We conducted a cross-sectional, observational study with prospective recruitment at the Instituto Ecuatoriano del Corazón (IECOREC), Guayaquil, Ecuador. Participant enrollment and study procedures were conducted after ethics approval and occurred from October 2021 to June 2022.

The research protocol was reviewed and approved by the Institutional Bioethics Committee of the Universidad Técnica de Manabí (UTM), in accordance with Ecuadorian national regulations for research involving human subjects (Protocol No. UTM-2021-007; approval letter No. UTM II 2018-011-OF; session date: October 13, 2021). Written informed consent was obtained from all participants prior to inclusion, in accordance with the Declaration of Helsinki and national guidelines.

Additionally, the protocol was reviewed by the Ethics and Bioethics Committee of the Instituto Universitario Italiano de Rosario (IUNIR), Argentina, as part of doctoral program requirements.

Eligible participants were adults aged 18–79 years with a clinical indication for 24-h ambulatory blood pressure monitoring (ABPM), either for initial hypertension screening or follow-up within primary prevention. Participants were required to be capable of providing informed consent and have an adequate echocardiographic acoustic window for three-dimensional assessment. We excluded patients with prior extracardiac target organ damage (stroke, advanced chronic kidney disease with eGFR <30 mL/min/1.73m²), significant chronic liver disease (Child-Pugh class B or C), active alcohol or drug dependence, current malignancy or cancer history within the past 5 years, hypertensive disorders of pregnancy, Parkinson’s disease, significant cognitive impairment, or cardiac arrhythmias that could impair ABPM accuracy. These criteria were applied to enhance internal validity and measurement reliability; however, they may reduce representativeness, since multimorbidity (including arrhythmias and chronic kidney disease) is common among hypertensive adults in routine practice (13).

A comprehensive medical history and physical exam were conducted. Collected data included demographics, cardiovascular risk factors (tobacco, alcohol, sedentary lifestyle, diet, occupational stress), comorbidities, and medication use. Anthropometric measures—body weight, height, waist circumference—were obtained with calibrated equipment following international protocols. Body mass index (BMI) was calculated as weight (kg) divided by height squared (m²). Office BP was measured after 5 min rest using an automated oscillometric device (Omron HEM-7120), with the average of 3 measurements recorded (14).

Waist circumference (WC) was measured at the midpoint between the lowest rib and the iliac crest during minimal respiration. Abdominal obesity categories were defined according to IDF/AHA/NHLBI harmonized criteria: normal (<94 cm men, <80 cm women), elevated risk (94–102 cm men, 80–88 cm women), and very high risk (>102 cm men, >88 cm women).

ABPM utilized a validated device (Microlife WatchBP O3 – AFIB, model 3MZ1-1A) following European Society of Hypertension and regional recommendations (7, 10). BP readings were scheduled every 20 min from 06:00 to 22:00 and every 30 min from 22:00 to 06:00. Quality criteria were ≥70% valid readings, with a minimum of 20 daytime and 7 nighttime successful recordings; compliance was documented via patient diary (7).

Hypertension thresholds were defined as 24-h mean ≥130/80 mmHg, daytime ≥135/85 mmHg, and nighttime ≥120/70 mmHg, consistent with contemporary guideline cutoffs for ABPM interpretation (7, 13). Pressure load was defined as the percentage of readings exceeding the corresponding thresholds, with >50% classified as abnormal during the respective periods. Circadian patterns were classified as dippers (10–20% nocturnal BP fall), non-dippers (<10%), extreme dippers (>20%), and reverse dippers (rise at night). For clarity, systolic (or diastolic) pressure load was defined as the proportion of valid SBP (or DBP) readings above the prespecified threshold over the 24-h, daytime, or nighttime period, and dipping pattern was defined as the percent decline in mean nighttime relative to daytime BP (7, 10, 15).

