# Routinely Available Inflammatory Biomarkers Are Not Associated With Target Lesion Revascularization After Coronary Intervention

## TL;DR

This study found that common inflammation markers do not predict the need for repeat heart procedures after stent placement, but they do predict other serious outcomes like death.

## Contribution

The study shows that inflammation markers are not linked to repeat revascularization after PCI, despite their role in predicting other adverse outcomes.

## Key findings

- Inflammatory biomarkers were not associated with target lesion revascularization or acute stent thrombosis.
- Elevated inflammation markers were significantly linked to all-cause mortality and major adverse cardiovascular events.
- The findings suggest that PCI should not be delayed due to high inflammation levels in patients with second-generation stents.

## Abstract

Biomarkers of inflammation are reliable predictors of adverse cardiovascular events in coronary artery disease. However, the association between systemic inflammation and percutaneous coronary intervention (PCI)-related adverse events remains widely unclear.

The objective of this study was to investigate the association of routinely assessed inflammatory biomarkers C-reactive protein, leukocytes, and neutrophil-to-lymphocyte ratio (NLR) with patient outcomes in an unselected patient cohort undergoing PCI.

A total of 7,412 patients (median age 64 years, 73.2% male) were enrolled in this single-center observational trial with a median follow-up time of 4.6 years. Target lesion revascularization (TLR) and acute stent thrombosis (ST) were defined as primary endpoints. Further endpoints included mortality, cardiovascular mortality, and 3-point major adverse cardiovascular events (MACE) (composite of cardiovascular mortality, myocardial infarction, and stroke). Cox proportional hazard regression was used for statistical analysis with a level of significance set at P < 0.01.

In the total study cohort, patients experiencing subsequent TLR (n = 488, 6.6%) had more comorbidities and underwent more complex primary interventions. Interestingly, no relation was found between systemic inflammation and subsequent TLR (eg, adjusted HR for C-reactive protein: 0.93 [95% CI: 0.85-1.03], P = 0.150), 30-day TLR (0.89 [95% CI: 0.75-1.05], P = 0.177), or acute ST (1.06 [95% CI: 0.79-1.42], P = 0.708) in multivariable analysis, neither in elective nor in acute interventions. All investigated inflammatory biomarkers were, however, significantly associated with all-cause mortality, cardiovascular mortality, and 3-point MACE, even after comprehensive adjustment for clinical and interventional parameters.

While our results emphasize the importance of systemic inflammatory activation for mortality and MACE, elevated baseline inflammatory parameters show no correlation with TLR or acute ST and, therefore, should not delay PCI in the era of second-generation drug-eluting stents.