Sodium‐Containing Pharmaceutical Products as Contributors to Cardiovascular Risk

Figures

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  Figure 1. Linear regression analyses describe the association between 24‐hour sodium excretiona and mean BP in the UK Biobank. 16 A, All participants (unadjusted; N=322 624); B, All participants (fully adjustedb; N=322 624); C, Excluding participants with Charlson score>0c (n=160 920; unadjusted); D, Excluding participants with Charlson score>0c (fully adjustedb) a24‐h sodium excretion was divided into sex‐specific quintiles to reduce the influence of outliers. bEach model was adjusted for age, lean body mass, ethnicity, family history of cardiovascular disease, smoking status, 24‐h potassium excretion, and Townsend deprivation score (calculated from census data on unemployment, non‐car ownership, and household overcrowding). cThe Charlson comorbidity score is a scoring system in which specific comorbid conditions are weighted based on their impact on survival. Scores range from 0 to 30, where 0 is no comorbid conditions. BP indicates blood pressure. Figure adapted with permission from Welsh et al. 16 Copyright ©2019, Wolters Kluwer Health, Inc.

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  Figure 2. Cumulative incidence of cardiovascular outcomes (composite of myocardial infarction, stroke, coronary revascularization, or cardiovascular death) with and without sodium interventions during long‐term follow‐up of the TOHP studies. 9 A, TOHP I; (B, TOHP II. TOHP assessed whether nonpharmacologic lifestyle changes, including reductions in sodium intake and weight loss alone and in combination, could reduce BP (TOHP I) or prevent incident hypertension (TOHP II) in individuals with overweight and prehypertension. Data are adjusted for age, sex, and clinic. CVD indicates cardiovascular disease; HR, hazard ratio; and TOHP, Trials of Hypertension Prevention. Figure adapted with permission from Cook et al. 9 Copyright © 2007, BMJ Publishing Group Ltd.

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  Figure 3. Impact of changing diet and sodium intake on BP in the DASH‐sodium trial. 11 A, DASH‐Sodium study design. After the 2‐wk run‐in period, participants were randomized to the DASH diet (high in fruits, vegetables, and low‐fat dairy) or a non‐DASH diet (a typical US diet). Participants consumed their assigned diet at each of the 3 sodium levels for 30 consecutive days, in random order, in a crossover trial. B, Mean differences in BP in the DASH and non‐DASH diets at each level of sodium intake; C, Changes in BP when patients switched between sodium levels within the DASH diet group; D, Changes in BP when patients switched between sodium levels within the control diet group. *P<0.05; **P<0.01; ***P<0.001. BP indicates blood pressure; and DASH, Dietary Approach to Stop Hypertension. Mean urinary sodium excretion was 3330, 2500, and 1500 mg/d in the high‐, intermediate‐, and low‐sodium groups, respectively. Figure based on Sacks et al. 11

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  Figure 4. Change in office and ambulatory BP when patients with hypertension switched between effervescent formulations of acetaminophen (paracetamol) (high‐sodium content) to noneffervescent tablets (low‐sodium content). 75 The ITT population included patients who met all eligibility criteria and had a measurement of the primary outcome (change in mean 24‐h systolic BP measured by) at the baseline visit; the PP population included patients who had completed the trial in the allocated arm and had final 24‐h systolic BP measurements. ΔC indicates change in BP when switching from noneffervescent to effervescent medication at basal visit; ΔE, change in BP when switching from effervescent to noneffervescent medication at final visit; ABPM, ambulatory blood pressure measurement; BP, blood pressure; DBP, diastolic blood pressure; ITT, intent to treat; PP, per protocol; and SBP, systolic blood pressure. Figure adapted with pemission from Benitez‐Camps et al. 75 Copyright © 2018, Wolters Kluwer Health, Inc.

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  Figure 5. Impact of changing from high‐sodium oxybate to low‐sodium oxybate on sodium excretion and systolic BP. 70 The mean±SD dosage was 8.0 (1.1) g/night for high‐sodium oxybate and 8.1 (1.1) g/night for low‐sodium oxybate. The mean difference in sodium content of medication was 1338.9 (190.7) mg. A, Change in urinary sodium excretion from baseline on high‐ vs low‐sodium oxybate. B, Proportion of patients with systolic BP <130 mm Hg after transitioning from high‐sodium oxybate to low‐sodium oxybate. Ambulatory BP monitoring was conducted at baseline and at the end of the study period using a device that automatically recorded BP every 20 min during daytime hours and every 30 min at night. Seated BP was assessed using an office BP measuring device at baseline and at the end of treatment. BP indicates blood pressure; IQR, interquartile range; and LSM, least squares mean. Figure adapted with permission from White et al. 70 Copyright © 2025, Wolters Kluwer Health, Inc.

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  Figure 6. Cumulative incidence of cardiovascular disease (A and C) or all‐cause mortality (B and D) after initiation of different formulations of acetaminophen (paracetamol) in individuals without hypertension (A and B) or with hypertension (C and D) during a 1‐year follow‐up period. 79 HR indicates hazard ratio. Figure adapted from Zeng et al. 79 Published under the terms of the Creative Commons CC BY license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.