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CLINICAL STATEMENTS AND GUIDELINES Circulation. 2025;152:e114–e218. DOI: 10.1161/CIR.0000000000001356 September 16, 2025 e131 protocols. Currently, few protocols exist for validating cuffless BP devices. The Institute of Electrical and Electronics Engineers validation standards recommend using a cutoff of <7 mm Hg for the mean absolute difference between test and reference devices.4 A sys tematic review and meta-analysis from 2022 evalu ated validation protocols of 15 cuffless devices; 12 of the 16 studies included in the analysis reported mean absolute difference data.1 Results revealed no statis tically significant differences between the wearable cuffless and reference devices, with a pooled mean difference of 3.42 mm Hg SBP (95% CI: −2.17 to 9.01 mm Hg) and 1.16 mm Hg DBP (95% CI: −1.26 to 3.58 mm Hg).1 Although these data are promising, the use of cuffless devices risks the underestimation or overestimation of BP due to the marked hetero geneity in the devices being tested. These limitations must be overcome before cuffless devices can be rec ommended for clinical use. In 2022, the International Organization for Standardization published a validation protocol (ISO 81060-3: 2022) for “continuous nonin vasive sphygmomanometers” that could be used for cuffless BP devices that continuously measure BP but may not be appropriate for outpatient use.5,6 In 2023, the European Society of Hypertension Working Group on BP Monitoring and Cardiovascular Variability rec ommended procedures for validating intermittent cuf fless BP devices.5 Scarce data exist on using these protocols to test cuffless BP devices. 3.2 Patient Diagnosis 3.2.1 Causes of Hypertension Synopsis Elevated BP and hypertension reflect a complex inter play of behavioral, environmental, hormonal, and genetic influences across the lifespan (Table 8). Diet quality is significantly associated with elevated BP and its se quelae.1–3 Among dietary factors influencing BP, higher sodium intake, lower potassium intake (measured by uri nary excretion), and alcohol overuse predominate; low in take of fiber, calcium, magnesium, and plant protein also influence BP.4–6 Weight gain,7 overweight or obesity, and related metabolic issues (ie, insulin resistance) contrib ute to the increase in BP and hypertension across the lifespan, particularly in recent decades.8,9 Factors such as increasing age, obesity, and insulin resistance influ ence how BP is affected by sodium, emphasizing the importance of lower sodium intake.5 Sleep disturbances (Section 3.2.3.3, “Obstructive Sleep Apnea”) and psycho social stressors can exacerbate,10–12 and increases in BP can be ameliorated by a higher level of physical activity and fitness (Section 5.1, “Lifestyle and Psychosocial Ap proaches”).13 Emerging data also implicate environmen tal exposures and chemical toxins (including air pollution and heavy metals) in the increases in BP.14,15 BP is a highly heritable trait,16 and hundreds of inde pendent genetic loci capable of affecting BP have been described to date.17,18 Each variant has small effects on BP alone, but collectively they may explain larger inter individual differences in BP.17,18 Nonetheless, all genetic loci described to date explain <10% of BP variance,18 indicating the importance of other factors and geneenvironment interactions. 3.2.2 White-Coat Hypertension and Masked Hypertension, and White-Coat Effect and Masked Uncontrolled Hypertension Recommendations for White-Coat Hypertension and Masked Hypertension, and White-Coat Effect and Masked Uncontrolled Hypertension Referenced studies that support the recommendations are summarized in the Evidence Table. COR LOE Recommendations 2a B-NR 1 In adults with untreated office SBP ≥130 mm Hg or DBP ≥80 mm Hg, and without office SBP ≥160 mm Hg or DBP ≥100 mm Hg, it is reasonable to exclude white-coat hypertension using out-ofoffice BP monitoring before a diagnosis of hypertension is made.1–5 2a B-NR 2 In adults with white-coat hypertension or masked hypertension, out-of-office BP monitoring is reasonable to exclude transition to a diagnosis of sustained hypertension.6–8 2a C-LD 3 In adults with apparent treatment-resistant hypertension on office BP, it is reasonable to exclude white-coat effect, a form of pseudoresis tance, using out-of-office BP monitoring.9–12 2a B-NR 4 In adults who are taking antihypertensive medication and have elevated office BP (office SBP ≥130 mm Hg or DBP ≥80 mm Hg) but do not have resistant hypertension or office SBP ≥160 mm Hg or DBP ≥100 mm Hg, it is reasonable to exclude white-coat effect using out-of-office BP monitoring.1,4,13 2b B-NR 5 In adults with untreated office SBP <130 mm Hg and DBP <80 mm Hg, it may be reasonable to exclude masked hypertension using out-of-office BP monitoring.5,13–15 2b B-NR 6 In adults who are taking antihypertensive medication and have office SBP <130 mm Hg and DBP <80 mm Hg, it may be reasonable to exclude masked uncontrolled hypertension using out-of-office BP monitoring.13–15 Table 8. Environmental, Behavioral, and Genetic Causes of Hypertension Dietary Intake Factors Nondietary Factors Higher sodium intake Genetic variants Lower potassium intake Overweight/obesity Lower calcium/magnesium intake Lower physical activity/fitness Lower diet quality (lower intake of fruits/vegetables, plant pro teins, fiber) Sleep disturbances (related to duration, quality, regularity, and/or disordered breathing) Alcohol intake Psychosocial stressors Air pollution Downloaded from http://ahajournals.org by on October 7, 2026