Salt, Hypertension, and Cardiovascular Disease

Catena, Cristiana; Colussi, GianLuca; Brosolo, Gabriele; Nait, Francesca; Pezzutto, Francesca; Martinis, Flavia; Sechi, Leonardo Antonio

doi:10.14205/2310-9556.2014.02.02.2

Cited by 2 publications

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“…6 Moreover, animal, epidemiological, and clinical studies suggest that high-sodium intake is associated with myocardial hypertrophy independently of blood pressure. 27 In the rat, increased dietary sodium intake causes cardiac hypertrophy, and salt restriction prevents LV hypertrophy induced by angiotensin II infusion. 28 Similarly, a high-sodium intake is associated with increased LV mass in both normotensive and hypertensive subjects, 29 and LV mass is decreased in response to dietary salt restriction.…”

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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“…Because blood pressure control in the population is a difficult task, prevention and treatment of hypertension through interventions on patients' lifestyle have been suggested as a cost-effective strategy [ 2 – 4 ]. Among these interventions, a reduction of dietary salt intake could be beneficial for blood pressure control and prevention of heart failure [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Salt, Aldosterone, and Parathyroid Hormone: What Is the Relevance for Organ Damage?

Catena

Colussi

Brosolo

et al. 2017

International Journal of Endocrinology

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Structured interventions on lifestyle have been suggested as a cost-effective strategy for prevention of cardiovascular disease. Epidemiologic studies demonstrate that dietary salt restriction effectively decreases blood pressure, but its influence on cardiovascular morbidity and mortality is still under debate. Evidence gathered from studies conducted in patients with primary aldosteronism, essential hypertension, or heart failure demonstrates that long-term exposure to elevated aldosterone results in cardiac structural and functional changes that are independent of blood pressure. Animal experiments and initial clinical studies indicate that aldosterone damages the heart only in the context of an inappropriately elevated salt status. Recent evidence suggests that aldosterone might functionally interact with the parathyroid hormone and thereby affect calcium homeostasis with important sequelae for bone mineral density and strength. The interaction between aldosterone and parathyroid hormone might have implications also for the heart. Elevated dietary salt is associated on the one hand with increased urinary calcium excretion and, on the other hand, could facilitate the interaction between aldosterone and parathyroid hormone at the cellular level. This review summarizes the evidence supporting the contribution of salt and aldosterone to cardiovascular disease and the possible cardiac and skeletal consequences of the mutual interplay between aldosterone, parathyroid hormone, and salt.

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Salt, Hypertension, and Cardiovascular Disease

Cited by 2 publications

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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

Salt, Aldosterone, and Parathyroid Hormone: What Is the Relevance for Organ Damage?

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