Hemoglobin, iron metabolism and angiographic coronary artery disease (The Ludwigshafen Risk and Cardiovascular Health

Tanja B Grammer1, Marcus E Kleber2, Günther Silbernagel3

  • 1Mannheim Institute of Public Health, Social and Preventive Medicine, Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany; Medical Clinic V (Nephrology, Hypertensiology, Endocrinology, Diabetolgy, and Rheumatology), Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany.

Atherosclerosis
|August 13, 2014
PubMed

Insights

Low hemoglobin and iron depletion are independently linked to coronary artery disease (CAD). This study clarifies their distinct roles in CAD development, offering insights into risk factors.

Area of Science:

  • Cardiology
  • Hematology
  • Biochemistry

Background:

  • Anemia is a known risk factor for coronary artery disease (CAD) and mortality.
  • The role of body iron stores in CAD development is debated.
  • Previous studies lacked simultaneous examination of hemoglobin and iron metabolism parameters.

Purpose of the Study:

  • To investigate the independent associations of hemoglobin levels and iron status with angiographically confirmed coronary artery disease (CAD).

Main Methods:

  • Cross-sectional study involving 1480 patients with stable CAD and 682 controls.
  • Assessed hemoglobin, iron status (ferritin, transferrin saturation), and sTfR/log10F index.
  • Used multivariate logistic regression to calculate odds ratios (OR) for CAD across quartiles of these markers.

Main Results:

  • Low hemoglobin and iron depletion were associated with increased odds of CAD.
  • Multivariate adjusted ORs for lowest vs. highest quartiles: Hemoglobin 1.62, Iron 2.05, Transferrin Saturation 1.69, Ferritin 1.98, sTfR/log10F 1.64.
  • Associations remained significant even after adjusting for each other, indicating independence.

Conclusions:

  • Both low hemoglobin and iron depletion are independently associated with angiographically defined CAD.
  • These findings highlight distinct pathophysiological pathways contributing to CAD risk.
Abstract

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