Do meals affect heart rate and symptoms in postural orthostatic tachycardia syndrome?

Most Americans consume on average three meals and three snacks a day; this is particularly true for women [1]. Given that the postprandial period depends on the meal composition, e.g., two hours for carbohydrates or eight hours for fats, we can infer that an ordinary person spends most of the day under the influence of food. In this context, it is well-known that meal consumption triggers significant changes in the cardiovascular system, whose actions primarily affect the splanchnic vascular bed, the largest blood volume reservoir of the human body. It can store nearly 25% of the total blood volume, which contributes to large and abrupt fluctuations in the stroke volume (SV) and blood pressure (BP) [2].

Food ingestion significantly increases the blood flow velocity in the superior mesenteric artery (SMA), which is responsible for the perfusion of major splanchnic organs (pancreas, small intestine, transverse colon). Figure a shows the SMA doppler flow velocity before and after ingesting 75g of glucose in a healthy subject; the SMA resistance index decreased by 18% after glucose ingestion denoting an increase in the splanchnic arterial blood flow. To compensate for this augmented splanchnic blood flow, the sympathetic nervous system is activated, which increases venous constriction, and restores the SV and cardiac output, to prevent any significant BP fluctuations. Patients with autonomic failure, who have impaired sympathetic function, cannot counteract food induced increase in splanchnic blood flow, which results in a high prevalence of postprandial hypotension [3].

Figure.

(a) Superior mesenteric artery flow (SMA) velocity before and after 75g glucose in one POTS patient. The left panel shows the SMA peak systolic (211 cm/s), diastolic (26 cm/s) flow velocity and the resistance index (RI, 0.88) during fasting conditions. The right panel shows an increase mostly in the diastolic (56.5 cm/s) flow velocity and a reduction in the RI 0.73 after 75g oral glucose. The systolic flow velocity did not change after oral glucose. (b) Effect of oral glucose intake on seated and standing heart rate (HR) and continuous blood pressure (BP) in one POTS patient. On the left panel, continuous BP and HR are shown during fasting conditions, the highest HR upon standing was 106 bpm. On the right panel, BP and HR are shown, 30-min after the ingestion of glucose 75g, the maximum increase HR was 147 bpm. The test was stopped because the patient elicited significant pre-syncopal symptoms.

Patients with postural orthostatic tachycardia syndrome (POTS), a common autonomic disorder, are also affected by the negative cardiovascular effect of meals. These patients, who can mount compensatory sympathetic activity in response to meals, also experience significant exacerbation of their POTS symptoms, typically with postprandial tachycardia instead of postprandial hypotension [4]. Anecdotally, many patients have reported some symptom improvement or mitigation following a low carbohydrate diet, and eating smaller meals throughout the day, rather than three larger meals per day [5].

The epidemiological data evaluating postprandial effects on POTS symptoms are scarce. We evaluated dietary influence on POTS symptoms in a large online, community-based survey between 2015 and 2021. The survey included a total of 8,919 POTS patients, this survey data was self-reported, and although participants reported a physician-diagnosis of POTS, this was not verified, which was a limitation in this study. Demographics and other characterization of this cohort, as well as study methodology, are described elsewhere [6]. The data showed a significant postprandial symptom burden in the POTS population. A majority of participants who reported a physician diagnosis of POTS conveyed an increase in their POTS symptoms following a high-carbohydrate meal (53% increased symptoms, 4% decreased symptoms, 16% no change, 27% not sure). This trend was also observed with high-fat meals (43% increased symptoms, 4% decreased symptoms, 18% no change and 36%not sure), whereas it was not with high-protein meals (15% increased symptoms, 18% decreased symptoms, 32% no change and 35% not sure). These findings persisted even after the analyses were stratified by sex and the presence of diabetes mellitus.

Several small studies have shown that meals induce important hemodynamic effects in POTS patients. Tani et. al. [4] found a significant increase in upright heart rate (HR) after POTS patients consumed a standardized meal compared to a pre-meal head up tilt test (133±5 bpm vs.121±5 bpm). Habek et al. [7] reported that a mixed meal significantly increased orthostatic tachycardia in POTS patients, which has implications for the HR diagnostic criteria in POTS. We measured continuous BP and HR in a 24 year old, white woman diagnosed with POTS while the patient moved from sitting to standing position, thereby mimicking typical daily activities. In this patient we observed a substantial elevation in the standing HR in this single case following a 75g glucose challenge (Figure b).

The underlying cause of the exaggerated postprandial orthostatic tachycardia in POTS patients is unknown. Certain gastrointestinal hormones with splanchnic vasodilatory properties could contribute to the pathophysiology of these symptoms. Suppression of the secretion of these peptides with octreotide (a somatostatin analogue), effectively reduced tachycardia and presyncopal symptoms in refractory POTS [8, 9]. Reducing carbohydrate intake or absorption (with acarbose) could also improve postprandial POTS symptoms. Shannon et al. [10] demonstrated a decrease in orthostatic tachycardia (123±23 bpm to 108±21 bpm) after rapid water ingestion (480mL of tepid tap water in less than 5 minutes). Additionally, post-prandial rapid water ingestion was tested in patients with autonomic failure, with a demonstrated reduction in orthostatic hypotension [10]. Although patients with orthostatic tachycardia were studied in a fasting state, future research could investigate the potential role of post-prandial water ingestion in mitigating orthostatic tachycardia in this patient group.

In conclusion, meals do matter in the evaluation and treatment of POTS. There are significant postprandial symptoms in POTS patients, which are related to exaggerated postprandial tachycardia. Possible mechanisms include enhanced splanchnic blood pooling, an increased secretion of vasoactive gastrointestinal hormones, or an excessive sympathetic nervous system response to food ingestion, either in isolation or in combination. Further mechanistic studies are needed to understand the underlying pathophysiology and response to dietary and pharmacological interventions, with the goal of developing new treatment approaches for POTS.

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