable effect on the heart. (Hypertension. 2010;56:865-870.)Key Words: left ventricular hypertrophy Ⅲ sodium intake Ⅲ hypertension Ⅲ aldosterone Ⅲ renin-angiotensin blockade A lthough left ventricular hypertrophy (LVH) is considered as an adaptative mechanism that preserves cardiac pump function in the presence of pressure or volume overload, it also represents a preclinical disease strongly predictive of cardiovascular morbidity and mortality in hypertension. 1 Moreover, some evidence indicates that reduction or aggravation of LVH, respectively, improves or enhances the risk of subsequent complications. [2][3][4] In the Pressioni Arteriose Monitorate e Loro Associazioni cohort of 398 treated subjects with essential hypertension, a prevalence of LVH of 19% was found when adequate control (Ͻ140/90 mm Hg) of blood pressure (BP) was achieved, whereas the prevalence of LVH was 29% in the presence of uncontrolled BP. 5 Because a number of treated patients exhibit levels of left ventricular mass (LVM) that exceed the need to sustain cardiac workload, it was suggested that nonhemodynamic factors may modulate or consistently influence the regression of LVH. 6 During the last decade, dietary sodium and aldosterone wer...

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“…As such, these studies establish both high dietary salt intake and excess aldosterone to be important and independent mediators of cardiovascular risk. 1,2 It is interesting, however, that animal models of hyperaldosteronism have consistently demonstrated that the unfavorable target-organ effects of aldosterone are in fact dependent on the concomitant dietary sodium intake. Beginning with landmark studies by Brilla and Weber, 3 it has been repeatedly demonstrated that the proinflammatory and profibrotic effects of excess aldosterone induced in end organs, including the heart, vasculature, and kidney, do not manifest unless the dietary salt intake is also excessive.…”

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confidence: 99%

Salt and Aldosterone

2010

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A very large number of experimental and human studies independently link high dietary salt intake and aldosterone excess to the development and progression of end-organ damage. Observational and dietary interventional studies clearly establish high diet salt intake as an important contributor to the development of hypertension, cardiac hypertrophy, and proteinuria. Likewise, observational data and studies of aldosterone blockade demonstrate that hyperaldosteronism significantly relates to level of blood pressure, intracardiac volumes, left ventricular mass, and urinary protein excretion. As such, these studies establish both high dietary salt intake and excess aldosterone to be important and independent mediators of cardiovascular risk. 1,2 It is interesting, however, that animal models of hyperaldosteronism have consistently demonstrated that the unfavorable target-organ effects of aldosterone are in fact dependent on the concomitant dietary sodium intake. Beginning with landmark studies by Brilla and Weber, 3 it has been repeatedly demonstrated that the proinflammatory and profibrotic effects of excess aldosterone induced in end organs, including the heart, vasculature, and kidney, do not manifest unless the dietary salt intake is also excessive. 4,5 That is, the deleterious tissue effects of aldosterone could be largely avoided by maintaining the rats on a low-salt diet.Until recently, such an interaction between sodium and aldosterone in humans, while anticipated, had not been clearly observed. Now, however, a growing body of data, including the article by du Cailar et al 6 in this edition of Hypertension, demonstrates that the blood pressure and target-organ effects of excess aldosterone and excess dietary sodium are in large part dependent on each other. That is, as had been predicted by animal models of excess aldosterone, endogenous aldosterone and dietary sodium consumption in hypertensive patients do not contribute in solo but instead act in concert to accelerate target-organ decline.Aldosterone, Dietary Sodium, and Target-Organ Damage du Cailar et al 6 measured plasma aldosterone levels, 24-hour urinary sodium excretion, and left ventricular mass index in 182 never-treated patients with primary hypertension. The patients were then treated with an angiotensin-converting enzyme inhibitor or an angiotensin receptor antagonist, with other agents added as needed for blood pressure control. After 3 years of treatment, the biochemical and echocardiographic assessments were repeated. In response to treatment, the reduction in left ventricular mass index was positively correlated with changes in systolic blood pressure, urinary sodium excretion, and plasma aldosterone. At the end of the treatment period, when the cohort was compared by tertiles of urinary sodium excretion and high or low aldosterone levels (ie, above or below the median), it was found that left ventricular mass index increased progressively in relation to increasing urinary sodium excretion in the high-aldosterone subjects. No such relation, h...

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Independent Relations of Left Ventricular Structure With the 24-Hour Urinary Excretion of Sodium and Aldosterone

Cited by 61 publications

References 37 publications

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

Dietary Salt Intake Is a Determinant of Cardiac Changes After Treatment of Primary Aldosteronism

Dietary Sodium, Aldosterone, and Left Ventricular Mass Changes During Long-Term Inhibition of the Renin-Angiotensin System

Salt and Aldosterone

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