Key result
Patients with coronary in-stent restenosis had a significantly higher prevalence of elevated baseline hsCRP (>3 mg/L) compared to patients without restenosis (90% vs 62.5%, p=0.007).
Why the study?
Inflammation plays a pivotal role in in-stent restenosis pathogenesis, prompting investigation of the hsCRP inflammatory response to PCI in CAD patients with versus without coronary in-stent restenosis.
Are high sensitivity C-reactive protein (hsCRP) levels elevated in CAD patients with in-stent restenosis compared to those without in-stent restenosis?
Case-Control (n=80)
No
Are high sensitivity C-reactive protein (hsCRP) levels elevated in CAD patients with in-stent restenosis compared to those without in-stent restenosis?
Patients with in-stent restenosis have substantially higher pre- and post-PCI hsCRP levels compared to controls without restenosis, suggesting that inflammation plays a key role in ISR pathogenesis.
Background: Inflammation plays a pivotal role in the pathogenesis of In-Stent Restenosis (ISR). High sensitivity C-reactive protein (hsCRP) is positively associated with major cardiovascular events. Aim: We aimed to investigate the hsCRP inflammatory response to Percutaneous Coronary Intervention (PCI) in Coronary Artery Disease (CAD) patients with coronary ISRvs.patients without ISR. Methods: This case-control study included 80 CAD patients previously treated with drug-eluting stent (DES) implantation. Patients had Coronary Angiography (CAG) because of chest pain or equivalent symptoms and were subdivided into 2 groups. Group A (n=40) included CAD patients with ISR. Group B (n=40) included age and gender-matched controls with CAD but without ISR. Serum hsCRP levels were obtained before PCI (baseline) and 8, 16, 24 h post-PCI. Results: At baseline (before intervention/CAG), the hsCRP level was increased in the ISR group compared with the No-ISR group (p=0.007). There were 36 (90%) patients in the ISR group who had a high hsCRP (>3 mg/L) compared with 25 (62.5%) patients in the No-ISR group. Also, there was a significant relationship between high hsCRP and the ISR. Patients with ISR had higher frequencies and percentages of elevated CRP than the no-ISR control group. This difference was maintained for all measurements, baseline, after 8, 16, and 24 h (p<0.05). Repeated measures analysis of variance (ANOVA) in the ISR group revealed that mean hsCRP differed significantly between serial measurements (p<0.001). In contrast, in the control group, the mean hsCRP did not differ significantly between the serial measurements (p=0.65). Most of our patients (n=66, 82.5%) had 1-vessel CAD disease, and the left anterior descending (LAD) coronary artery was significantly affected in 46 patients (57.5%). Management of restenosis was accomplished mainly by stenting by DES in 29 patients (72.5%). Conclusion: Patients with ISR had substantially higher pre- and post-PCI hsCRP levels than the no-ISR controls. This difference was maintained up to 24h post-PCI. Conversely, the mean hsCRP did not significantly differ at the follow-up points for the controls without ISR.
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Ismail et al. (2021) conducted a case-control in Coronary Artery Disease with previous drug-eluting stent implantation (n=80). In-stent restenosis (ISR) vs. No in-stent restenosis (No-ISR) was evaluated on Elevated baseline hsCRP (>3 mg/L) (p=0.007). Patients with coronary in-stent restenosis had a significantly higher prevalence of elevated baseline hsCRP (>3 mg/L) compared to patients without restenosis (90% vs 62.5%, p=0.007).
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