Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure

Damgaard, Morten; Norsk, Peter; Gustafsson, Finn; Kanters, Jørgen K.; Christensen, Niels Juel; Bie, Peter; Friberg, Lars; Gadsbøll, Niels

doi:10.1152/ajpregu.00738.2005

Cited by 89 publications

(85 citation statements)

References 30 publications

(31 reference statements)

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“…Decreased pulmonary artery and capillary wedge pressures without change in cardiac index and systemic vascular resistance was observed by Cody and colleagues 33 in New York Heart Association (NYHA) class III to IV patients with a very low sodium diet, but Damgaard and colleagues 34 noted a decrease in cardiac index and stroke volume and an increase in pulmonary vascular resistance with a low-sodium diet in NYHA class II to III patients. Two studies by Volpe and colleagues 35,36 concluded that moderate-to-high sodium intake had no hemodynamic effects on NYHA I to II patients Only consensus opinion of experts, case studies, or standard of care; FairϭBenefits exceed the harms but quality of evidence is not as strong; 1ϩ ϭ well-conducted meta-analysis, systemic reviews, or randomized controlled trials with low risk of bias.…”

Section: Physiological and Neurohormonal Responsesmentioning

confidence: 93%

Dietary Sodium Intake in Heart Failure

et al. 2012

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Section: Physiological and Neurohormonal Responsesmentioning

confidence: 93%

Dietary Sodium Intake in Heart Failure

et al. 2012

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“…In a previous study, Damgaard et al [15] addressed the adaptation of sodium excretion after an abrupt change in salt intake in both directions. Twelve healthy male subjects were submitted in a randomized order to 2 levels of salt intake (70 and 250 mmol/day; study F).…”

Section: U Na and V After An Abrupt Change In Sodium Intakementioning

confidence: 99%

“…Fluid intake was ad libitum. Their article showed how daily sodium excretion (U Na V) adapted, day after day, to these abrupt switches in salt intake [15], but U Na and V were not reported. Figure 2 shows these 2 variables along with the previously published U Na V. It appears clearly that V remained fairly constant over the whole period of observation in spite of marked changes in sodium excretion.…”

Section: U Na and V After An Abrupt Change In Sodium Intakementioning

confidence: 99%

Relationship between Sodium Intake and Water Intake: The False and the True

et al. 2017

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“…19 Similarly, a more recent therapeutic approach comprising high-dose oral furosemide and higher daily Na intake associated with fluid restriction has been reported to portend beneficial effects with very promising results in chronic HF patients; it is also likely to lower the incidence of hyponatremia in this patient population. [23][24][25][26] Vasopressin receptor antagonists (VRA), also called aquaretics or vaptans, represent the emerging strategy for treatment of HF-associated hyponatremia. Three types of vasopressin receptors have been identified with distinct functions: V1a, V1b, and V2.…”

Section: Newer Management Strategymentioning

confidence: 99%

Hyponatremia in Heart Failure: Revisiting Pathophysiology and Therapeutic Strategies

Kazory

2010

Clinical Cardiology

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Hyponatremia is frequently encountered in patients with heart failure (HF), and its association with adverse outcomes is well-established in this population. While hyponatremia is an independent marker for severity of HF, it is not certain whether it has a causal impact on the progression of the disease. There are no universally accepted consensus guidelines regarding therapeutic strategies for HF-associated hyponatremia and volume overload; current societal guidelines do not address management of this complication. Whereas thiazide diuretics are known to induce or worsen hyponatremia in this setting through a number of mechanisms, loop diuretics can be considered a readily available first-line pharmacologic therapy. Consistent with pathophysiology of the disease and mechanisms of action of loop diuretics, available clinical evidence supports such an approach provided that patients can be closely monitored. Use of vasopressin receptor antagonists is an emerging therapeutic strategy in this setting, and the efficacy of these agents has so far been shown in a number of clinical studies. These agents can be reserved for patients with HF in whom initial appropriate loop diuretic therapy fails to improve serum sodium levels. Scope of the ProblemHyponatremia, the most common electrolyte abnormality in hospitalized patients, is associated with increasing morbidity and mortality in various clinical settings, including heart failure (HF). In an analysis of the Organized Program To Initiate Life-Saving Treatment In Hospitalized Patients With Heart Failure (OPTIMIZE-HF) study comprising data on 47 647 admissions for acute decompensated HF (ADHF), 19.7% of the patients presented with hyponatremia, defined as a serum sodium (Na) level <135 mEq/L.1 This subgroup of patients demonstrated significantly worse outcomes and was more likely to require dialysis and inotropic agents. The in-hospital mortality rate was also significantly higher compared with those patients with normal serum Na levels (6% vs 3.2%, P < 0.0001). Nearly half of the study population had preserved left ventricular ejection fraction (LVEF), suggestingthat presence of hyponatremiais an independent predictor of outcomes in HF patients with both preserved as well as reduced LVEF, a concept that has been confirmed by other authors. 2,3 In another study on more than 4000 patients, Lee et al demonstrated that chronic hyponatremia (defined as serum Na level <136 mEq/L) increased the 30-day mortality by 53% and the 1-year mortality by 46% in patients admitted with a primary diagnosis of HF. 4 In addition to its impact on survival, in a study on patients withThe author is a consultant for Otsuka America Pharmaceutical, Inc. The author has no other funding, financial relationships, or conflicts of interest to disclose. a discharge diagnosis of HF in 49 US academic medical centers, hyponatremia was shown to significantly increase the hospital length of stay. 5 HF being the most common reason for hospitalization in patients age >65 years, and with an annual cost exceedi...

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Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure

Abstract: neuroendocrine responses to changes in sodium intake in compensated heart failure.

Cited by 89 publications

References 30 publications

Dietary Sodium Intake in Heart Failure

Dietary Sodium Intake in Heart Failure

Relationship between Sodium Intake and Water Intake: The False and the True

Hyponatremia in Heart Failure: Revisiting Pathophysiology and Therapeutic Strategies

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