Left ventricular mass was assessed via three-dimensional transthoracic echocardiography (Philips EPIQ CVx) performed by an experienced cardiologist blinded to ABPM results, following ASE/EACVI guidance (16, 17). LVH was defined as LVMI >115 g/m² (men) and >95 g/m² (women) using guideline criteria (16). Additional parameters included left ventricular ejection fraction (biplane Simpson), left atrial volume index, E/e′ ratio, and relative wall thickness (17).

Fasting serum samples assessed glucose, lipid profile, and serum creatinine. eGFR was calculated using the CKD-EPI 2021 equation (18).

Statistical analyses were performed using MedCalc® Statistical Software, version 23.3.7 (32-bit) (MedCalc Software Ltd., Ostend, Belgium).¹ Normality of continuous variables was assessed using the Shapiro–Wilk test. Results are reported as mean ± SD for normally distributed variables or median (IQR) for non-normally distributed variables. Categorical variables are expressed as frequencies and percentages.

Group comparisons between participants with and without LVH were performed using the Student’s t-test or Mann–Whitney U test for continuous variables, and the Chi-square test or Fisher’s exact test for categorical variables. Exact p-values are reported and interpreted cautiously, emphasizing magnitude and precision rather than dichotomizing findings as “significant” or “non-significant” (19).

The discriminative ability of ABPM parameters for detecting LVH was evaluated using receiver operating characteristic (ROC) curve analysis, calculating area under the curve (AUC) with 95% confidence intervals (CI), sensitivity, specificity, predictive values, likelihood ratios, and optimal cut-off points based on Youden’s index (20). Cutoff points derived from Youden’s index are presented as exploratory, data-driven thresholds and may be sample-dependent; external validation is required before clinical use as decision limits (20, 21). Diagnostic performance metrics are summarized in Table 1, and comparative ROC curves for systolic blood pressure parameters are illustrated in Figure 1.

Pre-specified subgroup analyses by sex, age category, antihypertensive treatment status, and blood pressure control were conducted on an exploratory basis to examine potential effect modification. However, given the modest overall sample size, the study was not powered for definitive subgroup comparisons; therefore, subgroup ROC results are not reported in detail (22, 23).

A total of 129 patients were screened, of whom 19 were excluded: 7 due to established extracardiac target organ damage, 5 for inadequate echocardiographic acoustic windows, 4 for incomplete ABPM recordings, and 3 were lost to follow-up. The final analytic cohort comprised 110 participants (Figure 2).

The median age was 53 years (IQR: 42–63), and 56.4% were men. LVH was identified in 34.5% of participants (n = 38), consistent with prevalence rates reported in hypertensive cohorts (5). A prior diagnosis of hypertension was present in 63.6% of participants, with a median disease duration of 4 years (IQR: 1–10); duration was significantly longer among those with LVH compared to those without (8 vs. 3 years; p = 0.011). The majority of patients (87.3%) were receiving antihypertensive therapy at enrollment.

Cardiovascular risk factors were highly prevalent: alcohol consumption (42.7%), tobacco use (38.2%), sedentary lifestyle (52.7%), poor dietary habits (81.8%), and occupational stress (69.1%). Among women, 62.5% were postmenopausal. Type 2 diabetes mellitus was present in 10% of the overall cohort, with a trend toward higher prevalence in the LVH group (18.4% vs. 5.6%; p = 0.072). Median eGFR was 90.5 mL/min/1.73 m² (IQR: 78.2–102.3), with no significant differences between groups. Table 2 summarizes baseline clinical and demographic characteristics.

Median systolic BP values were consistently higher in participants with LVH across all time periods: 24-h SBP (128 vs. 125 mmHg; p = 0.038), daytime SBP (133 vs. 130 mmHg; p = 0.043), and nighttime SBP (119 vs. 115 mmHg; p = 0.011). A dose–response pattern was observed, with LVH prevalence increasing across higher SBP strata: 80% among those with 24-h SBP ≥ 145 mmHg, 83.3% with daytime SBP ≥ 150 mmHg, and 72.7% with nighttime SBP ≥ 135 mmHg. In contrast, diastolic BP parameters showed no statistically significant associations with LVH status. Table 3 presents detailed ABPM findings stratified by LVH status.

