The Impact of Trait Anxiety on Blood Pressure Variability and Target Organ Damage in Hypertensive Patients: A Cross-Sectional Study

Abstract

Background

Hypertension is a leading global cardiovascular risk factor. Blood pressure variability (BPV) and target organ damage (TOD) are strong predictors of adverse cardiovascular outcomes. Trait anxiety is associated with sympathetic nervous system hyperactivity and hypothalamic-pituitary-adrenal axis dysregulation, both of which may elevate BPV and promote TOD. However, evidence linking trait anxiety to 24-hour BPV and subclinical TOD in hypertension remains limited. This study aimed to investigate the independent association of trait anxiety with BPV and TOD in hypertensive patients, and to clarify its clinical significance and novelty relative to existing literature.

Objective

This study aimed to investigate the relationship between trait anxiety and both target organ damage (TOD) and blood pressure variability (BPV) in hypertensive patients.

Methods

A cross-sectional observational study was conducted including 285 hypertensive patients. Trait anxiety was measured using the State-Trait Anxiety Inventory (STAI). Ambulatory blood pressure monitoring (ABPM) was performed to assess 24-hour BPV. Cardiac-ankle vascular index (CAVI) and left ventricular mass index (LVMI) were measured on the same day as ABPM after 15 minutes of supine rest to evaluate vascular and cardiac TOD. Multivariate regression and partial correlation analyses were used to examine independent associations.

Results

Among the 285 hypertensive patients, 142 were classified into the low trait anxiety group and 143 into the high trait anxiety group, with well-balanced baseline characteristics between groups. Compared with the low anxiety group, patients with high trait anxiety exhibited significantly higher 24-hour systolic and diastolic blood pressure variability (BPV), as well as elevated left ventricular mass index (LVMI) and cardio-ankle vascular index (CAVI) (all P<0.05). Further partial correlation and multivariate regression analyses demonstrated that trait anxiety was independently and strongly associated with 24-hour average real variability (ARV) of systolic blood pressure, 24-hour ARV of diastolic blood pressure, LVMI, and CAVI (all P<0.001). These associations remained statistically significant after adjustment for age, gender, BMI, hypertension duration, medication use, and laboratory confounders.

Conclusion

Trait anxiety is independently associated with increased 24-hour BPV and early TOD in hypertensive patients. As a modifiable psychological risk factor, trait anxiety may contribute to cardiovascular remodeling beyond mean blood pressure levels. Routine screening and anxiety intervention may help improve BPV control and reduce TOD progression. These findings provide new evidence for integrated psychological and cardiovascular management of hypertension.

Introduction

Around 1.39 billion people with hypertension were found in low and middle-income countries (LMICs) and high-income countries accounted for the remaining 1/4. There was a 440 million increase in the number of people with hypertension in LMICs between 2000 to 2010 which was much higher than the 27 million increases in HICs.¹ According to estimates, 10.7 million deaths, or 19.2% of all deaths, occurred in 2015 as a result of raised systolic blood pressure SBP [systolic blood pressure]> 110–115 mmHg. Worldwide, there were 7.8 million deaths associated with SBP 140 mmHg, accounting for 14.0% of all deaths.¹ An increased risk for coronary heart disease (CHD) as well as more severe atherosclerosis are both associated with hypertension, the primary risk factor for CHD. Heart failure and myocardial infarction are also made more likely due to an addition to left ventricular hypertrophy.

There is an elevated risk of cardiovascular events for short-term blood pressure variability (BPV), including variability that occurs over a 24h period. The development and severity of the damage in target organs such as kidney, blood arteries and heart are related to higher 24 hours BPV as research^2–8 can support. In addition, there is an independent correlation of increasing short-term BPV with an increased risk of cardiovascular events and death.⁹ One study showed that the risk of all-cause and cardiovascular death of hypertension patients was significantly increased by an increase in short-term BPV. This result was obtained from the Spanish ABPM Registry. More specifically, hazard ratios for all-cause death varied between 1.05 and 1.12 for every 1 standard deviation (SD) increase in daytime systolic BPV and for cardiovascular mortality, the range varied between 1.07 and 1.17.¹⁰

Despite the fact that BPV is affected by mean blood pressure, research shows that it has its own predictive power of cardiovascular risk. After adjusting for mean blood pressure, BPV still contains more information about prediction.¹¹ Also associated with an increased risk of cardiovascular events and death is BPV that is measured for an extended period of time, either in days or clinical visits. An increased risk of cardiovascular events and death from any cause was correlated with higher long-term BPV, according to one of the research projects.

