Abstract

Research scientists and physicians alike describe many different forms of inflammatory vascular disease, reporting each separate pathological entity in terms of individual causes, symptoms, signs, and physical findings Atherosclerotic plaque, recurrent plaque growth after angioplasty and stent implant, transplant rejection, arthritic disorders, and the inflammatory vasculitic syndromes such as giant cell arteritis or Takayasu’s disease, are all associated with increased inflammatory cell activation and severe arterial disease. Viewing these vasculitic disorders autonomously, as separate entities, leads to a risk of misdiagnosis, longer treatment, increased mortality, and in short limits treatment options. This has significant implications for morbidity and mortality. The very classifications on which we rely prevent us from seeing that inflammatory arterial disorders actually represent a continuum. We propose here that these separate classifications of vascular disease are artificial, that these vascular diseases represent a continuum of inflammatory arterial disorders, rather than separate pathological entities. We postulate that the underlying central cause for a wide spectrum of occlusive arterial diseases is an up-regulation of innate immune responses that drive ongoing arterial damage.

Highlights

  • Research scientists and physicians alike describe many different forms of inflammatory vascular disease, reporting each separate pathological entity in terms of individual causes, symptoms, signs, and physical findings Atherosclerotic plaque, recurrent plaque growth after angioplasty and stent implant, transplant rejection, arthritic disorders, and the inflammatory vasculitic syndromes such as giant cell arteritis or Takayasu’s disease, are all associated with increased inflammatory cell activation and severe arterial disease

  • We postulate that the underlying central cause for a wide spectrum of occlusive arterial diseases is an up-regulation of innate immune responses that drive ongoing arterial damage

  • Davies et al reported that acute inflammatory cell invasion into the surface of atherosclerotic plaques leads to plaque rupture

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Summary

Introduction

Research scientists and physicians alike describe many different forms of inflammatory vascular disease, reporting each separate pathological entity in terms of individual causes, symptoms, signs, and physical findings Atherosclerotic plaque, recurrent plaque growth after angioplasty and stent implant, transplant rejection, arthritic disorders, and the inflammatory vasculitic syndromes such as giant cell arteritis or Takayasu’s disease, are all associated with increased inflammatory cell activation and severe arterial disease. We postulate that the underlying central cause for a wide spectrum of occlusive arterial diseases is an up-regulation of innate immune responses that drive ongoing arterial damage.

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