Intercellular adhesion molecule-1 (ICAM-1) associates with 24-hour ambulatory blood pressure variability in type 2

Dana M Ciobanu1, Petru A Mircea2, Cornelia Bala1

  • 1Iuliu Hatieganu University of Medicine and Pharmacy, Faculty of Medicine, Department of Diabetes and Nutrition, Cluj-Napoca, Romania.

Cytokine
|February 5, 2019
PubMed

Insights

Blood pressure variability is linked to higher levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in type 2 diabetes patients. This suggests variability may drive endothelial dysfunction through these adhesion molecules.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Hypertension Research

Background:

  • Endothelial dysfunction is prevalent in hypertension and type 2 diabetes.
  • The role of blood pressure (BP) variability in influencing adhesion molecules like ICAM-1 and VCAM-1 is not fully understood.
  • Understanding these associations may clarify mechanisms of endothelial dysfunction.

Purpose of the Study:

  • To assess the association between circulating adhesion molecules (ICAM-1, VCAM-1) and ambulatory BP variability.
  • To investigate these links in patients with type 2 diabetes and control subjects.

Main Methods:

  • Included 55 type 2 diabetes patients with controlled BP, 55 with uncontrolled BP, and 28 controls.
  • Measured serum ICAM-1 and VCAM-1 using enzyme-linked immunosorbent assay.
  • Assessed BP variability via standard deviation of 24-hour ambulatory BP monitoring.

Main Results:

  • Uncontrolled BP group showed significantly higher ICAM-1 and VCAM-1 levels.
  • Higher ICAM-1 associated with increased daytime/24-hour diastolic BP variability and daytime systolic BP variability.
  • VCAM-1 associated with daytime systolic BP variability.

Conclusions:

  • Elevated 24-hour ambulatory BP variability may promote endothelial activation.
  • Increased circulating adhesion molecules (ICAM-1, VCAM-1) are linked to BP variability in type 2 diabetes.
  • Findings may enhance understanding of endothelial dysfunction mechanisms.
Abstract

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