ROC analysis revealed limited discriminative performance for LVH detection across all ABPM parameters, with all AUC values below 0.65. Among systolic parameters, daytime SBP demonstrated the highest discriminative ability (AUC = 0.620; 95% CI: 0.523–0.717; p = 0.047), followed by nighttime SBP (AUC = 0.592; 95% CI: 0.493–0.691; p = 0.106) and 24-h SBP (AUC = 0.591; 95% CI: 0.491–0.691; p = 0.126). Comparative ROC curves for these systolic parameters are illustrated in Figure 1.

Among diastolic parameters, nighttime DBP showed the best performance (AUC = 0.607; 95% CI: 0.508–0.706; p = 0.068), whereas 24-h DBP (AUC = 0.520; 95% CI: 0.419–0.621; p = 0.730) and daytime DBP (AUC = 0.515; 95% CI: 0.414–0.616; p = 0.807) demonstrated negligible discriminative ability.

Exploratory analysis of pressure load thresholds revealed that nighttime diastolic load >30% yielded high sensitivity (89.5%) but low specificity (29.2%; Youden’s J = 0.19), suggesting potential utility as a triage tool for ruling out very low-risk cases rather than for diagnostic confirmation. This threshold was derived from categorical analysis of pressure load (proportion of nocturnal readings exceeding DBP ≥ 70 mmHg) and represents a complementary approach to the continuous BP parameters evaluated in Table 1. As with all exploratory thresholds, external validation is required before clinical application (20, 21).

Pre-specified subgroup analyses by sex, age, treatment status, and BP control were explored; however, results are not reported in detail due to small strata sizes yielding imprecise ROC estimates with wide, overlapping confidence intervals that precluded reliable interpretation (22, 23).

Key strengths include the focus on a Latin American hypertensive cohort, the use of three-dimensional echocardiography as the reference standard for LVH assessment (supporting improved reproducibility in LV mass estimation compared with conventional approaches and aligning with ASE/EACVI guideline recommendations), and the comprehensive evaluation of daytime and nighttime ambulatory BP indices, supporting a detailed characterization of circadian BP patterns in this setting (10, 16, 17, 26).

In resource-constrained settings, ABPM should be prioritized for patients with suspected white-coat or masked hypertension, marked discordance between office BP and overall cardiovascular risk, or high risk of hypertension-mediated organ damage (including suspected LVH), consistent with guideline-based indications (6, 13). When echocardiography capacity is limited, a daytime SBP threshold around 134 mmHg may serve as a pragmatic triage criterion to prioritize imaging referral in hypertensive patients; this value should not be interpreted as a diagnostic cutoff for LVH and requires external validation (21, 27).

To maximize the clinical utility of ABPM, primary care implementation should include standardized training (appropriate cuff selection and placement, patient instructions and diary use, minimum quality criteria for valid readings and day/night distribution, and guideline-based interpretation) (14). At the health-system level, expanding access to validated ABPM devices within primary care networks, integrating ABPM into standardized hypertension evaluation pathways for high-risk patients, and adopting risk-based referral algorithms combining clinical risk factors with ABPM findings may improve targeting of echocardiography and specialist care (10, 14). Regional multicenter studies with harmonized ABPM and echocardiography protocols are needed to validate thresholds and develop integrated prediction models for HMOD in Latin America (3, 10).

Scientific and Societal Implications.

