Objectives: Pentraxins are a superfamily of multifunctional conserved proteins, some of which are components of the humoral arm of innate immunity and behave as functional ancestors of antibodies. They are divided into short (C reactive protein) and long pentraxins (pentraxin 3; PTX3). We investigated the diagnostic values of systematic arterial and coronary sinus (PTX3) in developing prediction models for estimating pretest probability of coronary artery disease (CAD) among an intermediate-risk population of patients with chronic stable angina.
Design: Cross-sectional analysis.
Setting: Referral cardiology hospital.
Participants: Patients with chronic stable angina, without evidence of previous CAD if they were referred for angiography.
Main outcome measures: All participants underwent diagnostic angiography. Prevalence rate ratio (PRR) of angiographically-determined coronary artery stenosis was separately examined in association with coronary sinus and femoral artery PTX3 concentrations using a general linear model. Duke treadmill score (DTS) was derived from the results of treadmill exercise cardiac stress testing. PTX3 data were collected in 100 patients with DTS-determined intermediate-risk chronic stable angina (aged 56.1 (1.1) years, 51 female).
Results: Both coronary sinus (PRR: 2.33, 95% CIs 1.64 to 3.31) and femoral artery PTX3 (PRR: 2.09, 95% CIs 1.46 to 2.97) independently predicted the prevalence rate of coronary artery involved with stenosis independent of the established CAD risk factors. Femoral artery PTX3 was highly correlated with coronary sinus PTX3 (β=0.8, 95% CIs 0.66 to 0.94; p value<0.001). When we added femoral artery PTX3 to the predictive models incorporating traditional CAD risk factors, net reclassification improvement indices were 40% (cutpoint-free) and 15% (cutpoint-based). In the presence of PTX3, high-density lipoprotein cholesterol (HDL-C) was no longer protective against CAD.
Conclusions: Gathering information on systemic arterial PTX3 may help more accurately reclassify DTS-determined patients with intermediate-risk chronic stable angina into more appropriate risk categories. PTX3 possibly, at least in part, mediates the protective effect on CAD of HDL-C.