24 MAY 2022
Our new findings demonstrate that controlling blood sodium could help Long QT patients prevent dangerous arrhythmias,” - Steven Poelzing, Associate professor at the Fralin Biomedical Research Institute.
Some Long QT syndrome patients are born with the disease, while others develop it as a result of natural aging, certain medications, tissue swelling, or heart disease.
As humans naturally age, heart muscle cells grow and require more calcium to contract. To sustain elevated calcium levels, heart muscle cells also need more sodium. As a result, the aging human heart naturally adapts ‘leaky’ sodium channels, allowing more sodium to enter the cell.
Long QT is diagnosed when the length of time it takes for a heartbeat to drop from its peak to baseline, the QT interval, is extended on an electrocardiogram reading.
“Our data suggests that the combination of tissue edema, elevated blood sodium, and faulty sodium channels trigger deadly heart arrhythmias,”
“Bringing the concept closer to the clinical setting will require teaching cardiologists on how parameters related to perinexal expansion and extracellular sodium levels may be monitored in a clinical environment.”
ORIGINAL RESEARCH article
Front. Nutr., 06 April 2023
Sec. Clinical Nutrition
Volume 10 - 2023 | https://doi.org/10.3389/fnut.2023.1073626
Evaluating the association between dietary salt intake and the risk of atrial fibrillation using Mendelian randomization
Sicen Wang1 Ye Cheng1,2 Qi Zheng3 Xin Su2* Yingjian Deng2*
Nutrients. 2020 Dec; 12(12): 3714. Published online 2020 Nov 30. doi: 10.3390/nu12123714
PMCID: PMC7761364PMID: 33266329
Left Ventricular Mass Reduction by a Low-Sodium Diet in Treated Hypertensive Patients †
Natale Musso,* Federico Gatto, Federica Nista, Andrea Dotto, Zhongyi Shen, and Diego Ferone
Abstract
Objective: To evaluate the left ventricular mass (LVM) reduction induced by dietary sodium restriction.
Patients and Methods: 138 treated hypertensives were given a simple sodium-restricted diet was advised. They had to avoid common salt loads, such as cheese and salt-preserved meat, and were switched from regular to salt-free bread.
Blood pressure (BP), 24-h urinary sodium (UNaV) and LVM were recorded at baseline, after 2 months. and after 2years.
Results:
In 76 patients UNaV decreased in the recommended range after 2 months and remained low at 2 years. In 62 patients UNaV levels decreased after 2 months and then increased back to baseline at 2 years.
The first group followed the diet advice for the long period. The second group did not follow the diet advice strictly.
Initially the two groups did not differ in terms of BP (134.3 ± 16.10/80.84 ± 12.23 vs. 134.2 ± 16.67/81.55 ± 11.18 mmHg, mean ± SD), body weight (72.64 ± 15.17 vs. 73.79 ± 12.69 kg), UNaV (161.0 ± 42.22 vs. 158.2 ± 48.66 mEq/24 h), and LVM index (LVMI; 97.09 ± 20.42 vs. 97.31 ± 18.91 g/m2).
After 2years. they did not differ in terms of BP (125.3 ± 10.69/74.97 ± 7.67 vs. 124.5 ± 9.95/75.21 ± 7.64 mmHg) and body weight (71.14 ± 14.29 vs. 71.50 ± 11.87 kg).
Significant differences were seen for UNaV (97.3 ± 23.01 vs. 152.6 ± 49.96 mEq/24 h) and LVMI (86.38 ± 18.17 vs. 103.1 ± 21.06 g/m2).
Multiple regression analysis: UNaV directly and independently predicted LVMI variations, either as absolute values (R2 = 0.369; β = 0.611; p < 0.001), or changes from baseline to +2years. (R2 = 0.454; β = 0.677; p < 0.001).
The prevalence of left ventricular hypertrophy decreased (29/76 to 15/76) in the first group while it increased in the less compliant patients (25/62 to 36/62; Chi2 p = 0.002). Conclusion: LVM seems linked to sodium consumption in patients already under proper BP control by medications.
The regression of the left ventricular mass, and the reversal of LVH, in severe hypertension under dietary sodium restriction is availabe in the existing research literature. In the papers by Walther Kempner, the rice-fruit diet, with its very low-sodium content, could normalize both the BP values and the cardiac mass. More recently, in hypertensive patients who actually restricted their sodium consumption, a reduction of the left ventricular mass was observed, even approaching the best pharmacological effect. Conversely, an increase in sodium/potassium ratio was associated with a higher LVMI in pre-hypertensive and hypertensive patients. The association between sodium intake and worsening of cardiac mass has been receiving widespread attention. The known linear relations between sodium intake and cardiovascular risk and between UNaV and LVH have even shown a stepwise increase, irrespective of BP values.
Experimental data attribute the sodium-induced LVH to actions mediated by the renin-angiotensin system without an increased sympathetic tone. Furthermore, the restriction of alimentary sodium reduces central BP independently of changes in peripheral BP. It follows that a high central BP, a stronger and independent predictor of cardiovascular morbidity and mortality, can induce a cardiac damage unrelated with peripheral BP.
Published On 11 Dec 2018
Too Much Salt In Diet Can Cause Irregular Heartbeat
Written By Medha Baranwal
After accounting for several other risk factors -- including age, body fat, blood pressure, and smoking -- the researchers found that salt consumption was independently associated with the risk of atrial fibrillation.
How Much Salt Should You Eat if there is a heart related problem?
If you’re living with congestive heart failure, it’s best if you limit the sodium in your diet to less than 1,500 milligrams a day.
That’s far less than the amount recommended for normal people -- 2,300 milligrams. But many Americans are taking 3,400 milligrams.
Dietary Sodium Intake in Heart Failure
Originally published24 Jul 2012
Americans consume ≈3700 mg sodium daily,11 whereas the US Department of Agriculture and the Department of Health and Human Services recommend 2300 mg daily intake for the general population, with a stricter recommendation of 1500 mg/d for those >50 years of age, blacks, or individuals with hypertension, diabetes mellitus, or chronic kidney disease.
Dietary Sodium Restriction Reverses Vascular Endothelial Dysfunction in Middle-Aged/Older Adults With Moderately Elevated Systolic Blood Pressure
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Hypertension
Kristen L. Jablonski, Matthew L. Racine, Candace J. Geolfos, Phillip E. Gates, Michel Chonchol, Matthew B. McQueen, and Douglas R. Seals
J Am Coll Cardiol. 2013 Jan, 61 (3) 335–343
Clinical significance
The concept that high sodium intake has adverse CV effects independent of BP has been advanced previously (9,12). High dietary sodium impairs EDD even in rodents that are salt-resistant and, thus, do not exhibit increases in BP in response to a high-salt diet (13,18,20). Acute impairment of EDD in normotensive adults after sodium loading also is BP independent (11), and adults with elevated SBP who report lower sodium intake have enhanced EDD independent of BP (16). The present results extend these findings to sodium restriction and lend support to the overall hypothesis that sodium intake not only elevates BP but also exerts other adverse influences (12). The effects of sodium restriction on endothelial function reported here also complement previous findings that reducing sodium intake can rapidly de-stiffen large elastic arteries (21), another independent vascular risk factor for CVD (40). The improvements in these 2 common forms of arterial dysfunction, both predictors of CV events (3,4,40), suggest that DSR has strong potential for reducing CVD risk via broad vasculoprotective effects.
https://www.jacc.org/doi/10.1016/j.jacc.2012.09.010
Ud. 12.6.2024
Pub. 31.5.2024
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