Although the use of iodinated contrast for percutaneous coronary intervention (PCI) has known toxicity issues, the association between the contrast volume-to-creatinine clearance (V/CrCl) ratio and perioperative myocardial infarction (PMI) is unclear. The present study is aimed to investigate the predictive value of V/CrCl ratio on the incidence of PMI, and to determine a relatively safe contrast media V/CrCl ratio cut-off value to prevent PMI undergoing elective PCI. The V/CrCl ratio were obtained from 5970 patients undergoing elective PCI for single-vessel lesions. Cardiac troponin I (cTnI) were measured at baseline, 8, 16, and 24 hours after PCI. PMI was defined as postprocedural > 5 × upper limit of normal. Receiver operating characteristic (ROC) curves were performed to identify the optimal sensitivity for the V/CrCl range. Multivariate regression model were used to assess the association between V/CrCl ratios and PMI. Eight hundred and ninety-seven patients (15.0%) developed PMI. There was a significant association between higher V/CrCl ratio and the development of PMI (P < 0.001 for the trend). ROC curve analysis indicated that V/CrCl ratio of 2.05 was a discriminator for PMI (area under the curve = 0.674). After adjusting for other potential risk factors, V/CrCl ratio > 2.05 remained significant associated with PMI (odds ratio, 1.921; 95% confidence interval, 1.311-2.815; P = 0.001). The finding of this study suggests the importance of minimizing the contrast media dose to avoid PMI development. Use of a contrast media dose based on renal function with a V/CrCl value < 2.05 might be valuable in preventing PMI.

Elevated serum uric acid (sUA) is associated with increasing risk of coronary heart disease (CHD). However, existing research is limited by potential confounders. Herein, our study aims to probe the association between sUA levels and the morphological characteristics of coronary plaque by a propensity score matching (PSM) analysis.

All 420 patients with CHD who had undergone optical coherence tomography of culprit lesions were included. Eligible patients were assigned into 2 groups according to sUA level: high-sUA group (sUA ≥ 6.0 mg/dL) and low-sUA group (sUA < 6.0 mg/dL). PSM was applied to control the balance of baseline characteristics.

After PSM, a total of 112 patients were included in our study (56 in each group). The high-sUA group showed a higher prevalence of TCFA (35.7% versus 16.1%, P = 0.03) and macrophage infiltration (33.9% versus 14.3%, P = 0.026) compared with the low-sUA group. Plaques in the high-sUA group had a wider maximum lipid arc (166.51° (115.77°, 224.14°) versus 142.29° (93.95°, 169.06°), P = 0.048), longer calcification length (6.77 (3.90, 20.55) mm versus 4.20 (1.95, 7.45) mm, P = 0.040), and thinner minimum fibrous cap thickness (43.81 (28.17, 62.26) μm versus 92.57 (46.25, 135.37) μm, P = 0.003). Correlation analysis indicated that the sUA value was inversely associated with the minimum fibrous cap thickness (r = −0.332, P = 0.015) and positively associated with the maximum lipid arc (r = 0.399, P = 0.003), average lipid arc (r = 0.347, P = 0.011), and calcification length (r = 0.386, P = 0.006).

The relationship between high-sUA levels and typical vulnerable features of plaques persisted after balancing the traditional risk factors.

Nonalcoholic fatty liver disease (NAFLD) is an emerging driver of cardiac arrhythmias. However, the relationship between NAFLD and malignant arrhythmia in non-ST-segment elevation myocardial infarction (NSTEMI) patients is still unclear.

In this study, 358 NSTEMI inpatients were enrolled. They all received 24-hour Holter monitoring after percutaneous coronary intervention. All inpatients were divided into two groups: the non-NAFLD group (236 cases, 65.9%) and the NAFLD group (122 cases, 34.1%). Compared with the non-NAFLD group, the NAFLD group had a significantly higher incidence of PVCs/hour > 5 (premature ventricular complexes, 32.0% versus 9.3%, P < 0.001), ventricular tachycardia (VT, 22.1% versus 5.9%, P < 0.001), and sinus arrest (SA, 7.4% versus 1.3%, P = 0.002). We found that NAFLD was closely associated with the occurrence of VT [unadjusted odds ratio (OR) 4.507, 95% confidence interval (CI) 2.263-8.974, P < 0.001] and SA (OR 6.186, 95%CI 1.643-23.291, P = 0.007). After adjusting for age, sex, body mass index, and other confounding factors, the above differences were still statistically significant (VT: OR 4.808, 95%CI 2.254-10.253, P < 0.001; SA: OR 9.589, 95%CI 2.027-45.367, P = 0.004).

