scholarly journals Increased risk of heart failure is associated with chronic habitual hypohydration that elevates serum sodium above 142 mmol/l suggesting lifelong optimal hydration as preventive measure

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
N.I Dmitrieva ◽  
D Liu ◽  
M Boehm

Abstract Background With increasing prevalence of heart failure (HF) owing to the aging population, identification of preventive measures that delay onset of the disease and their implementation become increasingly important. Recent studies demonstrated that chronic subclinical hypohydration accelerates degenerative changes and increases prevalence of many age-dependent degenerative diseases including heart failure (1). Worldwide surveys find wide differences in habitual water intake between and within countries and substantial prevalence of hypohydration in general population (2). Hypohydration elevates extracellular sodium triggering activation of water conservation mechanisms when serum sodium exceeds a threshold around 142 mmol/l. These adaptive responses include secretion of antidiuretic hormone and activation of the renin angiotensin aldosterone system (3), important contributors to pathogenesis of HF. Purpose The purpose of this study was to evaluate whether serum sodium concentration at middle age of 44–66 years as a measure of hydration habits is a significant predictor for left ventricular hypertrophy (LVH) and HF events 25 years later at age of 70–90 years. Methods Data from Atherosclerosis Risk in Communities (ARIC) study were obtained from the BioLINCC data repository. In ARIC study, 15,792 44–66 year-old participants were evaluated over 5 visits spanning 25 years (Figure 1A). Two separate logistic regression models were used in the study, where the dependent variable is diagnosis of LVH and HF at visit 5 (age:70–90 years), and the predictors are serum sodium concentration measured at visits 1 and 2 (age: 44–66 years), age, gender, total cholesterol, glucose, eGFR, BMI, smoking and hypertension statuses. Results Midlife serum sodium is associated with LVH and HF diagnosis 25 years later at visit 5 both with adjustment for age only (LVH: OR=1.24, 95% CI 1.15–1.34, P<0.001; HF: OR=1.06, 95% CI 1.02–1.10, P=0.006) and in fully adjusted model (LVH: OR=1.20, 95% CI 1.11–1.30, P<0.001; HF: OR=1.11, 95% CI 1.01–1.22, P=0.031) (Figure 1B). Cornell voltage criteria used for LVH diagnosis is elevated in participants with higher serum sodium and demonstrates sharper increase with age indicating accelerated hypertrophic LV remodeling (Figure 1C). These associations are reflected in increased prevalence of HF and LVH in 70–90 year-old participants whose middle age serum sodium exceeded 142 mmol/l (Figure 1D). Conclusions Habitual life-long hypohydration increases risk to develop LVH and HF. Keeping serum sodium below 142 mmol/l by drinking appropriate amount of liquids may slow down decline in cardiac function and decrease prevalence of HF. FUNDunding Acknowledgement Type of funding sources: Other. Main funding source(s): NHLBI Intramural program

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


2010 ◽  
Vol 40 (3) ◽  
pp. 121-127 ◽  
Author(s):  
Yi Fu ◽  
Zhan Chen ◽  
Alexandra I. F. Blakemore ◽  
Eric Orwoll ◽  
David M. Cohen

Copy number variation (CNV) is increasingly recognized as a source of phenotypic variation among humans. We hypothesized that a CNV in the human arginine vasopressin receptor-2 gene ( AVPR2) would be associated with serum sodium concentration based on the following lines of evidence: 1) the protein product of the AVPR2 gene is essential for renal water conservation; 2) mutations in the AVPR2 gene are associated with aberrant water balance in humans; 3) heritability of serum sodium concentration may be greater in females than in males; 4) the AVPR2 gene is X-linked; and 5) a common CNV spanning the AVPR2 gene was recently described in a non-Hispanic Caucasian population. We developed a highly reproducible assay for AVPR2 CNV. Among 279 subjects with measured serum sodium concentration in the Offspring Cohort of the Framingham Heart Study, no subjects exhibited CNV at the AVPR2 locus. Among 517 subjects in the Osteoporotic Fractures in Men Study (MrOS)—including 152 with hyponatremia and 183 with hypernatremia—no subjects with CNV at the AVPR2 locus were identified. CNV at the AVPR2 locus could not be independently confirmed, and CNV at the AVPR2 gene is unlikely to influence systemic water balance on a population-wide basis in non-Hispanic Caucasian subjects. A novel AVPR2 single nucleotide polymorphism affecting the reporter hybridization site gave rise to an artifactually low copy number signal (i.e., less than unity) in one male African American subject. Reanalysis of the original comparative genomic hybridization data revealed bona fide CNVs flanking—but not incorporating—the AVPR2 gene, consistent with our new genotyping data.


