Staying well hydrated reduce the risk of developing heart failure

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Staying well hydrated throughout life could reduce the risk of developing heart failure, according to research presented at ESC Congress 2021.

“Our study suggests that maintaining good hydration can prevent or at least slow down the changes within the heart that lead to heart failure,” said study author Dr. Natalia Dmitrieva of the National Heart, Lung, and Blood Institute, part of the National Institutes of Health, Bethesda, US.

“The findings indicate that we need to pay attention to the amount of fluid we consume every day and take action if we find that we drink too little.”

Recommendations on daily fluid intake vary from 1.6 to 2.1 litres for women and 2 to 3 litres for men. However, worldwide surveys have shown that many people do not meet even the lower ends of these ranges. Serum sodium is a precise measure of hydration status: when people drink less fluid, the concentration of serum sodium increases.

The body then attempts to conserve water, activating processes known to contribute to the development of heart failure.

Dr. Dmitrieva said: “It is natural to think that hydration and serum sodium should change day to day depending on how much we drink on each day. However, serum sodium concentration remains within a narrow range over long periods, which is likely related to habitual fluid consumption.”

This study examined whether serum sodium concentration in middle age, as a measure of hydration habits, predicts the development of heart failure 25 years later. The researchers also examined the connection between hydration and thickening of the walls of the heart’s main pumping chamber (left ventricle) – called left ventricular hypertrophy – which is a precursor to heart failure diagnosis.

The analysis was performed in 15,792 adults in the Atherosclerosis Risk in Communities (ARIC) study. Participants were 44 to 66 years old at recruitment and were evaluated over five visits until age 70 to 90.

Participants were divided into four groups based on their average serum sodium concentration at study visits one and two (conducted in the first three years): 135–139.5, 140–141.5, 142–143.5, and 144–146 mmol/l. For each sodium group, the researchers then analysed the proportion of people who developed heart failure and left ventricular hypertrophy at visit five (25 years later).

Higher serum sodium concentration in midlife was associated with both heart failure and left ventricular hypertrophy 25 years later. Serum sodium remained significantly associated with heart failure and left ventricular hypertrophy after adjusting for other factors related to the development of heart failure: age, blood pressure, kidney function, blood cholesterol, blood glucose, body mass index, sex and smoking status.

Every 1 mmol/l increase in serum sodium concentration in midlife was associated with 1.20 and 1.11 increased odds of developing left ventricular hypertrophy and heart failure, respectively, 25 years later.

The risks of both left ventricular hypertrophy and heart failure at age 70 to 90 began to increase when serum sodium exceeded 142 mmol/l in midlife.

Dr. Dmitrieva said: “The results suggest that good hydration throughout life may decrease the risk of developing left ventricular hypertrophy and heart failure. In addition, our finding that serum sodium exceeding 142mmol/l increases the risk of adverse effects in the heart may help to identify people who could benefit from an evaluation of their hydration level.

This sodium level is within the normal range and would not be labelled as abnormal in lab test results but could be used by physicians during regular physical exams to identify people whose usual fluid intake should be assessed.”


The Physiology of Hypohydration


Hypohydration is defined as a body water deficit caused by acute or chronic dehydration [1]. While extensive research has been conducted to identify the “elusive daily water requirement”, well summarized by Armstrong and Johnson [2] within this special issue, acute hypohydration studies have provided important insight into the integrative physiology of water balance in humans. Human hypohydration can be elicited experimentally through the use of water restriction, prolonged exercise, heat stress, diuretic administration, or a combination of methods [3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31].

In response to hypohydration-induced reductions in plasma volume and increases in plasma sodium ([Na+])/osmolality, the renin–angiotensin–aldosterone system becomes activated, thirst sensations increase, and arginine vasopressin (AVP, also referred to as anti-diuretic hormone) release increases [20,32,33,34,35,36,37,38,39,40].

A low extracellular fluid volume is sensed in the walls of the afferent arterioles proximal to the glomeruli and causes juxtaglomerular cells to secrete renin, which initiates a cascade culminating in increased circulating angiotensin II (Ang II) and aldosterone concentrations acting to increase [Na+] and water retention.

Central [Na+] sensing, which may be distinct from osmo-sensing [41], occurs in circumventricular organs including the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO) because both brain areas lack a complete blood–brain barrier (BBB) [42]. Specialized mechanical-stretch transient receptor potential vanilloid (TRPV) cation channels are one potential candidate thought to participate in osmo-sensing [43].

Nevertheless, these signals are communicated through neuronal projections to the median preoptic nucleus (MnPO) before activating thirst-promoting neurons in the paraventricular nucleus (PVN) of the hypothalamus via acid-sensing ion channel 1a (ASIC1a) by H+ ions exported from Nax-positive glial cells [44].

These signals are then

1) relayed to the lateral hypothalamus as well as the paraventricular hypothalamus and thalamus [45], and

2) stimulate AVP release from the posterior pituitary gland from upstream communication with the PVN and supraoptic nuclei [34,46].

Increased thirst sensations promote water intake [45,46]. Increased plasma [AVP] stimulate aquaporin-2-mediated water reabsorption from the luminal surface of renal collecting ducts to promote water retention [47]. Together, these integrated responses aim to restore body water homeostasis.

The following sections will discuss recent findings related to hypohydration and cardiovascular function. When applicable, we will mention the methods used to induce hypohydration (e.g., heat, exercise, fluid restriction, or diuretic) in humans because these methods have different side effects (e.g., diuretics promote iso-osmotic hypovolemia whereas heat stress promotes hyper-osmotic hypovolemia) [48].

Finally, for human hypohydration studies, we will report the resultant body mass deficit as the severity of hypohydration is defined as follows: mild hypohydration (1 to 5% body mass deficit), moderate hypohydration (5 to 10% body mass deficit), and severe hypohydration (>10% body mass deficit) [1].

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Figure 1
Summary of the physiological consequences of acute mild hypohydration in healthy humans. Further research is necessary to determine whether and how these acute effects influence the poor cardiovascular health outcomes associated with chronic inadequate water consumption. ↓, impaired or reduced; ↑, increased

reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723555/


Provided by European Society of Cardiology 

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