Because it gives more information on cardiovascular risk than that given by standard blood pressure measurements, BPV is of clinical relevance. The risks of cardiovascular events, TOD, and death are increased with both short- and long-term BPV, regardless of the mean blood pressure levels. Consequently, BPV is a very good complementary measurement for assessing cardiovascular risk.

A person who has trait anxiety is more likely to feel anxious in general in contrast to a person with state anxiety who is more likely to feel anxious in response to certain events.¹² People with a high level of trait anxiety are more susceptible to respond with anxiety and be hyper sensitive in response to a perceived danger. Numerous health issues have been linked to this prolonged manifestation, primarily through mechanisms related to all of the logic concerning the hypothalamic-pituitary-adrenal (HPA) axis dysfunction and sympathetic neurological business (SNS).

Exaggerated arousals of the sympathetic nervous system, such as fast heartbeat, hypertension and perspiration, are not uncommon in those which suffer from severe trait anxiety if they are under stress.¹³ Elevated cortisol levels annually may be an outcome of chronic trait anxiety that impedes on HPA axis function. In addition to making, it more difficult to regulate one’s emotions, this dysregulation may lead to a higher risk of developing diabetes, cardiovascular and immune-related illnesses.^14,15

Trait anxiety, being a constant personality trait, may affect psychological reactions, as well as physical health consequences such as target organ damage in hypertensive patients and blood pressure variability (BPV), according to their physiological correlates. Nevertheless, there is a lack of such research addressing such links specifically. Determining the role of trait anxiety in blood pressure variability (BPV) and target organ damage (TOD) of hypertensive persons is the main aim of this research.

Methods

Study Population

A total of 285 hypertensive patients were consecutively enrolled from the Cardiology Department of Beijing Friendship Hospital, Capital Medical University between January 2018 and December 2024. This was a cross-sectional observational study with all measurements obtained at baseline and no follow-up period. All participants underwent 24-hour ambulatory blood pressure monitoring, echocardiography, and arterial stiffness evaluation at baseline.

Anxiety was evaluated using the 40-item, 4-point State-Trait Anxiety Inventory (STAI).¹⁶ The 20-item Trait Anxiety Scale (T-AI) was applied to assess stable anxiety-related personality traits. Based on validated cut-off values,¹⁷ participants were divided into two groups: low trait anxiety (T-AI < 39, n = 142) and high trait anxiety (T-AI > 49, n = 143). Patients with T-AI scores of 39–49 (moderate trait anxiety) were excluded from between-group comparisons to maximize contrast in anxiety levels.

The Chinese version of the STAI demonstrated good construct validity and internal consistency in this sample (Cronbach’s α for trait anxiety = 0.717).^18,19 The study protocol was approved by the Ethics Committee of Beijing Friendship Hospital, Capital Medical University (approval No. 2025-P2-459-01). Written informed consent was obtained from all participants prior to any study procedures, including anxiety assessment and clinical measurements.

Inclusion and Exclusion Criteria

Inclusion Criteria: (1) Age 18–75 years; (2) Diagnosis of primary hypertension according to the 2018 ESC/ESH Guidelines for the management of arterial hypertension;²⁰ (3) Complete baseline clinical, laboratory, and imaging data available.Exclusion Criteria: (1) History of secondary hypertension; (2) Severe systemic diseases (eg., malignant tumor, neurological disorders, uncontrolled psychiatric disorders) (3) Participation in other concurrent clinical trials; (4) T-AI score of 39–49 (moderate trait anxiety);¹⁷ (5) Incomplete 24-hour ambulatory blood pressure monitoring data (successful readings < 80%).

