Hypertension remains one of the leading global public health challenges, significantly contributing to cardiovascular morbidity and mortality worldwide (1). The etiology of hypertension is multifactorial, with increasing evidence highlighting obesity—particularly central or visceral obesity—as a critical modifiable risk factor (2). Unlike generalized obesity measured by body mass index (BMI), visceral fat accumulation is more metabolically active and contributes to adverse cardiometabolic outcomes through mechanisms such as insulin resistance, systemic inflammation, and endothelial dysfunction (3,4).

The Visceral Adiposity Index (VAI) is a mathematical model that integrates waist circumference, BMI, triglycerides, and high-density lipoprotein cholesterol (HDL-C) to estimate visceral fat dysfunction (5). VAI offers a more precise representation of visceral adiposity and its metabolic consequences compared to traditional anthropometric parameters alone (6). Several studies have shown that higher VAI levels are associated with an increased risk of metabolic syndrome, type 2 diabetes mellitus, and cardiovascular events (7,8).

Despite the well-documented association between obesity and hypertension, the specific relationship between VAI and blood pressure components—systolic blood pressure (SBP) and diastolic blood pressure (DBP)—remains inadequately explored in diverse populations. Understanding this association could provide deeper insights into the pathophysiological mechanisms linking visceral adiposity and elevated blood pressure and may help refine risk stratification strategies in clinical practice.

A total of 200 adult participants, aged between 25 and 60 years, were recruited using convenience sampling. Individuals with known cases of secondary hypertension, thyroid disorders, chronic kidney disease, liver disease, or those on antihypertensive or lipid-lowering medications were excluded from the study to avoid confounding effects.

Anthropometric Measurements

Body weight and height were measured using a calibrated digital scale and stadiometer, respectively, with subjects wearing light clothing and no footwear. Body mass index (BMI) was calculated as weight in kilograms divided by height in meters squared (kg/m²). Waist circumference was measured at the midpoint between the lower margin of the last palpable rib and the top of the iliac crest, using a flexible measuring tape.

Biochemical Assessment
Fasting blood samples were collected after an overnight fast of 8–12 hours. Serum triglycerides and high-density lipoprotein cholesterol (HDL-C) levels were measured using an automated biochemical analyzer based on enzymatic colorimetric methods.

Blood Pressure Measurement
Systolic and diastolic blood pressure readings were taken in the sitting position after a 10-minute rest, using a standard mercury sphygmomanometer. Two readings were recorded at 5-minute intervals, and the average of the two was used for analysis.

Visceral Adiposity Index Calculation
VAI was calculated using the following sex-specific formulas developed by Amato et al.:

• For males:
  VAI = [WC / (39.68 + (1.88 × BMI))] × (TG / 1.03) × (1.31 / HDL-C)
• For females:
  VAI = [WC / (36.58 + (1.89 × BMI))] × (TG / 0.81) × (1.52 / HDL-C)

Where WC is waist circumference in cm, TG is triglycerides in mmol/L, and HDL-C is HDL cholesterol in mmol/L.

Statistical Analysis
Data were entered and analyzed using SPSS version 25.0 (IBM Corp., Armonk, NY). Continuous variables were expressed as mean ± standard deviation, and categorical variables as frequencies and percentages. Pearson correlation coefficients were calculated to assess the relationship between VAI and both systolic and diastolic blood pressure. Multivariate linear regression analysis was performed to adjust for potential confounders such as age, gender, smoking status, and physical activity level. A p-value of <0.05 was considered statistically significant.

A total of 200 participants were included in the final analysis, comprising 102 males (51%) and 98 females (49%). The mean age of the study population was 42.3 ± 9.6 years. Table 1 summarizes the baseline characteristics of the study population.

Table 1: Baseline Characteristics of the Study Population (n = 200)

A significant positive correlation was observed between VAI and both systolic and diastolic blood pressure. Pearson correlation analysis revealed a correlation coefficient of r = 0.48 (p < 0.001) between VAI and systolic BP, and r = 0.39 (p < 0.001) for diastolic BP.

Participants were divided into VAI quartiles to further analyze the relationship with blood pressure (Table 2). A progressive increase in both systolic and diastolic blood pressure was observed with increasing VAI quartiles.

Table 2: Mean Blood Pressure Values According to VAI Quartiles

Multivariate linear regression analysis (Table 3) demonstrated that VAI remained an independent predictor of both systolic and diastolic blood pressure after adjusting for age, gender, smoking status, and BMI. For every unit increase in VAI, systolic BP increased by 3.7 mmHg (p = 0.002) and diastolic BP by 2.4 mmHg (p = 0.004).

Table 3: Multivariate Linear Regression Analysis of VAI and Blood Pressure

As illustrated in Table 2 and Table 3, VAI shows a consistent and significant association with both SBP and DBP, independent of other confounders. This suggests that VAI may serve as a more precise marker than BMI alone in identifying individuals at risk of developing hypertension.

The present study demonstrates a significant and independent association between the Visceral Adiposity Index (VAI) and both systolic and diastolic blood pressure among adults. These findings support the growing body of evidence that visceral adiposity, as captured by VAI, plays a pivotal role in the pathogenesis of hypertension beyond the influence of general obesity indices such as BMI (1,2).

Our results revealed a positive linear relationship between VAI and blood pressure values, even after adjusting for confounding variables like age, sex, BMI, smoking, and physical activity. This aligns with the findings of Amato et al., who originally proposed VAI as a reliable indicator of visceral fat function and its cardiometabolic implications (3). Several studies have similarly validated the predictive value of VAI in identifying individuals at risk of hypertension and metabolic syndrome (4–6).

The underlying mechanisms linking visceral adiposity to elevated blood pressure are multifactorial. Visceral fat secretes various bioactive substances including adipokines, inflammatory cytokines, and components of the renin-angiotensin-aldosterone system (RAAS), all of which contribute to vascular resistance and endothelial dysfunction (7,8). Additionally, increased insulin resistance associated with visceral obesity may lead to sympathetic nervous system overactivity, sodium retention, and impaired natriuresis, further elevating blood pressure (9,10).

In our study, participants in the highest VAI quartile exhibited significantly higher mean systolic and diastolic blood pressure compared to those in the lowest quartile. Similar patterns have been documented in studies by Motamed et al. and Taverna et al., suggesting that VAI quartiles could be utilized in clinical risk stratification models for hypertension (11,12). Unlike BMI, which fails to differentiate between muscle and fat mass, VAI offers a composite index that reflects both adipose tissue quantity and function, giving it superior clinical relevance in cardiometabolic evaluations (13).

Another critical observation was the persistence of VAI as an independent predictor in multivariate regression, suggesting that the metabolic activity of visceral fat plays a stronger role in blood pressure regulation than total body weight alone. This supports the findings by Kaess et al., who reported that the ratio of visceral to subcutaneous fat was more strongly correlated with cardiometabolic risk factors than BMI or waist circumference alone (14).

Furthermore, gender-specific differences in visceral fat distribution and hormonal influences may also impact VAI and its relation to blood pressure. For example, women with central obesity are often found to have a higher cardiometabolic risk post-menopause due to estrogen decline and increased visceral fat deposition (15).

This study highlights a significant and independent association between the Visceral Adiposity Index (VAI) and both systolic and diastolic blood pressure. VAI may serve as a valuable, non-invasive marker for identifying individuals at increased risk of hypertension due to visceral fat accumulation. Integrating VAI into routine clinical assessments could enhance early detection and prevention strategies for cardiometabolic diseases.

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