2021 ◽  
Vol 8 ◽  
Author(s):  
Can Can Xue ◽  
Jing Cui ◽  
Xiao Bo Zhu ◽  
Jie Xu ◽  
Chun Zhang ◽  
...  

Aims: To examine the prevalence of primary epiretinal membranes (ERMs) and associated systemic factors.Methods: The cross-sectional, community-based Tongren Health Care Study enrolled participants who received regular health examinations in the Beijing Tongren Hospital from 2017 to 2019. Using fundus photographs, retinal specialists assessed the presence of ERMs and their systemic associations.Results: Primary ERMs were detected in 841/22820 individuals, with a prevalence of 3.7% [95% confidence intervals (CI): 3.4–3.9%] in the total study population (mean age: 44.5 ± 13.8 years) and 6.5% (95% CI: 6.1–7.0%) in individuals aged 40+ years. In multivariable analysis, a higher ERMs prevalence was associated with older age [odds ratio (OR): 1.10; P < 0.001], higher serum cholesterol concentration (OR: 1.14; P = 0.003) and higher serum sodium concentration (SSC) (OR: 1.12; P < 0.001). In women, a higher SSC, even within the normal range, was associated with an increased risk of ERMs (OR: 1.19; P < 0.001). Female participants with an SSC of 144–145mmol/L as compared with those with an SSC of 135–137 mmol/L had a 5-fold increased odds of having ERMs (All women: OR: 5.33; P < 0.001; Women aged 40+years: OR: 4.63; P < 0.001).Conclusion: Besides older age and higher serum cholesterol concentration, a higher SSC, even if within the normal range, was independently associated with a higher ERM prevalence in women.


2011 ◽  
Vol 68 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Philip L. Cyr ◽  
Katherine A. Slawsky ◽  
Natalia Olchanski ◽  
Holly B. Krasa ◽  
Thomas F. Goss ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Tamaki ◽  
H Yaku ◽  
E Yamamoto ◽  
N Ozasa ◽  
Y Inuzuka ◽  
...  

Abstract Background Impact of hyponatremia improvement on prognosis in patients with acute decompensated heart failure (ADHF) remains unclear. Methods Patients hospitalized for ADHF at 19 hospitals in Japan were enrolled between October 2014 and March 2016. Hyponatremia was defined as serum sodium concentration less than 135 mmol/l. Primary endpoint was composite of all-cause death and heart failure rehospitalization one year after discharge. Results Among 3805 patients enrolled, 486 patients with hyponatremia at admission showed higher in-hospital mortality (13.3% vs. 5.4%, p<0.001). Of 486 hyponatremic patients, 396 patients were discharged alive. One hundred forty-three patients showed persistent hyponatremia at discharge (group P), whereas 253 patients showed improvement of hyponatremia (group I). Baseline characteristics are shown in the table. Patients in group I showed higher sodium concentration at admission (132±3 mmol/l vs. 130±4 mmol/l, p<0.001) and more increase in serum sodium concentration at discharge (7±4 mmol/l vs. 1±5 mmol/l, p<0.001). One-year survival rate free from primary endpoint was not different between the groups (56.4% in group P vs. 58.5% in group I, p=0.79). After adjusting for confounders, improvement of hyponatremia was not associated with better prognosis (hazard ratio 1.00; 95% confidence interval 0.70–1.45, p=0.99). Hyponatremia improvement showed significant interaction with left ventricular ejection fraction (LVEF) less than 40% (p=0.01). In patients with LVEF<40%, improvement of hyponatremia was associated with better prognosis (hazard ratio 0.48, 95% confidence interval 0.28–0.85, p=0.01) whereas not in patients LVEF≥40%. Patient characteristics Group P (n=143) Group I (n=253) p value Age (years) 81 (72–86) 81 (72–87) 0.73 Female 71 (49.7) 110 (43.5) 0.24 Ischemic etiology 42 (29.4) 81 (32.0) 0.58 Prior hospitalization 62 (43.7) 98 (39.5) 0.42 SBP at admission (mmHg) 140±36 144±38 0.40 HR at admission (bpm) 92±23 95±29 0.27 Atrial Fibrillation 47 (32.9) 103 (40.7) 0.12 NYHA class IV 60 (42.2) 138 (54.8) 0.02 Intravenous inotropic use 35 (24.5) 59 (23.3) 0.80 LVEF <40% 54 (37.8) 95 (37.6) 0.97 Values are median (interquartile range), mean ± standard deviation or number (%). Conclusion Improvement of hyponatremia at discharge was not associated with better prognosis in patients hospitalized for ADHF.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Natasha Eftimovska-Otovikj ◽  
Natasha Petkovikj ◽  
Olivera Stojceva-Taneva

