High Sodium Intake in Patients With Postural Orthostatic Tachycardia Syndrome

A Practice "Worth Its Salt"

Blair P. Grubb, MD, FAHA


J Am Coll Cardiol. 2021;77(17):2185-2186. 

In the mid-1980s the introduction of head-up tilt-table testing provided not only a diagnostic modality for evaluating patients suffering from vasovagal syncope, but also a controlled environment where these episodes of orthostatic decompensation could be introduced and carefully observed. This allowed for investigators to accurately measure multiple physiologic parameters during tilt-induced episodes of vasovagal syncope, greatly enhancing our understanding of this disorder. In the course of these investigations, it became apparent that there were other conditions that could result in autonomically mediated periods of orthostatic intolerance. In 1993, Schondorf and Low[1] published a landmark paper describing a condition that has become known as postural orthostatic tachycardia syndrome (POTS). Subsequently, there has been an explosion of research on the nature and prevalence of this condition. POTS is currently defined as a chronic disabling disorder associated with excessive tachycardia and intensification of symptoms with standing that are relieved by lying down. In an expert consensus statement issued in 2015 by the Heart Rhythm Society, POTS was defined as a condition characterized by a recurrent increase of heart rate by 30 beats per min while upright, which occurs in the absence of orthostatic hypotension.[2] The syndrome appears to occur when a failure of the peripheral vasculature to maintain adequate constriction allows for excessive venous pooling to occur during upright posture. This excessive venous pooling in the lower one-half of the body results in a compensatory increase in both heart rate and myocardial contractility. Patients afflicted with POTS are often women and experience symptoms such as fatigue, exercise intolerance, palpitations, lightheadedness, dizziness, and near syncope. The onset of symptoms often occurs in the aftermath of an acute febrile illness (presumed to be viral), suggesting a potential autoimmune/auto-inflammatory etiology. Patients afflicted with POTS can be severely limited in their ability to perform daily activities to the point of disability. The patients thus affected can develop severe exercise intolerance leading to profound deconditioning. Although aggressive reconditioning programs can be helpful, there are individuals who are unable to complete these programs or are not helped by them.

Other therapeutic modalities that have been used include increasing salt and fluid intake, volume-expanding agents, vasoconstrictors, and heart rate–lowering agents. However, many studies involving therapeutic modalities in POTS have either been small in size or observational in nature.

Studies have demonstrated that POTS patients have a decreased volume of plasma and high serum norepinephrine levels that occur with standing. In addition, rapid volume expansion with intravenous saline solutions have been shown to reduce upright tachycardia and improve symptoms in patients suffering from POTS. It would be reasonable to assume, therefore, that increasing oral sodium intake would have a salutary effect on the physiologic derangements that occur in POTS. A quarter-century ago, a series of studies demonstrated that salt supplementation can increase plasma volume and orthostatic tolerance in patients with unexplained syncope as well as increasing baroreceptor sensitivity.[3,4] However, up until now, no one has prospectively evaluated whether increased dietary sodium intake would have similar effects in POTS.

In this issue of the Journal, the study by Garland et al.[5] provides a welcome answer to the question. In a well designed study, they compared the effects of a low-sodium (10 mEq sodium/day) versus a high-sodium diet (300 mEq sodium/day) on orthostatic heart rate and low blood pressure increases as well as orthostatic changes in serum norepinephrine, epinephrine, aldosterone, plasma renin activity (PRA), and plasma volume in both POTS patients and matched control subjects. They convincingly showed that compared with those on a low-sodium diet, subjects on a high-sodium diet demonstrated a smaller increase in heart rate and lower norepinephrine level, PRA, and aldosterone level while upright. Interestingly, blood volume was lower in POTS patients then that of healthy control subjects, even with a high-sodium diet. This finding matches well with previous data that many POTS patients are clinically hypovolemic. Interestingly, while orthostatic symptoms improved while on the high-sodium diet, the decline did not reach statistical significance. However, this may have been due to difficulties in the measurement tool used.

One question that has yet to be answered relates to whether the salubrious effects of high dietary sodium intake in POTS patients that were noted over a short period of time will continue if maintained over much longer periods of time. In addition, the potential problems with maintaining such intakes over long periods of time will need to be carefully evaluated.

Nevertheless, this superb study by Garland et al.[5] helps better establish our understanding of the pathophysiologic process taking place in POTS while at the same time providing good evidence for the augmentation of dietary sodium as one of the cornerstones of treatment. The field needs more such studies in our quest to better understand POTS and to elaborate therapeutic modalities to help those suffering from this debilitating illness.