Association of carotid body size with left atrial strain and peripheral hemodynamics in patients with hypertension:...

The carotid body (CB) is a key regulator of sympathetic tone, and its overactivity is implicated in the pathogenesis of neurogenic hypertension. While structural enlargement of the CB may reflect chronic autonomic dysregulation, its association with early markers of hypertension-mediated organ damage (HMOD) remains insufficiently characterized.

This exploratory study investigated whether carotid body size is associated with subclinical cardiac remodeling and peripheral vascular resistance in hypertensive patients.

We analyzed 49 patients with hypertension who underwent carotid computed tomography angiography (CTA) and comprehensive cardiovascular phenotyping. CB diameter was measured via CTA, and patients were categorized into Group 1 (CB < 2.5 mm, n = 22) and Group 2 (CB ≥ 2.5 mm, n = 27). Cardiac mechanics were assessed using two-dimensional speckle-tracking echocardiography (2DSTE), and hemodynamic parameters were evaluated via oscillometric pulse wave analysis.

Despite similar peripheral systolic and central blood pressure levels, Group 2 demonstrated significantly impaired left atrial (LA) mechanics and higher vascular resistance. Specifically, Group 2 had lower LA global peak atrial longitudinal strain (PALS) (23.88 ± 7.70% vs. 30.84 ± 11.40%, p = 0.014) and higher total vascular resistance (TVR) (1.56 ± 0.49 vs. 1.22 ± 0.18 s⋅mmHg/mL, p < 0.001) compared to Group 1. Augmentation index normalized to 75 bpm (AIx@75) was also elevated in the CB enlargement group (31.11 ± 7.91% vs. 24.36 ± 11.77%, p = 0.021). In multivariate linear regression analysis, LA diameter, TVR, and urinary microalbumin-to-creatinine ratio were independent determinants of CB size (Adjusted R² = 0.429, p = 0.022).

Carotid body enlargement is associated with impaired left atrial strain parameters and increased peripheral vascular load in patients with hypertension. These findings suggest that CB morphology may serve as a potential marker for early subclinical cardiovascular and renal alterations, reflecting a distinct neurovascular phenotype in hypertension.