Nearly one-third of all deaths globally are caused by cardiovascular disease (CVD), which continues to be the major cause of death[1]. Peripheral vascular disease, cerebrovascular disease, and coronary artery disease are all primarily caused by atherosclerosis. Endothelial dysfunction and lipid buildup in the artery wall are the first signs of the disease, which develops gradually over several decades before showing symptoms.

Traditionally, cardiovascular risk has been assessed using conventional lipid markers such total cholesterol, triglycerides, LDL cholesterol, and HDL cholesterol[2]. However, a significant percentage of cardiovascular events happen in people whose lipid profiles appear to be normal, indicating the need for more sensitive biomarkers[3].

The overall amount of atherogenic lipoprotein particles, such as LDL, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and lipoprotein (a), is represented by apolipoprotein B. On the other hand, HDL particles' main protein component, ApoA-I, exhibits anti-atherogenic properties. Thus, the ratio of ApoB to ApoA-I offers a comprehensive assessment of the equilibrium between protective and atherogenic lipoproteins[4].

An LDL-like core connected to apolipoprotein (a) makes up the genetically defined lipoprotein particle known as lipoprotein (a). Through pro-inflammatory, pro-thrombotic, and pro-atherogenic pathways, elevated Lp(a) levels have been linked to atherosclerosis. Beyond conventional lipid characteristics, recent research indicates that Lp(a) may independently contribute to cardiovascular risk[5-6].

Future cardiovascular events are predicted by carotid intima-media thickness, a validated surrogate marker of subclinical atherosclerosis. CIMT measurement enables the early identification of vascular alterations prior to the onset of clinical symptoms[7-8].

In this study, 400 adult patients' ApoB/ApoA-I ratio, Lp(a) levels, and early atherogenic alterations measured by CIMT were examined.

This hospital-based cross-sectional study was conducted in the Department of Biochemistry & Pathology of Mansarovar Medical College & MGU Hospital, Gadia, Sehore, M.P. A total of 400 adult patients aged 30–70 years attending outpatient and preventive health clinics were enrolled. Inclusion Criteria: 1. Adults aged 30–70 years. 2. Individuals willing to provide informed consent. 3. Patients undergoing routine cardiovascular risk assessment. Exclusion Criteria 1. Known coronary artery disease. 2. Previous stroke. 3. Chronic kidney disease. 4. Active inflammatory disorders. 5. Malignancy. 6. Pregnancy. 7. Lipid-lowering therapy initiated within the previous six months. Sample Size: The sample size of 400 was calculated assuming a prevalence of subclinical atherosclerosis of 40%, confidence level of 95%, and margin of error of 5%. Data Collection: Demographic and clinical data were collected using a structured questionnaire. Anthropometric Measurements Height (cm) Weight (kg) Body Mass Index (BMI) Blood pressure Laboratory Investigations After overnight fasting: Total cholesterol LDL cholesterol HDL cholesterol Triglycerides ApoB ApoA-I Lipoprotein(a) ApoB/ApoA-I ratio was calculated. Assessment of Early Atherogenic Changes CIMT was measured using high-resolution B-mode ultrasonography. Increased CIMT was defined as >0.8 mm. Statistical Analysis Data were analyzed using SPSS version 26.0. Continuous variables: Mean ± SD Categorical variables: Frequency and percentage Chi-square test Logistic regression analysis A p-value <0.05 was considered statistically significant.

Table 1: Baseline Characteristics of Study Participants (n=400)

Patients with increased CIMT were significantly older and had higher BMI, systolic blood pressure, and prevalence of diabetes and hypertension compared to those with normal CIMT. These findings indicate that traditional cardiovascular risk factors are strongly associated with early atherogenic change.

Table 2: Lipid Profile and Apolipoprotein Parameters

Subjects with increased CIMT exhibited significantly higher levels of total cholesterol, LDL-C, triglycerides, ApoB, ApoB/ApoA-I ratio, and Lp(a), along with lower HDL-C levels. This suggests that both conventional and novel lipid biomarkers are associated with subclinical atherosclerosis.

Table 3: Distribution of Increased CIMT According to ApoB/ApoA-I Ratio and Lp(a)

A significantly greater proportion of patients with ApoB/ApoA-I ratio ≥0.8 and Lp(a) ≥30 mg/dL had increased CIMT compared to those with lower values (p<0.001). These results demonstrate a strong relationship between elevated ApoB/ApoA-I ratio, Lp(a), and early atherogenic vascular changes.

Table 4: Multivariate Logistic Regression for Predictors of Increased CIMT

Multivariate logistic regression showed that ApoB/ApoA-I ratio and elevated Lp(a) remained significant independent predictors of increased CIMT after adjustment for traditional risk factors. This highlights their potential utility in identifying individuals at high risk for early atherosclerosis.

In a cohort of 400 adults, the current study assessed the function of Lp(a) levels and the ApoB/ApoA-I ratio as predictors of early atherogenic alterations. The results support the usefulness of these biomarkers in cardiovascular risk assessment by showing a substantial correlation between them and elevated CIMT[9]. ApoB concentrations and ApoB/ApoA-I ratios were considerably higher in participants with higher CIMT. ApoB is not just a measure of cholesterol level, but also of the quantity of circulating atherogenic particles[10]. This feature could account for its better predictive power when compared to traditional lipid measurements. Information from both pro-atherogenic and anti-atherogenic pathways is integrated by the ApoB/ApoA-I ratio. An imbalance favoring lipid deposition and plaque development is shown by elevated ratios[11]. In our investigation, the prevalence of elevated CIMT was considerably higher in those with ratios ≥0.8. Participants with higher CIMT also had significantly higher Lp(a) levels. Endothelial dysfunction and thrombosis may be caused by apolipoprotein (a)'s structural resemblance to plasminogen[12]. Ischemic stroke, calcific aortic valve disease, and coronary artery disease have all been linked to elevated Lp(a). Even after controlling for conventional risk variables, our multivariate analysis showed that the ApoB/ApoA-I ratio and Lp(a) remained independent predictors. These results corroborate earlier research showing that new lipid indicators offer further risk prediction beyond LDL cholesterol[13-15]. The findings are consistent with significant epidemiological studies that found the ApoB/ApoA-I ratio to be a strong predictor of myocardial infarction and cardiovascular events. In a similar vein, high Lp(a) has become a significant genetic risk factor for cardiovascular disease[16]. The clinical implications are significant. Traditional lipid profiles may underestimate risk in certain individuals. Measurement of ApoB, ApoA-I, and Lp(a) could improve early identification of patients requiring intensive preventive interventions. Objective CIMT assessment. Comprehensive lipid evaluation. Multivariate adjustment. Limitations Lack of long-term follow-up. Potential residual confounding. Future prospective studies are needed to establish causality and evaluate whether targeted reduction of ApoB/ApoA-I ratio and Lp(a) can reduce progression of atherosclerosis.

The present study demonstrates that elevated ApoB/ApoA-I ratio and increased lipoprotein(a) levels are strongly associated with early atherogenic vascular changes measured by CIMT. Both biomarkers independently predicted subclinical atherosclerosis after adjustment for conventional cardiovascular risk factors. Incorporation of ApoB/ApoA-I ratio and Lp(a) into routine cardiovascular risk stratification may facilitate earlier detection and intervention in high-risk individuals.

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