Systematic screening in patients with apparently resistant arterial hypertension identified a secondary etiology in 23.2% of cases, with primary aldosteronism being the most frequent cause (14.0%).
Cohort (n=1,062)
Systematic screening of patients with apparently resistant arterial hypertension identified a secondary cause in 23.2% of cases, predominantly primary aldosteronism.
Abstract Background Apparently resistant arterial hypertension (aRAH) represents a significant clinical challenge due to its association with poor cardiovascular outcomes. Previous research on aRAH has primarily focused on primary aldosteronism (PA), leaving the prevalence of other secondary hypertension etiologies under-investigated (1,2,3,4). This study addresses this gap by providing the largest and most comprehensive assessment of secondary hypertension causes in this population to date. Purpose To systematically assess the prevalence and distribution of secondary hypertension etiologies in a large cohort of patients with aRAH and to refine diagnostic strategies for identifying reversible causes of hypertension. Methods This retrospective cohort study included patients initially classified as having aRAH, defined as office blood pressure ≥140/90 mmHg despite treatment with at least three antihypertensive drugs (including a diuretic) and confirmed medication adherence (5). Ambulatory blood pressure monitoring (ABPM) was performed to exclude white-coat hypertension. All participants were referred to a specialized hypertension outpatient clinic for further evaluation. A structured screening protocol—including biochemical testing, imaging, and ABPM—was implemented to systematically assess potential secondary causes. Results Of the 1,117 patients evaluated, 55 were excluded due to unknown resistance status or uncertain secondary hypertension classification. Among the remaining 1,062 patients, 816 (77.0%) had no identifiable secondary hypertension etiology, while 246 (23.2%) were diagnosed with a secondary cause. Notably, PA was the most frequently identified etiology, accounting for 152 cases (14.0% of the total cohort), followed by renal parenchymal disease (38 cases, 3.6%), renovascular hypertension (37 cases, 3.5%), and pheochromocytoma/paraganglioma (11 cases, 1.0%). Less frequent causes included drug-induced hypertension (4 cases, 0.4%), hyperparathyroidism (2 cases, 0.2%), and hypercortisolism (2 cases, 0.2%). A breakdown of the distribution of secondary hypertension causes is illustrated in Figure 1. Conclusions This study highlights the high prevalence of secondary hypertension (23.2%) in patients with aRAH, with PA emerging as the most frequent etiology. These findings emphasize the necessity of systematic screening for secondary causes in resistant hypertension to facilitate targeted treatment and improve blood pressure control. A structured diagnostic approach—incorporating biochemical, imaging, and adherence assessments—is crucial for distinguishing pseudoresistance from true resistant hypertension. These findings align with previous evidence highlighting the need for a more proactive approach to hypertension subtyping in specialized clinics, as demonstrated by the variability in secondary hypertension prevalence across studies (Figure 2).Figure 1.Distribution Figure 2.Comparasion
Kvapil et al. (Sat,) conducted a cohort in Apparently resistant arterial hypertension (aRAH) (n=1,062). Structured screening protocol for secondary hypertension was evaluated on Prevalence of secondary hypertension etiologies. Systematic screening in patients with apparently resistant arterial hypertension identified a secondary etiology in 23.2% of cases, with primary aldosteronism being the most frequent cause (14.0%).