Baseline Data Collection and Laboratory Testing

Baseline characteristics included gender, age, height, weight, waist circumference, hip circumference, educational level, duration of hypertension, and family history of hypertension. Body mass index (BMI) and waist-to-hip ratio (WHR) were calculated. Fasting venous blood samples were collected in the morning, centrifuged at 4000 rpm for 15 minutes, and analyzed for total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), blood urea nitrogen (BUN), and creatinine (CR) using a Roche Cobas C501 automatic biochemical analyzer.

Ambulatory Blood Pressure (ABP) Monitoring

Twenty-four-hour ABP monitoring was performed using an automated portable device. Blood pressure readings were recorded every 30 minutes during daytime (6:00–22:00) and every hour during nighttime (22:00–06:00). Recordings with ≥80% successful readings were defined as valid. Parameters included 24-hour, daytime, and nighttime mean systolic blood pressure (SBP) and diastolic blood pressure (DBP). Blood pressure variability (BPV) was assessed using standard deviation (SD), coefficient of variation (CV), and average real variability (ARV).

Assessment of Left Ventricular Mass and Vascular Function

All measurements of left ventricular mass and vascular function were performed on the same day as 24-hour ABP monitoring, after at least 15 minutes of supine rest.

Left ventricular mass index (LVMI) was measured using a GE Vivid7 ultrasound system. Left ventricular end-diastolic diameter (LVEDd), interventricular septal thickness (IVST), and left ventricular posterior wall thickness (LVPWT) were measured. Left ventricular mass (LVM) was calculated using the Devereux formula, and LVMI was computed as LVM divided by body surface area (BSA).

Cardio-ankle vascular index (CAVI) was measured using an MB3000 arteriosclerosis detector to evaluate arterial stiffness. Cuffs were placed on bilateral upper arms and ankles. Electrocardiogram electrodes, a heart sound detector, and a plethysmographic detector were attached following standard protocols. CAVI values were automatically calculated by the device.

Statistical Methods

All statistical analyses were performed using SPSS 26.0 software. A priori sample size calculation was conducted using PASS 15.0, requiring at least 260 participants based on the principle of 10 participants per variable in regression analysis. Normally distributed continuous variables were presented as mean ± standard deviation (SD) and compared using one-way ANOVA. Non-normally distributed data were expressed as median (interquartile range) and compared using the Kruskal–Wallis test. Categorical variables were presented as percentages and compared using the chi-square test. Partial correlation analysis was used to explore associations between trait anxiety, BPV, LVMI, and CAVI after adjusting for confounders. Multiple linear regression was performed to identify independent predictors of BPV, LVMI, and CAVI. A total of 15 variables were included in the multivariate regression models based on clinical relevance and univariate analysis results. A two-sided P-value < 0.05 was considered statistically significant.

Results

Baseline Characteristics of Hypertensive Patients with Different Trait Anxiety Levels

This research involved 285 people with hypertension divided into two groups depending on their trait anxiety scores (the group with low anxiety (T-AI < 39, n = 142) and high anxiety (T-AI > 49, n = 143)). Gender, age, body mass index (BMI), education level, family history of hypertension, triglycerides, low-density lipoprotein (LDL-C), blood unit count (BUN), and creatinine ratio (CR) were all similar between two groups (all P > 0.05) as shown in Table 1.

Table 1.