NAFLD is associated with the occurrence of VT and SA in NSTEMI patients. It indicates that NAFLD might be a risk factor for malignant arrhythmias in post-NSTEMI patients.

N-terminal pro-B-type natriuretic peptide (NT-proBNP) is suggested to be altered in patients with systolic heart failure or acute coronary syndrome. We explored the relationship between left ventricular ejection fraction (LVEF) and levels of NT-proBNP in patients with unstable angina and type 2 diabetes mellitus and preserved LVEF.

Patients with unstable angina were divided into normal glucose tolerance (controls) and type 2 diabetes mellitus groups. The plasma NT-proBNP concentration was measured in these patients within 30 minute of admission for a comparative study. The severity of coronary arterial lesions was evaluated using Syntax scores. Results: NT-proBNP levels were not significantly different in patients with unstable angina and type 2 diabetes mellitus (median [quartiles]: 167.0 [66.1, 623.3] pg/mL) from those of controls (116.0 [69.8, 233.0], P = 0.278). Subsequent analyses indicated that ln (NT-proBNP) was positively associated with the following parameters: left ventricular end-diastolic diameter (r = 0.495, P = 0.019), left ventricular end-systolic diameter (r = 0.648, P = 0.001), and Syntax score (r = 0.567, P = 0.006); ln (NT-proBNP) was negatively associated with LVEF (r = −0.652, P = 0.001) in patients with unstable angina and type 2 diabetes mellitus. In multiple linear regression analysis, ln (NT-proBNP) levels were significantly independently correlated with the LVEF and Syntax score. However, no correlation was observed between ln (NT-proBNP) and each parameter in patients with unstable angina and normal glucose tolerance (controls).

The NT-proBNP level is independently correlated with the LVEF in patients with unstable angina and type 2 diabetes mellitus and preserved LVEF.

The efficacy of direct current (DC) cardioversion before catheter ablation (CA) for persistent atrial fibrillation (PerAF) patients remains controversial. We hypothesized that maintenance of sinus rhythm (SR) by pre-ablation DC cardioversion may predict the outcome of CA in patients with PerAF. A total of 383 PerAF patients with no or mild symptoms (EHRA I/II) who had undergone DC cardioversion before CA (301 males, 65 ± 10 years old, mean atrial fibrillation (AF) duration: 25 ± 47 months) were retrospectively enrolled. Whether or not SR was maintained at least 24 hour after DC cardioversion, patients were divided into two groups, namely, the DC-SR group and DC-AF group, and then all were followed until AF recurrence after CA. After DC cardioversion, 281 (73%) patients were categorized into the DC-SR group, and 102 (27%) were categorized into the DC-AF group. A total of 195 patients underwent CA at an average of 83 (54-145) days after DC cardioversion, including 161 (83%) in the DC-SR group and 34 (17%) in the DC-AF group. During follow-up (median: 15 [10-25] months), the number of patients who were free from AF was significantly higher in the DC-SR group compared with the DC-AF group (61.5% versus 38.3%, P < 0.0001). Multivariate analysis revealed that the DC-SR group (hazard ratio [HR]: 0.45, 95% confidence interval [CI]: 0.21-0.99, P = 0.047) and age at first AF diagnosis (HR: 0.95, 95% CI: 0.91-1.00, P = 0.039) were the independent predictors for being AF-free after CA. In conclusion, the 24-hour rhythm outcome of pre-ablation DC cardioversion and age at first AF diagnosis may predict the recurrence of AF after CA in patients with PerAF.

To compare the effects of dexmedetomidine (DEX) pretreatment, posttreatment, and whole-course pumping on myocardial protection during cardiac valve replacement.

One hundred and twenty patients undergoing cardiac valve replacement were randomly divided into the follow groups: DEX pretreatment (D1 group), DEX posttreatment (D2 group), DEX whole-course pumping (D3 group), and Control (C group). The concentrations of cardiac troponin I (cTnI), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), rate of spontaneous heart rebound after aortic opening, time to heart rebound, incidence of arrhythmia, and use of sufentanil and vasoactive drugs were recorded.

Compared with group C, the concentrations of cTnI, MDA, and TNF-α in the D1, D2, and D3 groups were lower, especially in the latter. The time to heart rebound was prolonged in all three groups (P < 0.05). The rate of automatic rebound was increased (P < 0.05) while the incidence of arrhythmia was decreased (P < 0.05) in all groups compared with group C. Group D3 had the highest rate of automatic rebound and the lowest incidence of arrhythmia. Compared with groups C and D2, the use of sufentanil and dopamine was lower in groups D1 and D3 (P < 0.05), especially in the latter.

