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Plasma heparin cofactor II activity is inversely associated with left atrial volume and diastolic dysfunction in

Takayuki Ise1, Ken-Ichi Aihara, Yuka Sumitomo-Ueda

  • 1Department of Medicine and Bioregulatory Sciences, The University of Tokushima Graduate School of Health Biosciences, 3-18-15 Kuramoto-cho, Tokushima, Japan.

Hypertension Research : Official Journal of the Japanese Society of Hypertension
|November 26, 2010
PubMed

Insights

Heparin cofactor II (HCII) activity inversely correlates with cardiac remodeling markers. Higher HCII levels are linked to reduced left atrial volume, wall thickness, and diastolic dysfunction, suggesting HCII as a therapeutic target.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Thrombin plays a key role in cardiac remodeling via protease-activated receptor-1.
  • Heparin cofactor II (HCII) inhibits thrombin in the cardiovascular system.
  • HCII may counteract cardiac remodeling processes.

Purpose of the Study:

  • To investigate the relationship between plasma HCII activity and cardiac geometry and diastolic function markers.
  • To assess HCII's potential role in mitigating cardiac remodeling.

Main Methods:

  • Echocardiography was used to measure cardiac geometry (LAVI, RWT, LVMI) and diastolic function (DcT, E/e' ratio).
  • Plasma HCII activity was measured in 304 elderly Japanese individuals without systolic heart failure.
  • Multiple regression analysis was employed to determine associations.

Main Results:

  • Plasma HCII activity showed significant inverse relationships with left atrial volume index (LAVI), relative wall thickness (RWT), deceleration time (DcT), and E/e' ratio.
  • No significant difference in mean plasma HCII activity was observed between males and females.
  • Plasma HCII activity was independently and inversely associated with cardiac remodeling, left atrial enlargement, and diastolic dysfunction.

Conclusions:

  • Plasma HCII activity is inversely associated with cardiac remodeling, including concentric changes, left atrial enlargement, and diastolic dysfunction.
  • These findings suggest that HCII's inactivation of cardiac tissue thrombin is a potential therapeutic target.
  • HCII may represent a novel therapeutic strategy for managing cardiac remodeling and atherosclerosis.

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