General Data About Hypertension Patients with Different Trait Anxiety Scores

	T-AI <39 (n = 142)	T-AI >49 (n = 143)	P value
Sex			0.861
Male	74 (52.11%)	76 (53.15%)
Female	68 (47.89%)	67 (46.85%)
Age
18–30	25.46±2.35	26.18±3.45	0.596
31–40	36.74±3.25	34.19±4.21	0.387
41–50	47.32±2.14	48.27±1.26	0.173
>50	57.68 ± 4.78	56.31 ± 3.12	0.726
BMI (kg/m2)	24.57 ± 5.28	26.31 ± 4.12	0.652
WHR	0.82 ± 0.05	0.85 ± 0.09	0.345
Educational level (college degree or above), n (%)	67 (47.18%)	72 (50.34%)	0.325
The duration of hypertension	3.69 ± 2.79	3.76 ±3.12	0.635
Family history of hypertension, n (%)	102 (71.83%)	97 (67.83%)	0.534
Current antihypertensive drugs
ACEI, n (%)	19 (13.38%)	21 (14.68%)	0.275
ARB, n (%)	56 (39.44%)	64 (44.75%)	0.568
Beta-blockers, n (%)	12 (8.45%)	7 (4.90%)	0.141
CCB, n (%)	98 (69.01%)	89 (62.24%)	0.128
Diuretic, n (%)	46 (32.39%)	47 (32.87%)	0.595
TC (mmol/L)	4.59 ± 0.63	4.68 ± 0.82	0.494
TG (mmol/L)	1.52 (0.97–1.98)	1.43 (1.15–1.97)	0.324
LDL-C (mmol/L)	2.46 ± 0.75	2.58 ± 0.51	0.259
BUN (mmol/L)	4.81 ± 1.47	4.76 ± 1.29	0.153
CR (μmol/L)	52.58 ± 10.23	51.77 ± 9.62	0.796

Abbreviations: ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; BUN, blood urea nitrogen; CR, creatinine; CCB, calcium channel blocker; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol; TG, triglyceride; WHR, waist-to-hip ratio.

Comparison of 24-Hour Ambulatory Blood Pressure in Hypertensive Patients

Compared with the low trait anxiety group, patients in the high trait anxiety group exhibited significantly higher daytime mean SBP, daytime mean DBP, 24-h mean SBP, and all 24-h BPV indices, including SBP-CV, DBP-CV, SBP-SD, DBP-SD, SBP-ARV, and DBP-ARV (all P < 0.05). No significant between-group difference was observed in nighttime mean SBP or 24-h mean DBP. Nighttime mean DBP was significantly lower in the high trait anxiety group (P < 0.001) as shown in Table 2, suggesting a distinct nocturnal BP pattern in these patients. Overall, high trait anxiety was associated with increased short-term blood pressure variability and an altered ambulatory BP profile.

Table 2.

Comparison of 24-Hour Ambulatory Blood Pressure in Hypertensive Patients

	T-AI <39 (n = 142)	T-AI >49 (n = 143)	P value
Daytime mean SBP (mmHg)	142.06 ± 11.28	152.13 ± 10.80	<0.001
Daytime mean DBP (mmHg)	85.19 ± 9.26	88.58 ± 11.23	0.003
Nighttime mean SBP (mmHg)	135.96± 12.38	137.35 ± 10.29	0.303
Nighttime mean DBP (mmHg)	82.67± 10.37	74.12 ± 6.85	<0.001
24-h mean SBP (mmHg)	136.23 ± 8.24	147.21 ± 9.72	<0.001
24-h mean DBP (mmHg)	82.47 ± 6.64	83.54 ± 9.21	0.262
24-h SBP CV (%)	11.64± 1.89	14.73 ± 2.21	<0.001
24-h DBP CV (%)	14.36 ± 2.25	15.27 ± 1.97	<0.001
24-h SBP SD	18.64 ± 2.16	23.53 ± 3.28	<0.001
24-h DBP SD	12.35 ± 1.65	12.90 ± 1.78	0.007
24-h SBP ARV	12.06 ± 4.53	18.96 ± 4.57	<0.001
24-h DBP ARV	6.29 ± 1.07	8.15 ± 1.32	<0.001

Abbreviations: ARV, average real variability; CV, coefficient of variation; DBP, diastolic blood pressure; SBP, systolic blood pressure; SD, standard deviation.

Comparison of Target Organ Damage in Hypertensive Patients

Table 3 indicates that compared to the low anxiety group, in the high anxiety group, the left CAVI, right CAVI and LVMI were significantly higher (P < 0.05). However, there was no difference between the groups concerning proteinuria.

Table 3.

