Related Experiment Video
Updated: Dec 4, 2025

Author Spotlight: Assessing the Cardiovascular Profile of Patients with Metabolic Syndrome
Published on: September 27, 2024
Correlation of Pre-Hypertension with Carotid Artery Damage in Middle-Aged and Older Adults
Jinkee Park1, Yongseong Na2, Yunjung Jang2
1Department of Sport Rehabilitation, Dong-Ju College, Busan 49318, Korea.
Insights
Pre-hypertension (PHT) is linked to increased carotid artery damage (CAD). This study found significant differences in carotid artery characteristics in adults with PHT compared to normotensive individuals, indicating a strong correlation.
Area of Science:
- Vascular Biology
- Cardiovascular Medicine
- Hypertension Research
Background:
- Carotid artery (CA) characteristics such as intima-media thickness (IMT), luminal diameters (LDs), and flow velocities (FVs) are established risk factors for cardiovascular diseases (CVDs).
- Pre-hypertension (PHT) is also recognized as an independent risk factor for CVDs.
- The relationship between PHT and CA damage (CAD) requires further investigation.
Purpose of the Study:
- To investigate the association between carotid artery damage (CAD) and pre-hypertension (PHT) in adults.
- To compare carotid artery characteristics between individuals with PHT and normotensive individuals.
Main Methods:
- A study involving 544 adults measuring blood pressures (BPs) and carotid artery (CA) characteristics using ultrasound.
- Analysis of covariance (ANCOVA) to compare CA characteristics between BP groups.
- Multinomial logistic regression to assess the risk of CAD associated with PHT.
Main Results:
- Significant differences in CA characteristics were observed between PHT and normotensive groups.
- Individuals with PHT showed significantly higher odds ratios for various CA parameters, including IMTmax, LDmax, LDmin, peak-systolic FV (PFV), end-diastolic FV (EFV), PFV/LDmin, EFV/LDmax, compliance, and β-stiffness compared to normotensive individuals (Model 2).
- After adjusting for age (Model 3), PHT remained associated with increased odds of altered LDmax, LDmin, EFV, PFV/LDmin, and EFV/LDmax.
Conclusions:
- Carotid artery damage (CAD) is closely correlated with pre-hypertensive status in adults.
- PHT is associated with detrimental changes in carotid artery structure and function.
- These findings highlight the importance of monitoring CA health in individuals with PHT to mitigate cardiovascular disease risk.
Abstract:
The intima-media thickness (IMT), luminal diameters (LDs), flow velocities (FVs), compliance, and β-stiffness of the carotid artery (CA) are considered as independent risk factors for cardiovascular diseases (CVDs). Pre-hypertension (PHT) is also an independent CVD risk factor. This study investigated the association between CA damage (CAD) and PHT. A total of 544 adults participated; their blood pressures (BPs) and CA characteristics were measured using a mercury-free sphygmomanometer and ultrasound. Analysis of covariance (ANCOVA) was performed to assess the differences in the CA characteristics according to the BPs, multinomial logistic regression to evaluate the risk of CAD associated with PHT. In ANCOVA, the CA characteristics of PHT were significantly different from normotensive. The odds ratios (ORs) of IMTmax, LDmax, LDmin, peak-systolic FV (PFV), end-diastolic FV (EFV), PFV/LDmin, EFV/LDmax, compliance, and β-stiffness of PHT were 4.20, 2.70, 3.52, 2.41, 3.06, 3.55, 3.29, 2.02, and 1.84 times higher than those of the normotensive, respectively, in Model 2. In Model 3 adjusted for age, the ORs of LDmax, LDmin, EFV, PFV/LDmin, and EFV/LDmax of PHT were 2.10, 2.55, 1.96, 2.20, and 2.04 times higher than those of the normotensive, respectively. Therefore, the present study revealed that CAD is closely correlated with pre-hypertensive status in adults.
Related Concept Videos
Hypertension III: Clinical Manifestations and Diagnostic Studies
Coronary Artery Disease I: Introduction
Hypertension II: Pathophysiology
Hypertension I: Introduction
Hypertension and Regulation of Blood Pressure
Coronary Artery Disease II: Pathophysiology

