Introduction: Diabetes mellitus is a major risk factor for myocardial infarction (MI), yet its molecular mechanisms exacerbating post-MI cardiac remodeling remain unclear.Methods: Type 2 diabetes mellitus mouse model was developed through a high-sugar and high-fat diet (HFD), followed by MI surgery. Four weeks post-surgery, cardiac function was evaluated via echocardiography, and cardiac pathology was examined using Masson's trichrome and wheat germ agglutinin staining. High-throughput sequencing identified differentially expressed mRNAs and long non-coding RNAs (LncRNAs) in diabetic mice with MI. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, along with LncRNA-target-gene analysis, were performed. Validation in human samples of diabetic patients with STEMI confirmed the influence of HFD on the expression of specific genes.Results: The results demonstrate that diabetes significantly impairs cardiac function, exacerbates cardiac fibrosis and hypertrophy. In addition, our extensive examination of human samples has conclusively demonstrated that diabetes significantly modulates the expression of genes (Rapgef5 and Ing1) within the cardiac tissue of individuals afflicted with STEMI, underscoring the intricate interplay between these conditions. In addition, we have found that Rapgef5 and Ing1 are involved in diabetes-mediated cardiomyocyte apoptosis and proliferation following myocardial infarction.Discussion: Diabetes aggravates post-MI remodeling via Rapgef5/Ing1-mediated apoptosis and proliferation, these findings highlight novel therapeutic targets for diabetic cardiovascular complications.

Background: Vascular calcification predicts adverse cardiovascular outcomes. CTRP9, an adiponectin paralog, has vascular protective effects. We evaluated the association of circulating CTRP9 with aortic valve calcification (AVC) and coronary artery calcification (CAC) in a cross-sectional observational study. Methods: Nine hundred coronary heart disease patients underwent echocardiography and optical coherence tomography; serum CTRP9 was measured in a subset. Logistic regression identified CAC determinants. ROC analysis assessed CTRP9 alone and combined with AVC for predicting severe CAC. AVC was modeled in ApoE−/− mice fed a Western diet for 24 weeks, with calcification markers analyzed via PCR and Western blot. Results: CTRP9 independently protected against CAC (OR = 0.156, 95% CI: 0.11–0.21, p < 0.05). CTRP9 predicted CAC severity (AUC = 0.74), and combining it with AVC improved prediction of severe CAC (AUC = 0.843). Kendall’s Tau-b indicated strong correlation between severe AVC and CAC (τb = 0.597, p < 0.001). Exogenous CTRP9 attenuated aortic valve calcification in mice. Conclusion: Lower CTRP9 levels associate with advanced AVC and greater CAC severity. Combining CTRP9 with AVC enhances risk prediction, highlighting CTRP9 as a potential biomarker and therapeutic target in vascular calcification.

Left main coronary artery (LMCA) spasm is an exceedingly rare but potentially fatal condition. We present a case of severe stenosis of LMCA found by coronary angiography (CAG) due to recurrent chest pain, and subsequently received coronary artery bypass grafting (CABG). Nine years later, the patient was readmitted to the hospital because of precordial discomfort. During hospitalization, CAG was performed once again and showed no significant stenosis in the LMCA, leading to the diagnosis of LMCA spasm. This case emphasizes to interventional cardiologists the critical need to consider the possibility of LMCA spasm when diagnosing LMCA lesions. It highlights the importance of thorough and proactive pretreatment and comprehensive clinical judgment to minimize the risk of misdiagnosis.