In addition, the relationship between post-surgical NLR and you can stent restenosis hasn’t been reviewed
Atherosclerosis is a progressive, complex and multifactorial disease. Inflammation plays an important role in all stages of the atherosclerosis development [13,14]. ISR has been attributed to neointimal hyperplasia in the early stage just after the procedure . Inflammatory cells may accelerate neointimal hyperplasia because of their release of growth and chemotactic factors or production of enzymes (e.g. matrix metalloproteinases), which can degrade extracellular constituents and facilitate cell migproportionn [17,18]. Neutrophils respond to different inflammatory stimuli resulting in release of various cytokines and cytotoxic/proteolytic enzymes that affect the vascular system datingranking.net/nl/cheekylovers-overzicht by numerous mechanisms such as induction of damage to endothelial cells, induction of the coagulation system . Lymphocyte count reflects a physiologic stress response to cortisol . The NLR has been shown to be a mation and closely related to increased cardiovascular mortality and morbidity [5,6]. The primary finding of our study is that the NLRratio level was a better independent predictor than NLRafter level for the occurrence of the ISR in patients who underwent superficial femoral artery stenting for lower extremity arteriosclerosis obliterans.
Into the issues, higher NLR shows two more protected paths; and that, it is a great deal more predictive than simply both factor alone
Our study observed that in patients presenting with restenosis within 12 months, the NLR increased after stent implantation. We find a positive correlation between the NLRratio and an occurrence of ISR (r=0.41; P<0.001). Patients with a NLRratio value > 37.5% had a 3.47-fold higher risk of ISR when compared with a NLRratio value < 37.5%. Patients with a NLRafter value > 4.3 had a 1.96-fold higher risk of ISR when compared with a NLRafter value < 4.3. Moreover, patients with a NLRchange > 1.24 had a 2.13-fold higher risk of ISR than did patients with a NLRchange value < 1.24. A NLRratio level > 37.5% had 77% sensitivity and 60% specificity for the prediction of ISR, A NLRchange level > 1.24 predicted ISR with 75% sensitivity and 77% specificity. The NLRchange in our study is higher than that reported in most other studies. For example, Balli et al. reported the neutrophil–lymphocyte ratio for prediction of in-stent restenosis in coronary stents. A NLRchange level > 0.58 had 81.8% sensitivity and 93.5% specificity for the prediction of ISR. This discrepancy might be caused by the different lesion sites studied. The superficial femoral artery stent might be affected by the compression, pulling and torsion of the thigh muscle, resulting in continuous vascular damage, while the coronary arteries are less affected by the muscle. Chang et al. reported that the NLRin advance of > 3.62 was independently and positively associated with a higher risk of early (within 1 year) ISR after stent implantation in patients with femoropopliteal chronic total occlusion. before levels and the occurrence of ISR. The differences may be: first, we excluded patients with active infection, chronic inflammation, malignancy, and copd. Inflammation is considered to play a key role in the pathophysiological process for many chronic diseases. Second, they mainly studied the chronic complete occlusion of femoral popliteal artery, while we mainly studied the superficial femoral artery, and the patients did not have severe limb ischemia.
Occurrence of ISR is a complex and multifactorial process . Inflammation appears to be one of the many risk factors for stent restenosis [22,23]. The inflammatory process plays an important role not only in initiation and progression of atherosclerosis but also in development of stent restenosis [24,25]. In general, the inflammation process contributes to stent restenosis by two distinct mechanisms, namely local vascular inflammation because of mechanical injury inflicted by stent implantation and a pre-existing systemic inflammatory state before the procedure. [22,23]. The association between systemic inflammation and ISR has been reported in various studies conducted on different inflammatory markers. Of those, CRP was the most frequently studied biomarker owing to its accurately reflecting systemic inflammation and being a strong predictor of cardiovascular outcomes . Our research is mainly discussed because of mechanical damage caused by stent implants, namely, local vascular inflammation. Donners reported that depending on endothelial damage during the PCI, increases in adhesive molecules and chemotactic factors are followed by the accumulation of inflammatory cells and pro-inflammatory molecules, such as interleukin-1 and 6, which mediate the development of neointimal proliferation. In our study, NLRratio was stronger independent predictors of short-term survival than other leukocytes. The predictive superiority of NLR may be due to 1 factor, NLR is a ratio of two different yet complementary immune pathways. Neutrophils are responsible for active ongoing nonspecific inflammation through secretion of many inflammatory mediators, like elastase , myeloperoxidase and oxygen free radicals that can facilitate plaque disruption. An increase in neutrophil count predicts an increase in neointima and undesirable outcomes of stent restenosis. Lymphocytes, in contrast, represent the regulatory pathway of the immune system. CD4, the main subtype of total lymphocyte count, reflects a physiologic stress response to cortisol .The neutrophil–lymphocyte ratio therefore reflects both the neutrophil of inflammation and the relative lymphocyte of cortisol-induced stress response.