The development of nanomaterials for delivering natural compounds has emerged as a promising approach for atherosclerosis therapy. However, premature drug release remains a challenge. Here, we present a ROS-responsive biomimetic nanocomplex co-loaded with Geniposide (GP) and Emodin (EM) in nanoliposome particles (LP NPs) for targeted atherosclerosis therapy. The nanocomplex, hybridized with the macrophage membrane (Møm), effectively evades immune system clearance and targets atherosclerotic plaques. A modified thioketal (TK) system responds to ROS-rich plaque regions, triggering controlled drug release. In vitro, the nanocomplex inhibits endothelial cell apoptosis and macrophage lipid accumulation, restores endothelial cell function, and promotes cholesterol effluxion. In vivo, it targets ROS-rich atherosclerotic plaques, reducing plaque area ROS levels and restoring endothelial cell function, consequently promoting cholesterol outflow. Our study demonstrates that ROS-responsive biomimetic nanocomplexes co-delivering GP and EM exert a synergistic effect against endothelial cell apoptosis and lipid deposition in macrophages, offering a promising dual-cell therapy modality for atherosclerosis regression.

PCSK9, which is closely related to atherosclerosis, is significantly expressed in vascular smooth muscle cells (VSMCs). Moreover, Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) mediated phenotypic transformation, abnormal proliferation, and migration of VSMCs play key roles in accelerating atherosclerosis. In this study, by utilizing the significant advantages of nano-materials, a biomimetic nanoliposome loading with Evolocumab (Evol), a PCSK9 inhibitor, was designed to alleviate atherosclerosis. In vitro results showed that (Lipo + M)@E NPs up-regulated the levels of α-SMA and Vimentin, while inhibiting the expression of OPN, which finally result in the inhibition of the phenotypic transition, excessive proliferation, and migration of VSMCs. In addition, the long circulation, excellent targeting, and accumulation performance of (Lipo + M)@E NPs significantly decreased the expression of PCSK9 in serum and VSMCs within the plaque of ApoE^−/− mice.

Acute coronary syndrome (ACS) encompasses a spectrum of cardiovascular emergencies arising from the obstruction of coronary artery blood flow and acute myocardial ischemia. Recent studies have revealed that thyroid function is closely related to ACS. However, only a few reports of thyrotoxicosis-induced ACS with severe atherosclerosis have been reported. A 33-year-old man, who had a history of hyperthyroidism without taking any antithyroid drugs and no history of coronary heart disease, experienced neck pain with occasional heart palpitations starting 3 mo prior that were aggravated after an activity. As the symptoms worsened at 21 d prior, he went to a hospital for treatment. The electrocardiogram examination showed a multilead ST segment elevation and pathological Q waves. Based on these findings and his symptoms, the patient was diagnosed with a suspected myocardial infarction and transferred to our hospital on July 2, 2020. He was diagnosed with a rare case of ACS due to coronary artery atherosclerosis in the anterior descending artery complicated by hyperthyroidism. A paclitaxel-coated drug balloon was used for treatment to avoid the use of metal stents, thus reducing the time of antiplatelet therapy and facilitating the continued treatment of hyperthyroidism. The 9-mo follow-up showed favorable results. This case highlights that atherosclerosis is a cause of ACS that cannot be ignored even in a patient with hyperthyroidism.