Comparison of Target Organ Damage in Hypertensive Patients

	T-AI <39 (n = 142)	T-AI >49 (n = 143)	P
Proteinuria, n (%)	2 (1.41%)	3 (2.10%)	0.067
CAVI (left)	6.92 ± 0.86	9.21 ± 0.48	<0.0001
CAVI (right)	7.01 ± 0.63	9.07 ± 0.32	<0.0001
LVMI	71.34 ±5.19	96.42 ± 2.27	<0.0001

Abbreviations: CAVI, cardio-ankle vascular index; LVMI, left ventricular mass index.

Correlation Analysis Between Trait Anxiety Scores and BPV, LVMI, CAVI

We performed a partial correlation analysis after considering potential confounders such as age, body mass index (BMI), duration of hypertension, antihypertensive drug use, TC, TG, BUN and CR. Trait anxiety levels were significantly correlated with several outcome measures such as 24-hour SBP ARV (r =0.817, P < 0.001), 24-hour DBP ARV (r = 0.816, P < 0.0001), LVMI (r=0.763, P < 0.0001), left CAVI (r= 0.829, P < 0.001), and right CAVI (r= 0.891, P < 0.001).

Multivariate Regression Analysis of Trait Anxiety Score, LVMI, and CAVI in Hypertensive Patients

The correlation between the levels of anxiety in the trait and LVMI and CAVI was investigated by multiple linear regression. Subsequent models were adjusted for gender, age, BMI, duration of hypertension, family history, current medicines, serological markers and 24-hour mean SBP/DBP. Even after taking into consideration any possible confounders, the analyses indicated a robust association for LVMI to increase by 7.195 g/m2 and CAV to increase by 8.256 for every 1 increase in the score of trait anxiety (Table 4).

Table 4.

Multivariable Regression Analysis of Trait Anxiety Scores with Left Ventricular Mass Index (LVMI) and Cardio-Ankle Vascular Index (CAVI) in Hypertensive Patients

	Regression Coefficient and 95% CI	P
LVMI
Model 1	8.512 (8.263–8.761)	<0.001
Model 2	8.718 (6.668–10.768)	<0.001
Model 3	7.195 (5.034–9.356)	<0.001
CAVI
Model 1	9.642 (8.208–11.076)	<0.001
Model 2	8.179 (6.897–9.461)	<0.001
Model 3	8.256 (6.6959.817)	<0.001

Notes: Model 1: no adjustment;Model 2: adjusted for sex, age, BMI, duration of hypertension, family history of hypertension, current antihypertensive drug use, and serological indexes;Model 3: Model 2 + 24-hour mean systolic blood pressure + 24-hour mean diastolic blood pressure.

Multivariate Regression Analysis of Trait Anxiety Score with 24-Hour SBP ARV and 24-Hour DBP ARV in Hypertensive Patients

After adjustment for sex, age, BMI, duration of hypertension, family history of hypertension, current antihypertensive medication, and serological indices, trait anxiety score remained independently associated with 24-h SBP ARV (β = 0.513, B = 8.457, 95% CI: 7.101 to 9.813, P < 0.001), 24-h SBP CV (β = 0.258, B = 7.481, 95% CI: 6.200 to 8.762, P < 0.001), 24-h SBP SD (β = 0.312, B = 6.154, 95% CI: 5.031 to 7.277, P < 0.001), 24-h DBP ARV (β = 0.472, B = 6.516, 95% CI: 5.757 to 7.275, P < 0.001), 24-h DBP CV (β = 0.201, B = 9.112, 95% CI: 7.938 to 10.286, P < 0.001), and 24-h DBP SD (β = 0.245, B = 8.214, 95% CI: 6.372 to 10.056, P < 0.001) as shown in Table 5. These findings indicate that trait anxiety is an independent determinant of increased short-term blood pressure variability in hypertensive patients.

Table 5.

