2 ± 13.6 versus 81.4 ± 18.4, P = 0.003), and borderline differences in angina stability (61.2 ± 26.5 versus 51.0 ± 23.7, P = 0.046) compared to patients in the OMT group. There were no significant differences in SAQ scores in the OMT group at baseline and during the FUP. There was a statistically significant increase in all five domains in the PCI group.Symptoms and QoL measured by the SAQ were significantly improved after CTO PCI compared to OMT alone.The aim of this study was to explore the pivotal genes or lncRNAs involved in the progression of atrial fibrillation (AF) -valvular heart disease (VHD). The mRNA profiling GSE113013 was obtained from the Gene Expression Omnibus database. The identification of differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs) was performed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were carried out for DEGs. Then, the construction of the protein-protein interaction (PPI) network was conducted. An lncRNA-miRNA-target ceRNA network was constructed after obtaining microRNAs (miRNA) related to DElncRNAs. Ultimately, key disease-related genes were screened. A total of 399 DEGs and 145 DElncRNAs were obtained. There were 283 nodes and 588 interaction pairs in the PPI network, and synaptosome-associated protein 25 (SNAP25) had higher degrees (degree = 22) in the PPI network. There were 65 interaction pairs in the ceRNA network. Here, Baculoviral IAP Repeat Containing 5 (BIRC5) was regulated by hsa-miR-1285-3p, which was regulated by lncRNA NPHP3-AS1. Gap Junction Protein Alpha 5 (GAJ5) was regulated by hsa-miR-4505, hsa-miR-1972, and hsa-miR-1199-5p. In particular, GAJ5 was enriched in the function of ion transmembrane transport regulation, whereas BIRC5 was enriched in the function of apoptosis-multiple species pathway. selleck kinase inhibitor Similarly, Potassium Inwardly Rectifying Channel Subfamily J Member 6 (KCNJ6) was enriched in the function of an ion channel complex. VENN analysis identified BIRC5 and GJA5 as key AF-related genes. KCNJ6, SNAP25, GJA5, BIRC5, hsa-miR-1285-3p, and lncRNA NPHP3-AS1 were likely to be associated with AF-VHD development.Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is erupting and spreading globally. Cardiovascular complications secondary to the infection have caught notice. This study aims to delineate the relationship of cardiac biomarkers and outcomes in severe cases of corona virus disease 2019 (COVID-19). One hundred forty-eight critically ill adult patients with COVID-19 were enrolled. From these patients, the demographic data, symptoms, cardiac biomarkers, treatments, and clinical outcomes were collected. Data were compared between survivors and non-survivors. Four patients in the non-survivor group were selected, and their cardiac biomarkers were collected and analyzed. Among the 148 patients, the incidence of cardiovascular complications was 19 (12.8%). Five of them were survivors (5.2%), and 14 of them were non-survivors (26.9%). Compared with the survivors, the non-survivors had higher levels of high-sensitivity cardiac troponin I, creatine kinase isoenzyme-MB, myoglobin, and N-terminal pro-brain natriuretic peptide (P less then 0.05). The occurrence of cardiovascular events began at 11-15 days after the onset of the disease and reached a peak at 14-20 days. COVID-19 not only is a respiratory disease but also causes damage to the cardiovascular system. Cardiac biomarkers have the potential for early warning and prognostic evaluation in patients with COVID-19. It is recommended that cardiac biomarker monitoring in patients with COVID-19 should be initiated at least from the 11th day of the disease course.Although it is well known that patients with hypertrophic cardiomyopathy (HCM) have serious adverse events, such as life-threatening arrhythmia and heart failure, the prediction of such evens is still difficult. Recently, it has been reported that one of the causes of these serious adverse events is microvascular dysfunction, which can be noninvasively evaluated by employing cardiac magnetic resonance (CMR) imaging.We analyzed 32 consecutive HCM patients via CMR imaging and myocardial scintigraphy and divided them into two groups ventricular tachycardia (VT) group and non-VT group. Myocardial perfusion studies were conducted quantitatively using the QMass® software, and each slice image was divided into six segments. The time-intensity curve derived from the perfusion image by CMR imaging was evaluated, and the time to 50% of the peak intensity (time 50% max) was automatically calculated for each segment.Although no difference was observed in various parameters of myocardial scintigraphy between the two groups, the VT group exhibited a higher mean of time 50% max and wider standard deviation (SD) of time 50% max in each segment than the non-VT group. The cutoff values were obtained by the receiver operating characteristic curves derived from the mean of time 50% max and SD of time 50% max. The two groups divided by the cutoff values exhibited significant differences in the occurrence of serious adverse events.CMR imaging may be useful for predicting serious adverse events of patients with HCM.Tachycardia-induced cardiomyopathy (TIC) is a potentially reversible cardiomyopathy caused by tachyarrhythmia. For atrial flutter (AFL) -induced TIC, a rhythm control strategy, such as catheter ablation, has been recommended. However, the efficacy of rate control has remained unclear due to the difficulty of achieving control using arrhythmic medications.We prospectively assessed 47 symptomatic heart failure (HF) patients with left ventricular ejection fraction (LVEF) less then 50% and suspected persistent AFL-induced TIC. Patients were divided into the rhythm control strategy (n = 22; treatment with catheter ablation or electrical cardioversion) and rate control strategy (n = 25; treatment with bisoprolol) groups. The latter was further divided into the strict rate control strategy (average heart rate less then 80 bpm) and lenient rate control strategy (average heart rate less then 110 bpm) subgroups. The primary outcome was left ventricular (LV) function recovery, which was defined as an increase in LVEF ≥ 20% or to a value of ≥ 55% after 6 months.