Enhanced plasma soluble CD40 ligand levels in essential hypertensive patients with blunted nocturnal blood pressure

Giovambattista Desideri1, Francesco Cipollone, Letizia Valeri

  • 1Department of Internal Medicine and Public Health, University of L'Aquila, Piazzale Salvatore Tommasi 1, 67100 Coppito, L'Aquila, Italy. giovambattista.desideri@cc.univaq.it

Insights

Essential hypertensives with blunted nocturnal blood pressure decrease have higher soluble CD40 ligand (sCD40L) levels. Elevated sCD40L is linked to increased carotid intima-media thickness, suggesting a role in vascular damage.

Area of Science:

  • Cardiovascular Medicine
  • Vascular Biology
  • Hypertension Research

Background:

  • Hypertension is associated with an increased risk of atherosclerotic disease, particularly in individuals with a blunted nocturnal blood pressure decrease.
  • Soluble CD40 ligand (sCD40L) plays a role in vascular damage related to cardiovascular risk factors.

Purpose of the Study:

  • To investigate the relationship between circulating sCD40L levels, circadian blood pressure patterns, and early carotid atherosclerosis in patients with essential hypertension.

Main Methods:

  • Plasma sCD40L concentrations and carotid intima-media thickness (IMT) were measured in never-treated hypertensive patients (dippers and nondippers) and matched normotensive controls.
  • Hypertensive participants were categorized based on their nocturnal blood pressure decrease (>10% for dippers, <10% for nondippers).

Main Results:

  • Nondippers exhibited significantly higher plasma sCD40L levels compared to dippers and normotensive controls.
  • Carotid IMT was elevated in both hypertensive groups versus controls.
  • sCD40L levels directly correlated with IMT and inversely with nocturnal systolic blood pressure decrease in hypertensive patients.

Conclusions:

  • Nondippers demonstrate elevated plasma sCD40L, potentially contributing to their heightened susceptibility to vascular damage.
  • sCD40L is identified as a key determinant of early carotid atherosclerosis in essential hypertension.
Abstract

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