Aspirin-free P2Y12 inhibitor monotherapy immediately after percutaneous coronary intervention: A systematic review.

Background: A modified antiplatelet therapy approach after percutaneous coronary intervention (PCI), specifically reducing dual antiplatelet therapy (DAPT) duration and transitioning to P2Y12 inhibitor monotherapy, may offer advantages in terms of bleeding risk reduction. However, the impact of initiating aspirin-free P2Y12 inhibitor monotherapy immediately after PCI is not yet fully understood. Methods: We systematically searched the PubMed and Embase databases until January 2024 for studies that examined the use of P2Y12 inhibitor monotherapy as a treatment approach without initial DAPT following PCI. Results: Four single-arm pilot prospective studies and 1 randomized controlled trial were included. In acute coronary syndrome patients with P2Y12 monotherapy following aspirin withdrawal immediately after PCI, the occurrence rates of the primary ischemic and bleeding endpoint were 2.91 % (8 out of 275 patients) and 1.09 % (3 out of 275 patients) respectively, whereas both the incidence rates of the primary ischemic and bleeding endpoints were 0.25 % (1 out of 407 patients) in individuals with stable coronary artery disease. In the STOPDAPT-3 trial comparing the effect of aspirin-free prasugrel monotherapy with standard DAPT after PCI, no differences were found in the primary ischemic or bleeding endpoints and most secondary outcomes (death, stroke, and myocardial infarction). However, there was an increased risk of coronary revascularization and stent thrombosis in the no-aspirin group. Conclusions: Single-arm studies suggest the safety and feasibility of aspirin-free P2Y12 inhibitor monotherapy without initial DAPT after PCI in selected patients with acute coronary syndrome or stable coronary artery disease. However, the safety and efficacy of this aspirin-free approach compared with standard DAPT strategies following PCI still require further investigation.

Oral anticoagulant therapy for patients with new-onset atrial fibrillation following acute myocardial infarction: A narrative review.

Background: To evaluate the advantages and disadvantages of anticoagulant therapy and provide a piece of information on anti-thrombotic treatment strategies for patients with new-onset atrial fibrillation (NOAF) and acute myocardial infarction (AMI). Methods: Literature from PubMed and Google scholar were screened until August 2022. Studies assessing oral anticoagulant (OAC) treatments for NOAF in patients with AMI were evaluated for inclusion. Results: Three retrospective cohort studies were included. In the study performed by Madsen et al., patients with previously diagnosed AMI with or without NOAF were followed up for 5.8 years. About 38% of NOAF patients with anticoagulant therapies, which could reduce long-term mortality [adjusted hazard ratio (HR): 0.69; 95% confidence interval (CI): 0.47-1.00]. Hofer et al. performed a single-center cohort study containing 1,372 patients with AMI with an 8.6-year follow-up period. Dual anti-thrombotic therapy (DAT) did not show the effect on the survival in NOAF (adjusted HR: 0.97; 95% CI: 0.65-1.57), while triple antithrombotic therapy (TAT) could reduce long-term cardiovascular mortality (adjusted HR: 0.86; 95% CI: 0.45-0.92). Petersen et al. also did a cohort study with 1-year follow-up duration. It showed that anticoagulant therapies demonstrated positive results (HR: 0.78; 95% CI: 0.41-1.47). Conclusion: Recent studies have shown that anticoagulant therapy in AMI-NOAF patients can obviously reduce the mortality of AMI-NOAF patients, especially OAC therapy. Further clinical trials could confirm these findings.

Ozone protects cardiomyocytes from myocardial ischemia-reperfusion injury through miR-200c/FOXO3 axis.

PURPOSE: Myocardial ischemia-reperfusion injury (I/R) is a detrimental process contributing to the pathological progression of coronary artery diseases. Studies indicate that miRNAs are implicated in ischemic heart disease, and ozone therapy could protect the heart from ischemic heart disease. In this study, we investigated the effect of ozone on miR-200c expression and the potential role of miR-200c in an I/R myocardial injury model. METHODS: A myocardial cellular model of I/R was established to detect the expression of miR-200c. Cardiomyocytes with I/R induction were treated with ozone as a cellular model to detect miR-200 expression and investigate its functional roles. The downstream target of miR-200c was predicted with Starbase online tools and validated by dual luciferase reporter assay. The function of miR-200c/FOXO3 axis in I/R was examined by CCK-8 proliferation and apoptotic assays. RESULTS: miR-200c was upregulated in primary cardiomyocytes of the I/R model. In cardiomyocyte cells, cell proliferation in the I/R group was significantly impaired, which could be partially rescued by miR-200c inhibitor or ozone treatment. Cell death detected by LDH release and apoptosis assay in the I/R model could also be inhibited by miR-200c inhibitor or ozone treatment. FOXO3 was identified as a downstream target of miR-200c, which was induced by ozone treatment and suppressed by miR-200c. Silencing FOXO3 abrogated the protective effect of ozone treatment on the I/R cell model. CONCLUSION: Overall, our results suggest that ozone plays a cardio-protective role in I/R through regulating miR-200/FOXO3 axis, and indicate that targeting miR-200/FOXO3 axis could potentially alleviate I/R.