Multivariable Regression Analysis of Trait Anxiety Scores with 24-Hour Systolic and Diastolic Blood Pressure Average Real Variability (ARV) in Hypertensive Patients

Outcome Variable	Standardized β	Regression Coefficient (B)	95% CI for B	P value
24-h SBP ARV	0.513	8.457	7.101–9.813	<0.001
24-h SBP CV	0.258	7.481	6.200–8.762	<0.001
24-h SBP SD	0.312	6.154	5.031–7.277	<0.001
24-h DBP ARV	0.472	6.516	5.757–7.275	<0.001
24-h DBP CV	0.201	9.112	7.938–10.286	<0.001
24-h DBP SD	0.245	8.214	6.372–10.056	<0.001

Notes: Adjusted for sex,age,body mass index (BMI),duration of hypertension,family history of hypertension,current antihypertensive drug use,and serological indices.

Abbreviations: ARV, average real variability; CV, coefficient of variation; DBP, diastolic blood pressure; SBP, systolic blood pressure; SD, standard deviation.

Discussion

This study systematically investigated the association between trait anxiety, left ventricular mass index (LVMI), and cardio-ankle vascular index (CAVI) in a well-characterized population of patients with primary hypertension. Consistent with our pre-specified objectives, the findings demonstrate that individuals with high trait anxiety exhibit significantly higher LVMI and increased arterial stiffness as measured by CAVI, compared to those with low trait anxiety. These observations align closely with the primary research aims and provide novel insights into the psychophysiological pathways underlying cardiovascular remodeling in hypertension.

Pathophysiological Mechanisms Underlying the Observed Associations

The positive correlation between trait anxiety and LVMI identified in this study is biologically plausible and supported by established pathophysiological frameworks.²¹ Although causality cannot be definitively established due to the cross-sectional design, the observed associations are consistent with known pathophysiological pathways suggesting a bidirectional or potentiating relationship between chronic anxiety states and cardiovascular remodeling. Chronic trait anxiety is characterized by sustained hyperarousal and dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, leading to persistent elevation of circulating cortisol levels.Long-term exposure to high cortisol promotes sodium and water retention, increases sympathetic nervous system (SNS) tone, and induces vasoconstriction—all of which contribute to chronic pressure overload and increased afterload on the left ventricle.This sustained hemodynamic stress triggers myocardial hypertrophy, as evidenced by the increased LVMI observed in our high-trait-anxiety group. Furthermore, anxiety-related psychological stress may exacerbate systemic inflammation, characterized by elevated pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6).These cytokines directly stimulate cardiac fibroblast proliferation and extracellular matrix deposition, facilitating the development of concentric left ventricular hypertrophy.^22,23

Similarly, the observed elevation of CAVI in patients with high trait anxiety reflects impairment of arterial elastic properties. Arterial stiffness is a key predictor of cardiovascular outcomes and is driven by multiple mechanisms linked to anxiety.^24,25 First, chronic SNS activation in anxiety induces vasoconstriction and enhances vascular smooth muscle cell contraction, acutely increasing arterial wave reflection and stiffness.Second, persistent stress triggers oxidative stress, with increased production of reactive oxygen species (ROS) leading to endothelial dysfunction and vascular smooth muscle cell proliferation. Endothelial damage impairs nitric oxide (NO) bioavailability, reducing vasodilatory capacity and promoting vascular remodeling. Third, anxiety-related conditions are associated with dyslipidemia and insulin resistance, which accelerate atherosclerotic processes and degrade arterial elastic fibers.Collectively, these pathophysiological pathways provide a robust mechanistic basis for the link between trait anxiety and increased arterial stiffness in hypertension.

Alignment with Previous Research and Broader Context

The current findings are consistent with prior clinical and epidemiological studies highlighting the adverse cardiovascular effects of psychological distress in hypertension.^26–28 For example, longitudinal studies have reported that anxiety disorders are associated with a 30–50% increased risk of incident cardiovascular events in hypertensive populations.²⁹ Our results extend these observations by demonstrating that even subclinical trait anxiety, in the absence of clinical anxiety disorders, is associated with measurable changes in cardiac structure and vascular function. This suggests that anxiety-related traits may represent a modifiable risk factor that contributes to the “hidden” cardiovascular burden of hypertension.

