Inflammatory Response Following Peripheral Endovascular Treatment Correlates with the Extent of Periprocedural Arterial Injury

Abstract

SUMMARY – The aim was to examine whether the postprocedural change in C-reactive protein (CRP) and fibrinogen levels was associated with the extent of periprocedural arterial injury caused by endovascular treatment (EVT). The study recruited 71 patients undergoing EVT. Eighty-four patients that underwent angiography served as a control group. CRP and fibrinogen were measured at baseline, and at 8, 24 and 48 hours following the procedure. In all experimental group patients, lesion complexity, percutaneous transluminal angioplasty (PTA) treated segment length, balloon inflation time and stented segment length were recorded. There was significant increase in plasma CRP and fibrinogen levels 48 hours following EVT (p<0.001). There was no significant difference in CRP and fibrinogen levels among different TASC groups. CRP levels were significantly higher in stent subgroup compared to PTA subgroup. Significant positive correlation was found between PTA treated segment length and CRP increase between 8 and 24 hours following EVT (r=0.313, p=0.02), balloon inflation time and CRP increase in the aforementioned time frame (r=0.270, p=0.03), as well as between CRP increase at 8 hours and stented segment length (r=0.535, p=0.01). This study showed that the arterial injury caused by EVT reflected on the level of inflammatory biomarkers.

Influence of concomitant percutaneous transluminal angioplasty with percutaneous coronary intervention on cardiovascular and limb outcomes in patients with chronic stable lower extremity artery diseases

“…However, concomitant PTA at the time of PCI still concerns various aspects, including procedure complexity, high contrast media exposure, repeated use of parenteral anticoagulants, multiple puncture sites and higher rates of ISR and acute thrombosis in PTA compared to PCI. PTA is also known to be followed by extensive systemic in ammation, which might promote coronary artery ISR (5,7). Therefore, the safety and e cacy of concomitant PTAs should be investigated thoroughly.…”

“…However, concomitant endovascular procedures at the time of PCI would increase the use of radiocontrast media and parenteral anticoagulants, which may increase the risk of renal impairment and bleeding (4). Moreover, these procedures may promote systemic in ammatory responses through extensive injuries to the diseased vessels (5), which may eventually result in coronary instent restenosis (ISR) during follow-up (6, 7). Because it is crucial to determine how concomitant PTA affects clinical outcomes following PCI, we investigated the impact of concomitant PTA on CV, limb and renal outcomes in patients who underwent PCI using the Korean National Health Insurance System (KNHIS) database.…”

Propolis ameliorates restenosis in hypercholesterolemia rabbits with carotid balloon injury by inhibiting lipid accumulation, oxidative stress, and TLR4/NF‐κB pathway

“…It is well-known that inflammatory cell infiltration occurs shortly after endothelial denudation, and monocyte infiltration contributes to restenosis (Kornowski et al, 1998). In addition, elevated CRP is considered to be a suggestive indicator of the degree of the inflammation in arterial disease and is associated with vascular restenosis (Turk et al, 2018). TNFα promotes the migration of VSMCs by upregulation of MMP-9 expression and promotes neointimal hyperplasia (Guo et al, 2014).…”

The association between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury in patients with carotid artery stenting

“…Increases in the levels of specific inflammatory biomarkers such as C-reactive protein and fibrinogen have been observed in patients undergoing endovascular interventions. 19,20 Shear stress during balloon inflation and vascular injury can facilitate events that trigger the inflammatory process, stimulating the production of proinflammatory molecules and the activation of circulating monocytes. Existing literature indicates that stent implantation itself provokes a marked inflammatory reaction.…”