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CLINICAL STATEMENTS AND GUIDELINES

Circulation. 2025;152:e114–e218. DOI: 10.1161/CIR.0000000000001356 September 16, 2025 e157

an SBP <130 mm Hg but were infrequent, with numbers needed to harm ranging from 508 for hypotension to 3222 for electrolyte abnormalities. The support for SBP <120 mm Hg versus <140 mm Hg was further demonstrated in the BPROAD (Blood Pressure Control Target in Diabetes) trial, with the incidence of MACE being significantly lower in those with type 2 diabetes (T2D).10

2 In the PREVER-Prevention trial, conducted in

adults who were not at high risk for CVD and had an average SBP between 120 and 139 mm Hg after 3 months of lifestyle counseling, treatment with once-daily low-dose chlorthalidone (12.5 mg) and amiloride (2.5 mg) significantly lowered BP, prevented hypertension, and reduced left ventric­ ular mass as an intermediate endpoint compared with placebo.5 3.	 In adults at high risk for CVD, participants in 2

trials6,15 were randomized to a DBP <80 mm Hg versus higher DBP antihypertensive treatment goal, concordant with randomization to an SBP goal of <12015 or <130 mm Hg.6 In one of these trials, CVD risk and all-cause mortality were sig­ nificantly reduced in the participants randomized to the lower compared with the higher DBP.6 The other trial failed to meet its recruitment goal and was substantially underpowered but resulted in a consistent, albeit nonsignificant, reduction for both outcomes in the participants randomized to the lower DBP target.15 J- and U-shaped associations between DBP and CVD events, including coronary heart disease, have been observed in analyses of nonrandomized clinical trial and disease regis­ try data sets, including a post-hoc analysis of the SPRINT.22 In randomized comparisons, however, CVD outcomes and all-cause mortality were bet­ ter in those randomized to an SBP goal of <120 versus <140 for every quintile of baseline DBP, including those with the lowest starting DBP (<68 mm Hg).22 Although there is no cutoff for level of DBP during antihypertensive treatment, careful monitoring of symptoms and attention to changes in eGFR are important. 4.	 In the PREVER-Prevention trial, conducted in adults

who were not at high risk for CVD and had an aver­ age DBP between 80 and 89 mm Hg, treatment with once-daily low-dose chlorthalidone (12.5 mg) and amiloride (2.5 mg) significantly lowered BP, prevented hypertension, and reduced left ventricular mass com­ pared with placebo.5 Although this is an intermedi­ ate endpoint, the results support lowering DBP and are consistent with guidance in an AHA Scientific Statement for those with a high lifetime risk of CVD, including young adults.23

5.2.8 Electrolyte Imbalances

Synopsis

Assessment of electrolytes is important in evaluating causes of hypertension and in monitoring adverse ef­ fects with treatment. A basic metabolic panel should be checked at the time of diagnosis of hypertension to evaluate for secondary hypertension, including primary or secondary aldosteronism (Section 3.2.3.1, “Primary Aldosteronism”) and other endocrine causes. A ba­ sic metabolic panel should be checked 2 to 4 weeks after initiation or dose titration of specific antihyper­ tensive medication classes, including diuretics, ACEi, ARB, and MRA. Common lab disturbances relate to changes in potassium, sodium, or creatinine. In addi­ tion to secondary causes of hypertension, hypokalemia may be caused by kaliuresis from thiazide-type and loop diuretics. Hyperkalemia may be caused by ACEi, ARB, MRA, and potassium-sparing diuretics especial­ ly when used in combination or in the setting of CKD. ACEi and ARB should not be used concurrently due to several trials demonstrating an increased risk for AKI or renal dysfunction.1–3 Hyponatremia may be caused by diuretics, in particular thiazide-type diuretics. Strat­ egies to mitigate electrolyte disturbances related to antihypertensive medications include dietary changes, electrolyte supplementation, and combination use of medications with complementary effects on electrolytes (eg, ACEi plus thiazide-type or loop diuretic, which may normalize potassium levels) (Section 5.2.6, “Medication Interactions”). Treatment of hyperkalemia, other than emergency treatment for life-threatening hyperkalemia, can also be managed with initiation of potassium-lower­ ing binders (including patiromer and sodium zirconium cyclosilicate), noting the importance of taking them (pri­ marily patiromer) mid-day apart from other medications to avoid interfering with absorption.4,5 If severe or lifethreatening electrolyte imbalances occur, the causative medication should be discontinued and the imbalance treated immediately.

Table 15.  Evidence-Based Strategies for Improving Antihypertensive Medication Adherence Evidence-Based Strategies for Improving Antihypertensive Medication Adherence Dose consolidation Single pill combination rather than separate pills Education/coaching by pharmacists and other health professionals Electronic/home blood pressure monitoring and feedback Integration of patient preferences and values/shared decision-making into management plan Medication synchronization and reminder aids Mindfulness-based stress reduction or counseling for high stress, anxiety, and/or depression Self-management interventions Modified with permission from Choudhry et al.21 Copyright 2022 American Heart Association Inc.

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