Association of Post-Saline Load Plasma Aldosterone Levels With Left
                    Ventricular Hypertrophy in Primary Hypertension

Catena, Cristiana; Verheyen, Nicolas; Url–Michitsch, Marion; Kraigher‐Krainer, Elisabeth; Colussi, GianLuca; Pilz, Stefan; Tomaschitz, Andreas; Pieske, Burkert; Sechi, Leonardo A.

doi:10.1093/ajh/hpv104

Cited by 8 publications

(8 citation statements)

References 40 publications

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“…Recently, in 90 untreated patients with primary hypertension we have reported an independent association of plasma aldosterone levels measured after an intravenous saline load with LVMI. 33 This finding suggested that a relatively inadequate ability of salt to suppress aldosterone secretion could contribute substantially to LV hypertrophy. du Cailar et al 34 evaluated 182 previously untreated hypertensive patients who were treated for 3 years with either angiotensinconverting enzyme inhibitors or angiotensin II receptor blockers.…”

Section: Discussionmentioning

confidence: 99%

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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%

“…* Value is calculated without aldosterone antagonists. Beta blocker, n (%) 17 (53) 4 (12) 19 (57) 6 (18) Calcium channel blocker, n (%) 18 (56) 10 (31) 20 (61) 11 (33) ACE inhibitor, n (%) 11 (34) 7 (22) 14 (42) 5 (15) Angiotensin receptor blocker, n (%) 8 (25) 3 (9) 7 (21) 4 (12) Alpha blocker, n (%) 4 ( …”

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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“…In 182 hypertensive patients who were treated for 3 years with either angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, du Cailar et al observed a direct relationship of the percentage change in ventricular mass with the absolute changes in urinary sodium and plasma aldosterone levels [ 52 ]. In 90 essential hypertensive patients free of clinically relevant cardiovascular complications, aldosterone levels measured after intravenous saline load were found to be independently related to left ventricular mass, suggesting that limited ability of salt to modulate aldosterone production could contribute to ventricular hypertrophy [ 53 ]. In 21 patients with primary aldosteronism, Pimenta et al found that urinary sodium independently predicts left ventricular mass [ 54 ].…”

Section: The Contribution Of Salt To Aldosterone-related Cardiac Dmentioning

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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“…It has also been shown that the post-SIT PAC is associated with the left ventricular mass, independent of age, body mass index, and BP. 22 It is possible that patients with suppressible aldosterone secretion have a milder phenotype and would not benefit from surgery. However, the post-SIT PAC was not associated with the outcome of adrenalectomy in our study.…”

Section: Comparison With Other Studiesmentioning

confidence: 99%

Suppression of Aldosterone Secretion After Recumbent Saline Infusion Does Not Exclude Lateralized Primary Aldosteronism

et al. 2016

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Guidelines recommend suppression tests such as the saline infusion test (SIT) to ascertain the diagnosis of primary aldosteronism (PA) in patients with a high aldosterone:renin ratio. However, suppression tests have only been evaluated in small retrospective series, and some experts consider that they are not helpful for the diagnosis of PA. In this study, we evaluated whether low post-SIT aldosterone concentrations do exclude lateralized PA. Between February 2009 and December 2013, 199 patients diagnosed with PA on the basis of 2 elevated aldosterone:renin ratio results and a high basal plasma or urinary aldosterone level or high post-SIT aldosterone level had a selective adrenal venous sampling. We used a selectivity index of 2 and a lateralization index of 4 to interpret the adrenal venous sampling results. Baseline characteristics of the patients were the following (percent or median): men 63%, 48 years old, office blood pressure 142/88 mm Hg, serum potassium 3.4 mmol/L, aldosterone:renin ratio 113 pmol/mU, plasma aldosterone concentration 588 pmol/L. The proportion of patients with lateralized adrenal venous sampling was 12 of 41 (29%) among those with post-SIT aldosterone <139 pmol/L (5 ng/dL) and 38 of 104 (37%) among those with post-SIT aldosterone <277 pmol/L (10 ng/dL). Post-SIT aldosterone levels were not associated with the blood pressure outcome of adrenalectomy. A low post-SIT aldosterone level cannot rule out lateralized PA, even with a low threshold (139 pmol/L). Adrenal venous sampling should be considered for patients who are eligible for surgery with elevated basal aldosterone levels even if they have low aldosterone concentrations after recumbent saline suppression testing.

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Association of Post-Saline Load Plasma Aldosterone Levels With Left Ventricular Hypertrophy in Primary Hypertension

Abstract: In patients with hypertension, aldosterone levels measured after intravenous saline load are related to LV mass independent of age, body mass, and blood pressure, suggesting that limited ability of salt to modulate aldosterone production could contribute to LVH.

Cited by 8 publications

References 40 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

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

Suppression of Aldosterone Secretion After Recumbent Saline Infusion Does Not Exclude Lateralized Primary Aldosteronism

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