Ozone protects cardiomyocytes against ischemia/reperfusion injury: Regulating the heat shock protein 70 (HPS70) expression through activating the JAK2/STAT3 Pathway.

Ischemia/reperfusion (I/R) injury causes complications in early coronary artery reperfusion for acute myocardial infarction (AMI). Ozone (O3) has been reported to be applied for protecting I/R injury, but its detailed mechanism remains unclear. Our study focused on the protective effect of O3 pretreatment on myocardial I/R injury and JAK2/STAT3 signaling and HSP70 regulation involving in the mediation. The rat hearts which were perfused and isolated as well as the cultured cardiomyocytes of neonatal rat were exposed to hypoxia/reoxygenation (H/R) and different concentrations of O3 followed by heat shock protein 70 (HSP70) siRNA treatment. The results showed O3 attenuated the suppression of cell viability induced by H/R and decreased the release of activity of creatine kinase (CK), lactate dehydrogenase (LDH) and apoptosis of cardiomyocytes in vitro. Moreover, O3 also activated the JAK2/STAT3 signaling, upregulated the expression of HSP70 both in vitro and vivo, and decreased the index of apoptosis of cardiomyocytes caused by I/R as well as myocardial infarct area in vivo. In addition, HSP70 siRNA and JAK2 inhibitor AG490 inhibited the cardioprotective effect of O3. And the expression of HSP70 increased by ozone was reduced by AG-490. In conclusion, our results demonstrated that ozone protects cardiomyocytes in I/R injury through regulation of the expression of HSP70 by activating the JAK2/STAT3 pathway.

Analysis of therapeutic effectiveness and prognostic factor on argon-helium cryoablation combined with transcatheter arterial chemoembolization for the treatment of advanced hepatocellular carcinoma.

OBJECTIVE: The objective of this study was to evaluate the effectiveness on argon-helium cryoablation combined with transcatheter arterial chemoembolization (TACE) in treating advanced hepatocellular carcinoma (HCC) and its influence factor. MATERIALS AND METHODS: This trial was approved by the Guangzhou Panyu Central Hospital Ethics Committee. This was a prospective, single-center study conducted in Guangzhou Panyu Central Hospital. After informed consent was obtained, the prospective randomized clinical data of 120 patients with advanced HCC were collected. Based on the therapeutic scheme, the patients were divided into control group (TACE + argon-helium cryoablation) and observed group (TACE group). All the patients were followed up for 60 months. The pre- and post-operative cancer situation, hepatic function situation, complete remission (CR) rate, total effective rate, and survival time were evaluated. The short-term and long-term effectiveness were compared between the two groups. RESULTS: Both the CR rate and total effective rate of the combination group were significantly higher than those of TACE group (P < 0.05). Liver function damage of the combination group was lower than those of TACE group. The survival rate of the combination group was significantly longer than that of TACE group P < 0.05). The Cox regression model revealed that ages, tumor diameter, tumor periportal location, and liver function (Child-Pugh) were significant variables influencing survival time P < 0.05). CONCLUSION: For the treatment of advanced HCC, argon-helium cryoablation combined with TACE is obviously effective and safe. The ages, tumor diameter, tumor periportal location, and grade of liver function (Child-Pugh) have obvious impacted the treatment effectiveness.

Targeting activated hepatic stellate cells (aHSCs) for liver fibrosis imaging.

Following injurious stimuli, quiescent hepatic stellate cells (qHSCs) transdifferentiate into activated HSCs (aHSCs). aHSCs play pivotal roles in the onset and progression of liver fibrosis. Therefore, molecular imaging of aHSCs in liver fibrosis will facilitate early diagnosis, prognosis prediction, and instruction and evaluation of aHSC-targeted treatment. To date, several receptors, such as integrin αvß3, mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF-IIR), collagen type VI receptor (CVIR), platelet-derived growth factor receptor-ß (PDGFR-ß), vimentin, and desmin, have been identified as biomarkers of aHSCs. Corresponding ligands to these receptors have also been developed. This review will discuss strategies for developing aHSC-targeted imaging in liver fibrosis.