Abstract Background and Aims We are uncertain about whether dialysate sodium improves overall health and well-being for people on haemodialysis, since there are a mixture of probably good and bad effects. Dialysate sodium is one of the most easy changeable parameter which can influence hemodynamic stability, echocardiography and laboratory parameters. The aim of the study was to investigate whether dialysis patients will have some beneficial effects of dialysate sodium set up according to serum sodium. Method 77 nondiabetic subjects (41men; 36women) performed 12 months hemodialysis (HD) sessions with dialysate sodium concentration setup at 138 mmol/L, followed by additional 24 month ssessions wherein dialysate sodium was set up according to pre-HD serum sodium concentration. Interdialytic weight gain (IDWG), echocardiography, laboratory parameters and survival were analysed. Results Sodium individualization resulted in significantly lower IDWG by using individualized sodium according to pre HD serum sodium compared to standard dialysate sodium (2.17±0.79 vs 1.93±0.64 kg, p&lt;0,001). In all patients we confirmed positive sodium gradient and univariate regression analysis showed that by increasing the sodium gradient by 1 mmol/L, IDWG increased by an average of 0.189% and 7,1% changes in IDWG can be explain by changing of the sodium gradient. Echocardiography analysis showed an increase of 2.04 mm of left ventricular diastolic diameter (LVDD) by increasing the sodium gradient for 1mmol/L and significantly increased left ventricular mass (LVM) of 35.69 gr by 1kg increase of IDWG. Laboratory analysis showed statistical significant increase in Kt/V, URR (urea reduction rate), serum albumin and hemoglobin by using individualized dialysed sodium compared to standard dialysate sodium, respectively (1.50±0.24 vs 1.36±0.22; 70.80±5.24 vs 67.00±6.23%; 38.23±3.80 vs 34.46±2.53 g/L; 120.32±10.14 vs 114.62±10.34 g/L, p&lt;0.001). We confirmed significant decrease in serum potassium, with no change in other electrolities (5.62±0.60vs 5.15±0.94). During the study, 7 patients died and binary logistic regression univariate analysis showed that significant predictors of mortality in patients dialyzed with individualized sodium dialysis according to pre-HD plasma sodium concentrations were Kt/V, URR, and CRP (C reactive protein). Analysis showed that patients with Kt/V lower than 1,2 have 8.8 times higher risk for death compared to patients with Kt/V&gt;1,2, URR lower than 65% have 10,9 times higher risk compared to URR&gt;65% and CRP higher than 10 mg/L have 10.2 times higher risk for death compared to patients with CRP lower than 10 mg/L Conclusion Individualization of dialysate sodium according to pre HD serum sodium concentration result in better IDWG control, improvement of fluid overload and regression of left ventricular hypertrophy, better dialysis adequacy and higher survival compared to standard dialysate sodium.


2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


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