Myocardial ischemia‐reperfusion injury (MIRI) is a major cause of heart failure in patients with coronary heart disease (CHD). Mitochondrial dysfunction is the crucial factor of MIRI; oxidative stress caused by mitochondrial reactive oxygen species (ROS) aggravates myocardial cell damage through the mitochondria‐dependent apoptosis pathway. Asiatic acid (AA) is a type of pentacyclic triterpene compound purified from the traditional Chinese medicine Centella asiatica, and its protective pharmacological activities have been reported in various disease models. This study is aimed at investigating the protective effects of AA and the underlying mechanisms in MIRI. To achieve this goal, an animal model of MIRI in vivo and a cell model of oxygen‐glucose deprivation/reperfusion (OGD/R) in vitro were established. The results show that AA exerts a protective effect on MIRI by improving cardiac function and reducing cardiomyocyte damage. Due to its antioxidant properties, AA alleviates mitochondrial oxidative stress, as evidenced by the stable mitochondrial structure, maintained mitochondrial membrane potential (MMP), and reduced ROS generation, otherwise due to its antiapoptotic properties. AA inhibits the mitogen‐activated protein kinase (MAPK)/mitochondria‐dependent apoptosis pathway, as evidenced by the limited phosphorylation of p38‐MAPK and JNK‐MAPK, balanced proportion of Bcl‐2/Bax, reduced cytochrome c release, inhibition of caspase cascade, and reduced apoptosis. In conclusion, our study confirms that AA exerts cardiac‐protective effects by regulating ROS‐induced oxidative stress via the MAPK/mitochondria‐dependent apoptosis pathway; the results provide new evidence that AA may represent a potential treatment for CHD patients.

Atherosclerosis (AS) is one of the leading causes of death among the elderly, and is primarily caused by foam cell generation and macrophage inflammation. Rutin is an anti-inflammatory, anti-oxidant, anti-allergic, and antiviral flavonoid molecule, known to have anti-atherosclerotic and autophagy-inducing properties, but its biological mechanism remains poorly understood. In this study, we uncovered that rutin could suppress the generation of inflammatory factors and reactive oxygen species (ROS) in ox-LDL-induced M2 macrophages and enhance their polarization. Moreover, rutin could decrease foam cell production, as shown by oil red O staining. In addition, rutin could increase the number of autophagosomes and the LC3II/I ratio, while lowering p62 expression. Furthermore, rutin could significantly inhibit the PI3K/ATK signaling pathway. In summary, rutin inhibits ox-LDL-mediated macrophage inflammation and foam cell formation by inducing autophagy and modulating PI3K/ATK signaling, showing potential in treating atherosclerosis.

Asiatic acid inhibits cardiac hypertrophy by blocking interleukin- 1β-activated nuclear factor-κB signaling in vitro and in vivo

Coronary sinus thrombosis (CST) is a rare and severe disease that remains underrecognized in clinical practice. Most documented cases fall within the acute category, with non-specific symptoms, rapid progression, and a high mortality rate. In contrast, some cases follow an insidious course, leading to the formation of partial or incomplete thrombi that may not cause immediate death but can progress to severe complications over time. This review study the pathophysiology, clinical presentations, diagnostic challenges, and the association with persistent left superior vena cava (PLSVC), emphasizing the utility of imaging modalities such as Echocardiography, Computed Tomography, Magnetic Resonance Imaging and Venography. For management, anticoagulation remains the cornerstone of treatment for CST, with surgical thrombectomy reserved for severe or refractory cases. Post-treatment follow-up is highlighted as essential for monitoring recurrence and managing complications. In brief, the aim of this review is to enhance the understanding of CST and improve clinical outcomes through early recognition, tailored interventions, and multidisciplinary care.

To investigate the relationship of preoperative high-sensitivity cardiac troponin T (hs-cTnT) with early postoperative hypoxemia (EPH) following off-pump coronary artery bypass grafting (OPCAB). Records of patients undergoing OPCAB between 2018 and 2022 were reviewed. Baseline characteristics and postoperative arterial blood gas analysis were derived from the cardiovascular surgery electronic medical records. Preoperative hs-cTnT levels were measured routinely in all patients. Logistic regression analyses were performed to test the association of preoperative hs-cTnT with EPH. A total of 318 OPCAB patients were included, who had a preoperative hs-cTnT test available for review. Before surgery, 198 patients (62%) had a rise in hs-cTnT level (≥14 ng/L) and 127 patients (40%) had a more severe hs-cTnT level (≥25 ng/L). The preoperative hs-cTnT level was associated with EPH (odds ratio per ng/L, 1.86; 95% confidence interval 1.30–2.68; p < 0.001), prolonged intensive care unit stay (odds ratio, 1.58; 95% confidence interval 1.08–2.32; p = 0.019), and delayed extubating time (odds ratio, 1.63; 95% confidence interval 1.15–2.34; p = 0.007). On multivariable analysis, adjusted for BMI, hypertension, smoking status, serum creatinine, and cardiac function, preoperative hs-cTnT remained an independent factor associated with EPH. Elevation of hs-cTnT concentrations are significantly associated with EPH after OPCAB. Review of presurgical hs-cTnT concentration may help identify patients who would benefit from OPCAB to improve surgical risk assessment.