Our findings support the use of ABPM as a complementary tool to characterize circadian BP patterns and to support risk stratification in hypertensive patients in resource-constrained settings. Given modest discrimination, ABPM indices should not replace echocardiography for LVH diagnosis; rather, they may help prioritize referral for imaging when capacity is limited. Broader implementation requires standardized training and quality criteria for ABPM acquisition and interpretation, and multicenter regional validation to ensure that any proposed thresholds are appropriate for diverse Latin American healthcare contexts (10, 13, 21).

This study was conducted in a single tertiary cardiovascular center with a modest sample size (n = 110). These design features may limit the precision of our estimates, increase the likelihood of type II error, and introduce referral-related selection bias. Accordingly, our results should be interpreted as exploratory and primarily applicable to urban, referred hypertensive adults in coastal Ecuador rather than to the broader and heterogeneous Latin American population, where ancestry, comorbidity burden, treatment patterns, and healthcare access differ across countries and levels of care. Larger multicenter studies across diverse Latin American settings (including primary, secondary, and tertiary care, as well as urban and rural populations) are needed to validate the ABPM cutoff values and diagnostic performance for LVH suggested by our data (10, 13, 26).

Because of the cross-sectional design, ABPM parameters and LVH were assessed at a single time point. This design permits only the identification of associations and does not allow robust causal inference, determination of temporal directionality, or evaluation of LVH progression/regression or long-term prognosis. Reverse causation, residual confounding, and selection/referral bias cannot be excluded; therefore, predictive or etiologic interpretations should be avoided (11, 12). Prospective cohort studies and treatment-response designs are required to determine whether ABPM-derived indices and thresholds predict incident LVH and whether changes in ambulatory BP are associated with LV mass regression over follow-up (30, 33).

Several exclusion criteria were applied to enhance the internal validity of ABPM and echocardiographic measurements. Patients with clinically significant arrhythmias were excluded because irregular RR intervals and frequent ectopy can impair the accuracy and reproducibility of oscillometric blood pressure measurement and increase the variability of ambulatory indices, as highlighted in contemporary guidance on blood pressure measurement and device validation (14, 34). Likewise, patients with advanced chronic kidney disease or established extracardiac hypertension-mediated organ damage were not included because CKD and end-stage kidney disease are strong, independent determinants of LV hypertrophy and abnormal LV geometry (e.g., through volume overload, anemia, and neurohormonal activation). However, these exclusions reduce the representativeness of our cohort, since multimorbidity, CKD, and overt cardiovascular disease are common among hypertensive patients in routine practice, including in Latin American populations. Our findings should therefore be interpreted as applicable primarily to relatively low-to-moderate risk ambulatory hypertensive adults, and future studies including patients with arrhythmias, CKD, and clinical HMOD—using validated measurement protocols for irregular rhythms—are needed to evaluate external validity of the diagnostic performance and exploratory ABPM thresholds suggested by our data (13, 14).

The study was not powered for robust subgroup analyses. Although stratified analyses by sex, age, antihypertensive treatment status, and blood pressure control were pre-specified, small numbers in several strata resulted in unstable and imprecise estimates. In line with methodological guidance on subgroup reporting, we therefore did not present detailed subgroup results and identify heterogeneity assessment as a priority for future, adequately powered multicenter studies (22, 23, 35).

Because diagnostic discrimination was modest (AUCs generally <0.65), individual ABPM parameters should not be used as stand-alone tests to diagnose or exclude LVH. Limited sensitivity for some thresholds implies a risk of false-negative classification; therefore, echocardiography remains necessary for definitive LVH assessment, and ABPM should be positioned as a complementary tool for risk stratification and triage rather than a replacement for imaging (21, 24).

Future studies should evaluate multivariable prediction models integrating ABPM parameters with clinical factors (e.g., age, sex, antihypertensive treatment, metabolic comorbidities, and hypertension duration) to assess whether discrimination improves beyond single BP-derived indices (25, 28). Prospective multicenter studies are needed to validate ABPM thresholds and assess whether ABPM indices predict incident LVH or longitudinal changes in LV mass (30, 33).