BACKGROUND With the development of percutaneous coronary intervention (PCI), the number of interventional procedures without implantation, such as bioresorbable stents (BRS) and drug-coated balloons, has increased annually. Metal drug-eluting stent unloading is one of the most common clinical complications. Comparatively, BRS detachment is more concealed and harmful, but has yet to be reported in clinical research. In this study, we report a case of BRS unloading and successful rescue. CASE SUMMARY This is a case of a 59-year-old male with the following medical history: “Type 2 diabetes mellitus” for 2 years, maintained with metformin extended-release tablets, 1 g PO BID; “hypertension” for 20 years, with long-term use of metoprolol sustained-release tablets, 47.5 mg PO QD; “hyperlipidemia” for 20 years, without regular medication. He was admitted to the emergency department of our hospital due to intermittent chest pain lasting 18 hours, on February 20, 2022 at 15: 35. Electrocardiogram results showed sinus rhythm, ST-segment elevation in leads I and avL, and poor R-wave progression in leads V1–3. High-sensitivity troponin I level was 4.59 ng/mL, indicating an acute high lateral wall myocardial infarction. The patient’s family requested treatment with BRS, without implantation. During PCI, the BRS became unloaded but was successfully rescued. The patient was followed up for 2 years; he had no episodes of angina pectoris and was in generally good condition. CONCLUSION We describe a case of a 59-year-old male experienced BRS unloading and successful rescue. By analyzing images, the causes of BRS unloading and the treatment plan are discussed to provide insights for BRS release operations. We discuss preventive measures for BRS unloading.

Heart failure (HF) continues to pose a significant global health burden, necessitating accurate prognostic tools to guide patient management. This mini-review presents grading systems, frailty scales, and scoring models, followed by challenges and future directions. We traces the evolution of stratification and prognostic assessments in HF, beginning with the foundational NYHA functional classification and progressing to the advanced prognostic scores currently in use. We examine the historical significance and clinical relevance of NYHA grades, which have long been pivotal in evaluating HF severity. The review then shifts focus to contemporary prognostic scores, including the Seattle Heart Failure Model (SHFM), the Heart Failure Survival Score (HFSS), and emerging tools leveraging machine learning (ML) and big data. We explore specific challenges encountered in current clinical practice and outline future directions. By highlighting the strengths and limitations of these tools, this mini-review aims to provides a critical appraisal of stratification and scoring models for HF to inform their optimal application in clinical practice, ultimately enhancing patient care and outcomes in HF.

Background: Ischemic heart failure (IHF) severely impacts patients’ quality of life and leads to frequent hospitalizations, increased healthcare costs, and increased mortality rates, thus posing a substantial global health challenge. Myocardial ischemia is a primary trigger of HF. Yixintai granules (YXT), a traditional Chinese medicine (TCM) formulation, have demonstrated clinical benefits in HF treatment; however, their underlying mechanisms remain unclear. Methods: The components of YXT absorbed into the blood were identified using ultra-high-performance liquid chromatography coupled with mass spectrometry (UHPLC-MS/MS). The key regulatory mechanisms underlying its therapeutic effects on HF were clarified using network pharmacology, and the binding affinity of key YXT components to proteins associated with the LPS/TLR4/NF-κB pathway was assessed through molecular docking. In vivo experiments involved the establishment of an HF rat model through the ligation of the left anterior descending coronary artery. In vitro experiments utilized an H9C2 cell injury model induced by lipopolysaccharide (LPS), which was subsequently treated with YXT-containing serum. Results: UHPLC-MS/MS analysis identified 2,581 active components in the YXT and 1,055 active components in the YXT-containing serum. Network pharmacology indicated that the expression of pro-inflammatory cytokines mediated by the LPS/TLR4/NF-κB pathway and glucolipid metabolic disorders may significantly contribute to the anti-HF effects of YXT. Subsequent in vivo experiments revealed that YXT enhanced cardiac function, reduced myocardial fibrosis, and improved mitochondrial morphology in HF rats. Additionally, it lowered inflammatory cytokine levels and was associated with altered glucose and lipid metabolic profiles and inhibition of the LPS/TLR4/NF-κB signaling pathway. In vitro experiments revealed that YXT-containing serum alleviated LPS-induced H9c2 cardiac cell injury, reduced reactive oxygen species and inflammatory cytokine levels, and was associated with altered glucose and lipid metabolic profiles and inhibition of the LPS/TLR4/NF-κB signaling pathway. Conclusion: YXT improved cardiac function and attenuated fibrosis and ultrastructural damage in IHF rats, with effects associated with LPS/TLR4/NF-κB signaling inhibition, reduced inflammation, and altered glucose/lipid metabolic profiles.