In the broader context of translational medicine, this study reinforces the need for integrated psychocardiological approaches in the management of hypertension. Current clinical guidelines primarily focus on pharmacological and lifestyle interventions, but our findings suggest that psychological assessment and intervention should be integrated into routine clinical care. For instance, routine screening for anxiety traits in hypertensive patients, particularly those with suboptimal blood pressure control or evidence of end-organ damage, may identify high-risk individuals who would benefit from targeted psychosocial support.³⁰

Conclusion

This cross-sectional study demonstrates that trait anxiety is independently and significantly associated with increased 24-hour blood pressure variability (BPV), elevated left ventricular mass index (LVMI), and higher cardio-ankle vascular index (CAVI) in patients with primary hypertension. These findings are consistent with our study objectives and confirm that trait anxiety serves as a potentially modifiable psychological risk factor for cardiovascular remodeling beyond mean blood pressure levels. Pathophysiologically, the observed associations are supported by sympathetic overactivation, HPA axis dysregulation, chronic inflammation, oxidative stress, and endothelial dysfunction, which collectively promote hemodynamic instability and target organ damage. Despite these novel insights, several knowledge gaps and limitations should be acknowledged. First, the cross-sectional design precludes definitive causal inference; prospective longitudinal studies with repeated measurements are needed to clarify temporal relationships. Second, the single-center recruitment may limit generalizability, and multicenter research involving diverse ethnic and demographic groups is warranted. Third, mediating factors such as sleep quality, medication adherence, and dietary patterns were not evaluated, representing important avenues for further investigation. Based on the present results, we recommend routine screening for trait anxiety using validated scales in hypertensive patients, especially those with suboptimal BP control or early target organ damage. Integrated management strategies combining antihypertensive treatment with psychological interventions (eg., cognitive-behavioral therapy, stress reduction) may improve BPV control and attenuate cardiovascular remodeling. Future research should focus on large-scale prospective cohorts and randomized controlled trials to verify the causal link and evaluate the clinical efficacy of anxiety-targeted interventions. In summary, trait anxiety is a clinically relevant determinant of BPV and subclinical target organ damage in hypertension. Routine psychological assessment and targeted intervention may facilitate more personalized and effective cardiovascular risk reduction.

Funding Statement

This research did not receive any specific grant from the public, commercial, or not-for-profit funding agencies.

Data Sharing Statement

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Ethics Clearance

This study strictly adhered to the Helsinki Declaration. This research project has been approved by Ethics Committee of Beijing Friendship Hospital, Capital Medical University (Tongzhou Branch) (Ethical number: 2025-P2-459-01) and operated in strict accordance with ethical standards. In this study, we respect and protect the rights and privacy of participants and ensure the confidentiality of their personal information.

1. Participants’ informed consent: We explained the purpose, process, risks and benefits of the study to all individuals involved in the study orally or in writing, and obtained their informed consent. Participants have the right to know that their participation is voluntary and can withdraw from the study at any time.

2. Data confidentiality and privacy protection: We have taken appropriate measures to protect the privacy of participants’ personal information. We will not disclose or disclose any personal information that may lead to the identification of participants. In the research report, we will treat the participants’ information anonymously.

3. Assessment and management of potential risks: We assessed the potential risks that may be involved in the study during the project design stage and took appropriate measures to reduce or manage these risks. We guarantee that participants will not suffer any physical or psychological harm because of participating in the study.

4. Research data use: We will strictly abide by the principles of legality and transparency in data use to ensure the correct use and interpretation of research data. We will try our best to avoid data misunderstanding and abuse, and only use the data for research purposes.

The purpose of this statement is to ensure the ethical compliance of research projects and protect the rights and privacy of participants. If you have any further questions or doubts, please feel free to contact us.

Informed Consent Statement

All the selected patients were informed and agreed to the study and provided an informed consent to participate.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that there is no competing interest associated with the manuscript. In relation to this research, the authors have no competing interests. Scientific impartiality and freedom from commercial or other influences were ensured in the course of data collection, data analysis, interpretation, and paper production. The study followed all appropriate ethical standards and the confidentiality and rights of the study subjects was carefully guarded.