Myocardial ischemia remains one of the principal causes of mortality and morbidity worldwide, necessitating novel approaches to facilitate early diagnosis and subsequent risk evaluation following reperfusion. Although advancements in wearables capable of ECG (electrocardiogram) monitoring have been initiated, these devices have encountered barriers due to limited capacities to encapsulate the temporally complex nature of ischemic events, notably in risk stratifying reperfusion injury. In this paper, we describe a framework that leverages bionic, wearable ECG sensor technologies along with multimodal large language models using a coherent temporal modeling effort to address the intertwining of fine-grained temporal dependencies, heterogeneous biomedical modalities, and interpretable risk stratification. Our temporally hierarchical fusion transformer utilizes a cross-granularity attention mechanism to model intrabeat, interbeat, and long-term dependencies all simultaneously. The validation of our system was carried out using 4 datasets across n = 108,778 patients, 17,173 of whom were ischemia-positive cases (4,627 from PTB-XL, 5,243 from MIMIC-Ⅳ, 6,891 from CODE-15%, and 412 in the wearable cohort). The area under receiver operating characteristic curve (AUROC) for the model for ischemia was 0.947, and the C-index for post-reperfusion risk stratification was 0.923, with a relative AUROC improvement of 4.8% to 9.5% over the best baseline in each dataset. Importantly, we achieved an average lead time of 18.4 min prior to the ischemic event to allow the clinician to enact interventions. Ultimately, this research demonstrates a prototype of an intelligent cardiovascular care monitoring system that couples advanced sensing with clinical decision support.

Atherosclerosis is a chronic inflammatory metabolic disease with a complex pathogenesis. However, the exact details of its pathogenesis are still unclear, which limits effective clinical treatment of atherosclerosis. Recently, multiple studies have demonstrated that the gut microbiota plays a pivotal role in the onset and progression of atherosclerosis. This review discusses possible treatments for atherosclerosis using the gut microbiome as an intervention target and summarizes the role of the gut microbiome and its metabolites in the development of atherosclerosis. New strategies for the treatment of atherosclerosis are needed. This review provides clues for further research on the mechanisms of the relationship between the gut microbiota and atherosclerosis.

Percutaneous coronary interventions have progressed through the era of plain balloon dilation, bare-metal stent insertion to drug-eluting stent treatment, which has significantly reduced the acute occlusion and restenosis rates of target vessels and improved patient prognosis, making drug-eluting stents the mainstream interventional treatment for coronary artery disease. In recent years, drug-coated balloons (DCBs) have become a new treatment strategy for coronary artery disease, and the drugs used in the coating and the coating technology have progressed in the past years. Without permanent implant, a DCB delivers antiproliferative drugs rapidly and uniformly into the vessel wall via the excipient during a single balloon dilation. Many evidence suggests that DCB angioplasty is an effective measure for dealing with in-stent restenosis and de novo lesions in small coronary vessels. As more clinical studies are published, new evidence is emerging for the use of DCB angioplasty in a wide range of coronary diseases, and the indications are expanding internationally. Based on the latest research from China and elsewhere, the Expert Writing Committee of the Chinese Expert Consensus on Clinical Applications of Drug-Coated Balloon has updated the previous DCB consensus after evidence-based discussions and meetings in terms of adequate preparation of in-stent restenosis lesions, expansion of the indications for coronary de novo lesions, and precise guidance of DCB treatment by intravascular imaging and functional evaluation.

N6-methyladenosine (m6A) RNA methylation is an emerging area of epigenetics, which is a reversible and dynamic modification mediating by 'writers' (methylase, adding methyl groups, METTL3, METTL14, and WTAP), 'erasers' (demethylase, deleting methyl groups, FTO and ALKBH5), and 'readers' (YTHDF1-3, YTHDC1 and YTHDC2). Recent studies in human, animal models and cell levels have disclosed a critical role of m6A modification in regulating the homeostasis of metabolic processes and cardiovascular function. Evidence from these studies identify m6A as a candidate of biomarker and therapeutic target for metabolic abnormality and cardiovascular diseases (CVD). Comprehensive understanding of the complexity of m6A regulation in metabolic diseases and CVD will be helpful for us to understand the pathogenesis of CVD. In this review, we discuss the regulatory role of m6A in metabolic abnormality and CVD. We will emphasize the clinical relevance of m6A dysregulation in CVD.