Cardiovascular disease, particularly coronary artery disease, is the leading cause of death in humans worldwide. Coronary heart disease caused by chemotherapy affects the prognosis and survival of patients with tumors. The most effective chemotherapeutic drugs for cancer include proteasome inhibitors, tyrosine kinase inhibitors, immune checkpoint inhibitors, 5-fluorouracil, and anthracyclines. Animal models and clinical trials have consistently shown that chemotherapy is closely associated with coronary events and can cause serious adverse cardiovascular events. Adverse cardiovascular events after chemotherapy can affect the clinical outcome, treatment, and prognosis of patients with tumors. In recent years, with the development of new chemotherapeutic drugs, new discoveries have been made about the effects of drugs used for chemotherapy on cardiovascular disease and its related mechanisms, such as inflammation. This review article summarizes the effects of chemotherapeutic drugs on coronary artery disease and its related mechanisms to guide efforts in reducing cardiovascular adverse events during tumor chemotherapy, preventing the development of coronary heart disease, and designing new prevention and treatment strategies for cardiotoxicity caused by clinical tumor chemotherapy.

Purpose The effects of combing evolocumab and statin on the clinical outcome and physiological function of coronary arteries in STEMI patients with non-infarct-related artery (NIRA) disease are still unclear. Methods A total of 355 STEMI patients with NIRA were enrolled in this study, who underwent combined quantitative flow ratio (QFR) at baseline and after 12 months of treatment with statin monotherapy or statin plus evolocumab. Results Diameter stenosis and lesion length were significantly lower in the group undergoing statin plus evolocumab. While the group exhibited significantly higher minimum lumen diameter (MLD), and QFR values. Statin plus evolocumab (OR = 0.350; 95% CI: 0.149–0.824; P = 0.016) and plaque lesion length (OR = 1.223; 95% CI: 1.102–1.457; P = 0.033) were independently associated with rehospitalization for unstable angina (UA) within 12 months. Conclusion Evolocumab combined with statin therapy can significantly improve the anatomical and physiological function of the coronary arteries and downregulate the re-hospitalization rate due to UA in STEMI patients with NIRA.

Fusion genes are recurrent molecular aberrations in acute myeloid leukemia, with signi cant diagnostic and therapeutic value. The identi cation of novel fusion genes provides advanced biomarkers for diagnosis and facilitates the discovery of drug targets. Here we report a male AML patient with presence of PIEZO1::CBFA2T3 and INO80C::SETBP1 fusion genes detected by RNA sequencing. As far as we know, it is the rst time PIEZO1::CBFA2T3 and INO80C::SETBP1 are identi ed in AML patients.

Fusion genes are recurrent molecular aberrations in acute myeloid leukemia, with significant diagnostic and therapeutic value. The identification of novel fusion genes provides advanced biomarkers for diagnosis and facilitates the discovery of drug targets. Here we report a male AML patient with presence of PIEZO1::CBFA2T3 and INO80C::SETBP1 fusion genes detected by RNA sequencing. As far as we know, it is the first time PIEZO1::CBFA2T3 and INO80C::SETBP1 are identified in AML patients.

Background The relationship between serum IL-38 and major adverse cardiovascular events (MACE) in patients with ST elevation myocardial infarction (STEMI) remains unclear. Methods In the present study, 589 STEMI patients were included, the serum level of IL-38 was measured. The median follow-up time was 720 days, the STEMI patients were divided into high IL-38 (IL-38>6.49ng/mL) and low IL-38 groups (IL-38≤6.49ng/mL) to compare the probability of MACE. Results Plasma IL-38 levels were significantly lower in STEMI patients than in SAP patients (4.0±2.2 vs 6.9±3.2 ng/mL, P < 0.001). Ninety-three STEMI patients met the defined MACE study endpoint. The incidence of MACE was significantly lower in patients with high IL-38 group than in patients with low IL-38 group (7.8% vs 23.7%, P < 0.001). Low plasma IL-38 levels were independently associated with the occurrence of MACE (OR = 0.90, P < 0.001). Conclusion We get a conclusion that low plasma levels of IL-38 are independently associated with the occurrence of MACE.