Markers of Inflammation and Rapid Coronary Artery Disease Progression in Patients With Stable Angina Pectoris

TLDR

Endothelial and macrophage activation contribute to atherogenesis and plaque vulnerability, potentially driving rapid coronary artery disease progression. The study aimed to evaluate whether serum inflammatory markers predict rapid coronary artery disease progression in patients with chronic stable angina. A cohort of 124 chronic stable angina patients, followed for an average of 4.8 months, was assessed for CAD progression defined by ≥10 % diameter reduction of ≥50 % stenosis, ≥30 % reduction of <50 % stenosis, new ≥30 % stenosis, or total occlusion. Rapid CAD progression occurred in 28 % of patients and was independently predicted by elevated neopterin, hs‑CRP, MMP‑9, soluble ICAM‑1, and prior unstable angina, confirming that higher inflammatory and endothelial activation markers are linked to faster disease progression.

Abstract

Background— Both endothelial cell activation and macrophage activation play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapid coronary artery disease (CAD) progression. We sought to assess the association between serum inflammatory markers and rapid CAD progression in patients with chronic stable angina pectoris. Methods and Results— We studied 124 chronic stable angina pectoris patients (84 men; mean age, 61±10 years) who were on a waiting list for coronary angioplasty for a mean time of 4.8±2.4 months. CAD progression was defined as ≥10% diameter reduction of a pre-existing stenosis ≥50%, ≥30% diameter reduction of a stenosis &lt;50%, development of a new stenosis ≥30% in a previously normal segment, or progression of any stenosis to total occlusion. CAD progression occurred in 35 patients (28%). After adjustment with binary logistic regression, neopterin ( P &lt;0.001), high-sensitivity C-reactive protein ( P =0.017), matrix metalloproteinase-9 ( P =0.002), soluble intercellular adhesion molecule 1 ( P &lt;0.001), and previous history of unstable angina ( P =0.01) were independent predictors of rapid CAD progression. The association between rapid disease progression and inflammatory markers remained significant even when presence of complex lesions was introduced into the multivariate model. Conclusions— Rapid CAD progression in patients with stable angina pectoris is associated with increased C-reactive protein levels and raised concentrations of biochemical markers of endothelial and macrophage activation.