Arterial Neovascularization and Inflammation in Vulnerable Patients

TLDR

Atherosclerosis can lead to myocardial infarction, stroke, or peripheral arterial disease, and inflammation and pathological neovascularization are thought to trigger plaque rupture or erosion, causing arterial thrombosis. The study tested whether arterial inflammation and angiogenesis are increased throughout the arterial tree in patients who have experienced cardiovascular events compared to those without such events, by quantifying inflammatory infiltrate and microvascular networks postmortem. The authors used tissue microarray technology to analyze full‑thickness arterial sectors from 22 symptomatic and 27 asymptomatic patients, quantifying inflammatory infiltrate and microvascular networks. Vulnerable patients had 2‑ to 4‑fold higher intimal macrophage content and a denser, hyperplastic vasa vasorum network across iliac, carotid, and renal arteries, indicating that high macrophage infiltration and vasa vasorum hyperplasia are hallmarks of symptomatic atherosclerosis and a pan‑arterial disease.

Abstract

Atherosclerosis is complicated by cardiovascular events such as myocardial infarction, stroke, or peripheral arterial occlusive disease. Inflammation and pathological neovascularization are thought to precipitate plaque rupture or erosion, both causes of arterial thrombosis and cardiovascular events. We tested the hypothesis that arterial inflammation and angiogenic events are increased throughout the arterial tree in vulnerable patients, ie, in patients who suffered from cardiovascular events, compared with patients who never suffered from complications of atherosclerosis.In a postmortem study, we quantified the inflammatory infiltrate and microvascular network in the arterial wall of iliac, carotid, and renal arteries. Tissue microarray technology was adapted to investigate full-thickness arterial sectors. We compared 22 patients with symptomatic atherosclerosis with 27 patients who never had suffered from any cardiovascular event. The absolute intimal macrophage content was 2- to 4-fold higher in vulnerable patients at all 3 arterial sites analyzed (P<0.05). Patients with symptomatic atherosclerosis had a denser network of vasa vasorum than patients with asymptomatic disease (33+/-2 versus 25+/-2 adventitial microvessels per 1 mm2; P=0.008). Hyperplasia of vasa vasorum was an early and macrophage infiltration was a late sign of symptomatic atherosclerosis.High intimal macrophage content and a hyperplastic network of vasa vasorum characterize vulnerable patients suffering from symptomatic atherosclerosis. These changes are uniformly present in different arterial beds and support the concept of symptomatic atherosclerosis as a panarterial disease.