scholarly journals The Effect of Dietary Sodium Restriction on Vascular Stiffness in Hypertension

2020 ◽  
Author(s):  
Henrique Cotchi Simbo Muela ◽  
Mujimbi José Viana ◽  
António Gerson Bastos Francisco ◽  
Isaura da Conceição Almeida Lopes ◽  
Valeria Aparecida Costa-Hong

Increased salt consumption is believed to induce high blood pressure (BP)-mediated organ damage, although it is not yet clear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. Exceeding dietary sodium intake is acknowledged to be the main modifiable environmental risk factor for cardiovascular events that accounts for an increase in blood pressure and induces hypertension (HTN)-related target organ damage. Arterial stiffness is well known as an independent cardiovascular risk factor, and sodium intake may be a determinant of arterial stiffness. Even so, the studies that investigated the effect of dietary sodium reduction intake on arterial stiffness in humans provided inconclusive results. Therefore, we aim to perform a review of the available evidence of salt restriction and arterial stiffness and its impact on hypertensive patients.

Author(s):  
Federica Nista ◽  
Federico Gatto ◽  
Manuela Albertelli ◽  
Natale Musso

Salt intake is too high for safety nowadays. The main active ion in salt is sodium. The vast majority of scientific evidence points out the importance of sodium restriction for decreasing cardiovascular risk. International Guidelines recommend a large reduction in sodium consumption to help reduce blood pressure, organ damage, and cardiovascular risk. Regulatory authorities across the globe suggest a general restriction of sodium intake to prevent cardiovascular diseases. In spite of this seemingly unanimous consensus, some researchers claim to have evidence of the unhealthy effects of a reduction of sodium intake, and have data to support their claims. Evidence is against dissenting scientists, because prospective, observational, and basic research studies indicate that sodium is the real villain: actual sodium consumption around the globe is far higher than the safe range. Sodium intake is directly related to increased blood pressure, and independently to the enlargement of cardiac mass, with a possible independent role in inducing left ventricular hypertrophy. This may represent the basis of myocardial ischemia, congestive heart failure, and cardiac mortality. Although debated, a high sodium intake may induce initial renal damage and progression in both hypertensive and normotensive subjects. Conversely, there is general agreement about the adverse role of sodium in cerebrovascular disease. These factors point to the possible main role of sodium intake in target organ damage and cardiovascular events including mortality. This review will endeavor to outline the existing evidence.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Costantino Mancusi ◽  
Valentina Trimarco ◽  
Maria Angela Losi ◽  
Grazia Canciello ◽  
Carmine Morisco ◽  
...  

Author(s):  
Anping Cai ◽  
Lin Liu ◽  
Mohammed Siddiqui ◽  
Dan Zhou ◽  
Jiyan Chen ◽  
...  

Abstract BACKGROUND Hypertensive patients with increased serum uric acid (SUA) are at increased cardiovascular (CV) risks. Both the European and American hypertension guidelines endorse the utilization of 24 h-ambulatory blood pressure monitoring (24 h-ABPM) for hypertensive patients with increased CV risk. While there is difference in identifying uric acid as a CV risk factor between the European and American guidelines. Therefore, it is unknown whether 24 h-ABPM should be used routinely in hypertensive patients with increased SUA. METHODS To address this knowledge gap, we investigated (i) the correlation between SUA and 24 h-ABP; (ii) the association between SUA and blood pressure (BP) phenotypes (controlled hypertension [CH], white-coat uncontrolled hypertension [WCUH], masked uncontrolled hypertension [MUCH], and sustained uncontrolled hypertension [SUCH]); (iii) the association between SUA and target organ damage (TOD: microalbuminuria, left ventricular hypertrophy [LVH], and arterial stiffness) according to BP phenotypes. RESULTS In 1,336 treated hypertensive patients (mean age 61.2 and female 55.4%), we found (i) there was no correlation between SUA and 24 h, daytime, and nighttime systolic blood pressure/diastolic blood pressure, respectively; (ii) in reference to CH, SUA increase was not associated WCUH (odds ratio [OR] 0.968, P = 0.609), MUCH (OR 1.026, P = 0.545), and SUCH (OR 1.003, P = 0.943); (iii) the overall prevalence of microalbuminuria, LVH, and arterial stiffness was 2.3%, 16.7%, and 23.2%, respectively. After adjustment for covariates, including age, sex, smoking, body mass index, diabetes mellitus, and estimated glomerular filtration rate, there was no association between SUA and TOD in all BP phenotypes. CONCLUSIONS These preliminary findings did not support routine use of 24 h-ABPM in treated hypertensive patients with increased SUA.


Sign in / Sign up

Export Citation Format

Share Document