Systemic immune-inflammation index and in-stent restenosis in patients with acute coronary syndrome: a single-center retrospective study.

BACKGROUND: In-stent restenosis (ISR) has been shown to be correlated with inflammation. This study aimed to examine the relationship between systemic immune-inflammation index (SII, an innovative inflammatory biomarker) and ISR in acute coronary syndrome (ACS) patients after drug-eluting stent (DES) implantation. METHODS: Subjects who were diagnosed with ACS and underwent DES implantation were enrolled retrospectively. All individuals underwent follow-up coronary angiography at six to forty-eight months after percutaneous coronary intervention (PCI). SII was defined as [(platelet count × neutrophil count)/lymphocyte count], and Ln-transformed SII (LnSII) was carried out for our analysis. Multivariate logistic regression analysis was employed to assess the association between LnSII and DES-ISR. RESULTS: During a median follow-up period of 12 (11, 20) months, 523 ACS patients who underwent follow-up angiography were included. The incidence of DES-ISR was 11.28%, and patients in the higher LnSII tertile trended to show higher likelihoods of ISR (5.7% vs. 12.1% vs. 16.0%; P = 0.009). Moreover, each unit of increased LnSII was correlated with a 69% increased risk of DES-ISR (OR = 1.69, 95% CI 1.04-2.75). After final adjusting for confounders, a significant higher risk of DES-ISR (OR = 2.52, 95% CI 1.23-5.17) was found in participants in tertile 3 (≥ 6.7), compared with those in tertiles 1-2 (< 6.7). Subgroup analysis showed no significant dependence on age, gender, body mass index, current smoking, hypertension, and diabetes for this positive association (all P for interaction > 0.05). CONCLUSION: High levels of SII were independently associated with an increased risk of DES-ISR in ACS patients who underwent PCI. Further prospective cohort studies are still needed to validate our findings.

Comparing the efficacy of angiotensin receptor-neprilysin inhibitor and enalapril in acute anterior STEMI patients after primary percutaneous coronary intervention: a prospective randomized trial.

Background: For patients with heart failure (HF), the effect of angiotensin receptor-neprilysin inhibitors (ARNIs, sacubitril/valsartan) on cardiac remodeling has been found to be superior to angiotensin-converting enzyme inhibitors (ACEI). However, little data have described the impact of early-initiation ARNI in patients with acute anterior ST-segment elevation myocardial infarction (STEMI). Methods: In this prospective, randomized, double-blind, parallel-group trial, we enrolled 131 anterior STEMI patients who were treated with primary percutaneous coronary intervention (PCI) between February 2019 and December 2019. All patients received standard STEMI management and were divided into 2 groups (ARNI/enalapril). Primary efficacy outcomes were the between-group difference in change (from baseline to 4-, 12-, and 24-week) in N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration, left ventricular ejection fraction (LVEF), and left ventricular end-systolic volumes and end-diastolic volumes (LVESV and LVEDV). Secondary outcomes were determined by a composite of death, reinfarction, outpatient HF or HF hospitalization, malignant arrhythmia, and stroke. Safety outcomes included worsening renal function, hypotension, hyperkalemia, angioedema and cough. Results: We found that NT-proBNP concentration decreased more in the ARNI group than in the enalapril group [4 weeks: ratio of ARNI vs. enalapril 0.36, 95% confidence interval (CI): 0.24 to 0.52, P<0.001; 12 weeks: 0.54, 95% CI: 0.35 to 0.79, P<0.001; 24 weeks: 0.53, 95% CI: 0.32 to 0.83, P<0.001). When compared to the enalapril group, the ARNI group patients had a significant reduction in LVEDV (P<0.001) and LVESV (P<0.001), and an improvement in LVEF (P=0.011) at 24 weeks. Secondary outcomes occurred in 13 participants (20.3%) in the ARNI group and 22 participants (34.4%) in the enalapril group [hazard ratio (HR), 0.56; 95% CI: 0.28 to 1.12; P=0.102]. The incidence of outpatient HF or HF hospitalization in the ARNI group was significantly lower than that in the enalapril group (HR, 0.36; 95% CI: 0.14 to 0.94; P=0.037). There were no significant differences in the safety between the 2 groups. Conclusions: For patients with acute anterior STEMI undergoing primary PCI, early initiation of ARNI provided significant clinical benefits. Trial Registration: Chinese Clinical Trial Registry (ChiCTR2100042944) registered on February 1, 2021.

Blood microRNA 202-3p associates with the risk of essential hypertension by targeting soluble ST2.

MicroRNA (miR)-202-3p has attracted a great deal of attention in the fields of oncology, gynecology, and metabolic disorders. However, its role in cardiovascular diseases remains to be clarified. We previously found that disruption of miR-202-3p mediated regulation of expression of soluble (s)ST2, a decoy receptor for interleukin (IL)-33, promotes essential hypertension (EH). In the present study, we first measured miR-202-3p expression levels in the blood of 182 EH cases and 159 healthy controls using TaqMan assays. miR-202-3p levels were shown to be significantly higher in EH cases than controls (fold change = 3.58, P<0.001). Logistic regression analysis revealed that higher miR-202-3p expression was associated with an increased occurrence of EH (adjusted odds ratio (OR): 1.57; 95% confidence interval (CI), 1.36-1.82; P<0.001). Addition of miR-202-3p to traditional risk factors showed an additive prediction value for EH. Further functional experiments indicated that miR-202-3p could be induced by angiotensin II (Ang II) and inhibited by Ang II-triggered soluble ST2 (sST2) expression in a negative feedback manner. Moreover, blood miR-202-3p levels were negatively correlated with sST2 expression in vivo. Our study shows that blood miR-202-3p levels were significantly associated with the occurrence of EH. These findings indicate that miR-202-3p exerts a protective role against EH by antagonizing the induction of sST2 by Ang II.