Age, rather than hypertension duration, drives coronary endothelial degradation: an in situ post-mortem analysis

Arterial hypertension drives coronary vascular remodeling, yet disentangling the independent effects of physiological aging and chronic hemodynamic overload on the endothelium (CD31) and glycocalyx (CD138) in situ remains challenging. Most clinical studies evaluate soluble circulating markers, while direct morphological evidence of tissue-level spatial degradation is scarce.

This observational post-mortem study evaluated coronary artery fragments from 30 deceased patients (10 controls, 20 with essential hypertension) using immunohistochemistry and digital pathology. To mitigate confounding bias caused by age discrepancies and acute pre-mortem systemic stressors in the control group (e.g., fatal trauma), multivariable linear regression modeling with robust standard errors was applied exclusively to the hypertensive cohort to isolate the independent impacts of chronological age and hypertension duration.

Within the hypertensive cohort, chronological age emerged as a significant independent factor inversely associated with CD31 expression area (β = -0.74, 95% CI: -0.98 to -0.50, p = 0.016). The duration of hypertension was not independently associated with CD31 loss (p = 0.076). Furthermore, the multivariable model for CD138 did not reach overall statistical significance (for age: β = -0.17, 95% CI: -0.42 to 0.07, p = 0.200; for hypertension duration: β = 0.21, 95% CI: -0.06 to 0.48, p = 0.130). However, a robust positive correlation was observed between CD31 and CD138 tissue expression levels (R = 0.50, p = 0.025), indicating synchronized structural degradation.

Chronological age, rather than the chronicity of hypertension, is significantly associated with reduced CD31 expression in the coronary arteries of hypertensive patients. The positive correlation between CD31 and CD138 expression highlights a synchronized spatial degradation of the endothelium and its protective glycocalyx. These findings highlight the critical necessity of isolating physiological senescence from pathological remodeling in vascular research.