The Fibrosis-5 Index Predicts Major Adverse Cardiovascular Events in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

This study aimed to evaluate the fibrosis-5 (FIB-5) index as a marker of liver fibrosis for major adverse cardiovascular events (MACE) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). A total of 406 STEMI patients were enrolled in the study. Over an average follow-up of 27 months, 143 of the patients developed MACE. The patients were subgrouped into tertiles based on the FIB-5 index and Kaplan-Meier survival (MACE-free) curves were plotted, showing statistically significant differences (log-rank test, P < .001). In the adjusted Cox regression model, the hazard ratio (HR) of MACE was 1.95 (95% CI 1.21-3.13; P = .006) in tertile 3 and 0.98 (95% CI 0.97-1.00; P = .013) for per unit increase in the FIB-5 index. The area under the curve (AUC) of the FIB-5 index predicting the occurrence of MACE in STEMI patients after PCI was 0.645 (95% CI 0.590-0.701; P < .001). Low FIB-5 may be a useful predictor of MACE in STEMI patients undergoing PCI.

Impact of plaque characteristics on percutaneous coronary intervention-related microvascular dysfunction: insights from angiographic microvascular resistance and intravascular ultrasound.

Background: The correlation between percutaneous coronary intervention (PCI)-related microvascular dysfunction (MVD) and plaque characteristics remains unclear. To investigate this correlation and its prognosis, we assessed changes in MVD by angiographic microvascular resistance (AMR) and intracoronary ultrasound scans after PCI. Methods: We conducted a retrospective study that enrolled 250 patients with coronary artery disease between July 2016 and December 2018. We collected demographic characteristics, laboratory tests, coronary angiography (CAG) and intracoronary ultrasound findings. We calculated quantitative flow ratio (QFR) and AMR by CAG. The endpoint was vessel-oriented composite outcomes (VOCOs). Results: After 47 exclusions, we divided 203 cases into a deteriorated group (n=139) and an improved group (n=64) based on AMR change after PCI. Compared with the improved group, the deteriorated group had smaller lumen area [3.03 (interquartile range, 2.20-3.91) vs. 3.55 mm2 (interquartile range, 2.45-4.57), P=0.033], higher plaque burden [78.92% (interquartile range, 73.95-82.61%) vs. 71.93% (interquartile range, 62.70-77.51%), P<0.001], and higher proportion of lipidic components (13.86%±4.67% vs. 11.78%±4.41%, P=0.024). Of 186 patients who completed 4.81±1.55 years follow-up, 56 developed VOCOs. Receiver-operating characteristic (ROC) curve analysis showed post-PCI AMR and VOCOs correlation (area under the curve: 0.729, P<0.001). Multivariate regression analysis showed post-PCI AMR >285 mmHg·s/m correlated with adverse outcome (hazard ratio =4.350; 95% confidence interval: 1.95-9.703; P<0.001). Conclusions: Intravascular ultrasound (IVUS) imaging and AMR revealed an association of post-PCI MVD with a smaller lumen area, more severe plaque burden, and a higher percentage of lipidic components. Post-PCI MVD was an independent risk factor for poor prognosis.

Investigating the Correlation between Serum Amyloid A and Infarct-Related Artery Patency Prior to Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction Patients.

Serum amyloid A (SAA) is a cardiovascular risk factor and may serve as a predictor of infarct-related artery (IRA) patency in patients with ST-segment elevation myocardial infarction (STEMI). We measured SAA levels in STEMI patients who underwent percutaneous coronary intervention (PCI) and investigated their association with IRA patency. According to the Thrombolysis in Myocardial Infarction (TIMI) flow grade, 363 STEMI patients undergoing PCI in our hospital were divided into an occlusion group (TIMI 0-2) and a patency group (TIMI 3). The SAA level before PCI was significantly higher in STEMI patients with IRA occluded than in those with patent ones. At a cutoff value of 36.9 mg/L, SAA had a sensitivity of 63.0% and a specificity of 90.6% (area under the ROC curve [AUC] = .833, 95% CI: .793-.873, P < .001). Multivariate logistic regression analysis showed that SAA was an independent predictor of IRA patency in STEMI patients before PCI (odds ratio [OR] = 1.041, 95% CI: 1.020-1.062, P < .001). SAA can be used as a potential predictor of IRA patency in STEMI patients before PCI.

Simvastatin Alleviates Intestinal Ischemia/Reperfusion Injury by Modulating Omi/HtrA2 Signaling Pathways.

PURPOSE: The objective of this research was to survey the therapeutic action of simvastatin (Sim) on intestinal ischemia/reperfusion injury (II/RI) by modulating Omi/HtrA2 signaling pathways. METHODS: Sprague Dawley rats were pretreated with 40 mg/kg Sim and then subjected to 1 hour of ischemia and 3 hours of reperfusion. The blood and intestinal tissues were collected, pathologic injury was observed, the contents of serum tumor necrosis factor-α and interleukin-6 (IL-6) were estimated, and superoxide dismutase, methane dicarboxylic aldehyde, and cysteinyl aspartate specific proteinase-3 (caspase-3) levels, as well as the expressions of Omi/HtrA2 and caspase-3, were measured in the intestinal tissues. RESULTS: Sim preconditioning mitigated the damnification of intestinal tissues by decreasing oxidative stress, inflammatory damage, and apoptosis and downregulating the expression of Omi/HtrA2 compared to the ischemia/reperfusion group, while Sim+Ucf-101 significantly augmented this effect. CONCLUSION: These results suggest that Sim may alleviate intestinal ischemia/reperfusion injury by modulating Omi/HtrA2 signaling pathways.