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Published on: September 22, 2020

In concomitant coronary and peripheral arterial disease, inflammation of the affected limbs predicts coronary artery

Gregorio Brevetti1, Federico Piscione, Plinio Cirillo

  • 1Department of Clinical Medicine and Cardiovascular and Immunological Sciences, University of Naples Federico II, Naples, Italy. brevetti@unina.it

Atherosclerosis
|March 25, 2008
PubMed

Insights

Peripheral arterial disease (PAD) inflammation in affected limbs may worsen coronary artery disease (CAD) by impairing coronary artery endothelial function (CAEF). This suggests PAD mechanistically contributes to CAD progression.

Area of Science:

  • Cardiovascular Medicine
  • Vascular Biology
  • Inflammation Research

Background:

  • Concomitant peripheral arterial disease (PAD) in coronary artery disease (CAD) patients indicates more severe coronary atherosclerosis.
  • The inflammatory status of affected limbs in PAD may impair coronary artery endothelial function (CAEF).

Purpose of the Study:

  • To investigate if inflammation in affected limbs of PAD patients impacts CAEF.
  • To determine if blood from PAD-affected limbs activates human coronary artery endothelial cells (HCAECs).

Main Methods:

  • Measured neutrophil myeloperoxidase content (NMPOxC) and plasma interleukin-6/C-reactive protein in aorta, femoral vein, and coronary sinus of CAD+PAD and CAD-alone patients.
  • Assessed CAEF using the cold pressure test and incubated HCAECs with patient serum.
  • Analyzed transfemoral gradients of inflammatory markers and their correlation with CAEF.

Main Results:

  • CAD+PAD patients showed higher NMPOxC and interleukin-6 across the femoral circulation compared to coronary circulation and healthy controls.
  • Transfemoral gradients of NMPOxC and interleukin-6 correlated significantly with CAEF, especially post-exercise.
  • Serum from PAD-affected limbs induced MCP-1 release from HCAECs in vitro.

Conclusions:

  • Inflammatory triggers from PAD-affected circulation may activate endothelium at distant sites, impacting CAEF.
  • PAD may play a mechanistic role in CAD progression, beyond being a cardiovascular risk marker.
Abstract

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