What does this research mean for the field?

Post-PCI high-sensitivity C-reactive protein (hs-CRP) is independently associated with adverse cardiovascular outcomes in stable coronary artery disease patients, providing prognostic information beyond baseline inflammatory status. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine whether post-procedural high-sensitivity C-reactive protein provides prognostic information independent of baseline inflammatory status and renal function following elective percutaneous coronary intervention in stable coronary artery disease.

August 27, 2026Journal of Clinical MedicineOpen Access

Inflammatory Response After Elective PCI and Subsequent Outcomes in Stable Coronary Artery Disease

Q: What is the clinical evidence from this study?

Study design: Cohort. Population: Stable coronary artery disease (n=496). Intervention: Post-PCI high-sensitivity C-reactive protein (hs-CRP) vs. Baseline (pre-PCI) hs-CRP / lower post-PCI hs-CRP. Primary outcome: Composite of death, myocardial infarction, stroke, or repeat revascularization (HR 1.43, 95% CI 1.05-1.96, p=0.025).

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Key result

Higher post-PCI hs-CRP linked to ~43% greater risk of major events per doubling.

HR 1.43
95% CI 1.05-1.96
P=0.025
n=496

Why the study?

In stable coronary artery disease, it was unclear whether post-procedural inflammation provides prognostic information distinct from baseline inflammatory status and post-procedural renal function.

Does post-procedural hs-CRP elevation predict adverse cardiovascular outcomes independently of baseline inflammatory status and post-procedural renal function in patients with stable CAD undergoing elective PCI?

Key Points

To determine whether post-procedural high-sensitivity C-reactive protein provides prognostic information independent of baseline inflammatory status and renal function following elective percutaneous coronary intervention in stable coronary artery disease.
Analyzed 496 consecutive patients with stable coronary artery disease undergoing elective percutaneous coronary intervention.
Measured post-PCI high-sensitivity C-reactive protein (hs-CRP) and creatinine at 18–24 hours post-procedure, evaluating a composite endpoint of death, myocardial infarction, stroke, or repeat revascularization over a median follow-up of 10 months.
Employed multivariable Cox proportional hazards models with log-transformed hs-CRP adjusted for baseline hs-CRP, renal function, albumin, and procedural factors.
The primary composite endpoint occurred in 43 patients (8.7%) over a median follow-up of 10 months.
Post-PCI hs-CRP was independently associated with the composite endpoint after adjustment for pre-PCI hs-CRP, post-PCI creatinine, and albumin (HR 1.43 per doubling, 95% CI 1.05–1.96, p = 0.025), and remained significant after procedural adjustment (HR 1.54, p = 0.008), whereas pre-PCI hs-CRP was not independent (p = 0.083).
Post-PCI creatinine was independently associated with the endpoint across all models (HR 1.16 per 0.1 mg/dL, p = 0.001) and identified a high-risk group largely non-overlapping with elevated hs-CRP.

Study Design

Type

Cohort (n=496)

Multicenter

Structured PICO

Population

496 adult patients with stable coronary artery disease undergoing elective percutaneous coronary intervention, followed for a median of 10 months.

Exposure

Measurement of post-PCI high-sensitivity C-reactive protein (hs-CRP) and creatinine 18-24 hours after elective PCI

Outcome

Composite of death, myocardial infarction, stroke, or repeat revascularization during follow-upcomposite

Main Result

Hazard Ratio: 1.43 (95% CI 1.05–1.96)

p-value: p=0.025

In patients with stable CAD undergoing elective PCI, post-procedural hs-CRP and creatinine levels provide independent prognostic information for adverse cardiovascular events beyond baseline inflammatory status.

Limitations

Single-center observational design with a modest number of composite endpoint events (43), limiting generalizability and precluding causal inference.
Relatively short follow-up period (median 10 months).
Small number of acute coronary syndrome events (n=16) precluded subclassification into STEMI and NSTEMI.
Post-PCI creatinine was measured at 18-24 hours, earlier than the conventional 48-72 hour window for contrast-induced nephropathy.
Exploratory ROC analyses did not account for censoring or variable follow-up.
Exclusion of patients on chronic dialysis means renal findings do not extend to end-stage renal disease.
Patient-level discharge medication use and adherence during follow-up were not captured.
Modest number of events relative to covariates
Single-center observational design
Calcified-lesion status and IVUS use were not systematically captured
Patient-level discharge medication use and adherence during follow-up were not systematically captured

Implication

Post-PCI hs-CRP may refine risk stratification beyond baseline inflammation in elective PCI; leaves open whether serial monitoring or anti-inflammatory interventions alter outcomes.

Abstract

Background/Objectives: Inflammation contributes to atherosclerotic progression and may intensify after percutaneous coronary intervention (PCI). In stable coronary artery disease (CAD), whether post-procedural inflammation is prognostically distinct from baseline inflammatory status and post-procedural renal function remains unclear. Methods: We studied 496 consecutive patients with stable CAD undergoing elective PCI. The primary outcome was a composite of death, myocardial infarction, stroke, or repeat revascularization. Post-PCI high-sensitivity C-reactive protein (hs-CRP) and creatinine were measured 18–24 h after PCI. Multivariable Cox models used clinically prespecified covariates, with hs-CRP log-transformed (hazard ratio [HR] per doubling) and additionally adjusted for its pre-PCI level; discrimination was assessed by ROC analysis with bootstrap internal validation. Results: The endpoint occurred in 43 patients (8.7%) over a median follow-up of 10 months. Post-PCI hs-CRP was independently associated with the endpoint after adjustment for pre-PCI hs-CRP, post-PCI creatinine, and albumin (HR 1.43 per doubling, 95% CI 1.05–1.96, p = 0.025), and after further adjustment for angiographic and procedural characteristics (HR 1.54, p = 0.008); pre-PCI hs-CRP was not independent (p = 0.083). Post-PCI creatinine was independently associated in every model (HR 1.16 per 0.1 mg/dL, p = 0.001) and identified a largely non-overlapping high-risk group. Conclusions: After elective PCI in stable CAD, post-PCI hs-CRP was independently associated with adverse outcomes and provided prognostic information beyond baseline hs-CRP and procedural characteristics in the fitted models, rather than merely reflecting baseline inflammatory status. Post-PCI renal function was a complementary, largely independent risk signal.

Discussion

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Published by Journal of Clinical Medicine · CC BY

Cite This Study

Dalgıç et al. (2026) conducted a cohort in Stable coronary artery disease (n=496). Post-PCI high-sensitivity C-reactive protein (hs-CRP) vs. Baseline (pre-PCI) hs-CRP / lower post-PCI hs-CRP was evaluated on Composite of death, myocardial infarction, stroke, or repeat revascularization (HR 1.43, 95% CI 1.05-1.96, p=0.025). Post-PCI hs-CRP was independently associated with a composite of death, myocardial infarction, stroke, or repeat revascularization (HR 1.43 per doubling) beyond baseline inflammatory status.

synapsesocial.com/papers/6a8fea0d10c91c1e926221b6 https://doi.org/10.3390/jcm15176557

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Implication

Post-PCI hs-CRP may refine risk stratification beyond baseline inflammation in elective PCI; leaves open whether serial monitoring or anti-inflammatory interventions alter outcomes.

Inflammatory Response After Elective PCI and Subsequent Outcomes in Stable Coronary Artery Disease

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

Inflammatory Response After Elective PCI and Subsequent Outcomes in Stable Coronary Artery Disease

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

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