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There are many clinical scoring criteria for predicting the risk of death in patients with acute ST-segment elevation myocardial infarction (STEMI), but most of the indicators are complex to calculate and are not suitable for use in primary hospitals. Neutrophil to lymphocyte ratio (NLR) and red cell distribution width (RDW) are blood routine indicators that are easy to obtain and may help primary hospitals to evaluate the risk of death in patients with STEMI. Our aim was to explore the predictive value of NLR combined with RDW in the long-term prognosis of patients with STEMI after emergency percutaneous coronary intervention (PCI). A total of 181 patients with STEMI who underwent emergency PCI in the Affiliated Hospital of Pu-tian University from January 2017 to August 2018 were selected. Clinical profile, prognosis of all patients were collected. P value < 0.05 was considered significant. In all patients, cardiovascular death during the follow-up period was defined as cardiovascular death group, and surviving during the follow-up period was defined as survival group. There were no significant differences in demography and comorbidities between the two groups. The differences between the two groups in NLR, RDW, C-reactive protein, N-terminal-pro B type natriuretic peptide were statistically significant (P < 0.01). Binary logistic regression analysis showed that NLR (OR = 1.122, 95% CI 1.041 ~ 1.210, P = 0.003) and RDW (OR = 1.288, 95% CI 1.126 ~ 1.472, P = 0.0005) were important predictors of mortality in patients with STEMI (P < 0.05). Kaplan–Meier analysis showed that as the NLR increased, the risk of death increased (P < 0.001). In conclusion, NLR and RDW are independent predictors of cardiovascular death in patients with STEMI, and they have a certain predictive value.

Objectives: To investigate the effect and mechanism of sacubitril/valsartan on myocardial fibrosis in rats following experimental myocardial infarction and in TGF-β1-treated myocardial fibroblasts.Methods: Male Sprague-Dawley (SD) rats were subjected to coronary artery ligation to establish myocardial infarction and intragastrically fed vehicle, valsartan (Val, 32 mg/kg, once-daily) or sacubitril/valsartan (Sac/Val, 68 mg/kg, once-daily) for 4 weeks. In parallel, myocardial fibroblasts (MFs) isolated from neonatal SD rats were exposed to hypoxia and treated with TGF-β1 (5 ng/ml) plus vehicle, Val (107–10–5 M) or Sac/Val (107–105 M). Rat cardiac function and fibrosis were measured by echocardiography and histological method, respectively. MFs viability and collagen synthesis were determined by cell counting kit-8 and enzyme-linked immunosorbent assay, respectively. Protein expressions of TGF-β1, Smad3, phosphorylated Smad3 (p-Smad3), and p-Smad3 subcellular localization were detected by immunoblotting and immunocytochemistry.Results: Sac/Val significantly improved cardiac structure and function in rats after myocardial infarction, including decreased left ventricular end-diastolic diameter and interventricular septal thickness, increased ejection fraction, and reduced myocardial collagen volume fraction and type Ⅰ and type Ⅲ collagen levels, and this effect was superior to that of Val. Besides, Sac/Val inhibited myocardial TGF-β1 and p-Smad3 protein expression better than Val. Mechanically, Sac/Val significantly attenuated TGF-β1-induced proliferation and collagen synthesis of MFs, and inhibit Smad3 phosphorylation and nucleus translocation, and this effect outperformed Val. Overexpression and silencing of Smad3 enhanced and reversed the inhibitory effects of Sac/Val on TGF-β1-induced collagen synthesis by MFs, respectively.Conclusions: Sacubitril/valsartan improves cardiac function and fibrosis in rats after experimental myocardial infarction, and this effect is related to the inhibition of collagen synthesis in myocardial fibroblasts by inhibiting the TGF/Smads signaling pathway.

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