During cardiac valve replacement, DEX pretreatment, posttreatment, and whole-course pumping could have myocardial protective effects. The latter showed better effects.

Data on the combined use of aortic Inoue-Balloon catheter and self-expandable transcatheter valve for patients undergoing transcatheter aortic valve replacement (TAVR) are lacking. This study aimed to assess the feasibility and safety of this combination, particularly in patients who cannot be safely managed with balloon-expandable valves.

Between 2018 and 2021, 140 consecutive patients who had Inoue-Balloon catheters with self-expandable valves were retrospectively examined. Self-expandable transcatheter valves were deployed using the heart team approach in patients with calcification on the left ventricular outflow tract, which could not be safely addressed with the current-generation balloon-expandable valves.

The 20- and 22 mm Inoue-Balloon catheters were used with the 26- and 29 mm Evolut valves, respectively. According to the Valve Academic Research Consortium-2 criteria, the procedural success rate was 95.0%, with an early safety at 30 days rate of 6.5%. A total of 27 patients required post-dilation with the same Inoue-Balloon catheter used for pre-dilation after adjustment to appropriate sizes. Post-dilation, with balloon size adjusted to be 1.4 ± 0.9 mm larger than that in pre-dilation, was effective in 19 out of 27 patients (70.3%) for decreasing paravalvular leak after transcatheter valve deployment. The procedural complication rates between patients with and without post-dilation were not different.

The combined use of the size-adjustable Inoue-Balloon catheter and self-expandable valve is safe, particularly in patients who cannot be safely managed with balloon-expandable valves. However, further studies are warranted to elucidate concerns regarding the durability of self-expandable transcatheter valves after post-dilation using the Inoue-Balloon catheter.

It was unclear whether there are discrepancies among the efficacy and safety of different doses of empagliflozin in patients with heart failure with reduced ejection fraction (HFrEF). The aim of this study was to compare the efficacy and safety of 25 mg and 10 mg of empagliflozin in HFrEF patients.

In this 3-month, single-center, open-label, randomized, positive-controlled, parallel-group study, 100 patients with HFrEF were divided into two groups, namely, groups A (n = 50) and B (n = 50), which were given 25 mg/day and 10 mg/day of empagliflozin, respectively. Cardiac function indexes at baseline and at the end of the third month were compared between the two groups, as well as adverse events during the 3-month follow-up period. The primary outcome of this study was the change in the left ventricular ejection fraction (LVEF), and the secondary outcomes were the change in the left ventricular end-diastolic diameter (LVEDD) and the incidences of hypotension, acute kidney injury (AKI), and genitourinary infections.

At the end of the third month, the changes in the LVEF and LVEDD were greater in group A than those in group B (P < 0.05). During the 3-month follow-up period, the differences in the incidences of hypotension, AKI, and genitourinary infections between the two groups were statistically insignificant (P > 0.05).

The results from this study suggested that 25 mg of empagliflozin might be better than 10 mg in improving heart function in HFrEF patients, and the safety profiles of 25 mg and 10 mg of empagliflozin are comparable. Further studies are expected to substantiate our speculations.

A high prevalence of heavy menstrual bleeding (HMB) has been reported in women with Fontan circulation. Cyanosis has been reported to contribute to HMB, and menstruation has been suggested to affect cardiac status in women with congenital heart disease. This study aimed to evaluate the relationship between the amount of menstrual flow and cardiac status in women with Fontan circulation.

Twenty women who had undergone the Fontan procedure were prospectively investigated and the amount of their menstrual flow was evaluated using a questionnaire. Participants were divided into two groups-small and large menstrual bleeding groups-and their clinical data, including the results of hematological tests and echocardiographic findings, were evaluated.

One (5%) woman showed primary amenorrhea. Eight of the remaining 19 (42%) women were included in the large menstrual bleeding group. Women with large menstrual bleeding showed a significantly higher hematocrit level (47.1% [36.2%-50.3%] versus 42.1% [35.3%-44.9%], P = 0.006) and longer QRS duration (106 [92-172] ms versus 88 [78-140] ms, P = 0.008), as well as a lower fractional area change (37.4% [35.6%-47.2%] versus 47.0% [38.2%-55.7%], P = 0.010) and global longitudinal strain (−10.5% [−14.9% to −6.6%] versus −13.9% [−20.5% to −7.8%], P = 0.041) of the dominant ventricle on echocardiography, than women with small bleeding.

Erythrocytosis, longer QRS duration, and reduced ventricular function were related to increased menstrual bleeding in women with Fontan circulation. These functions may be interrelated with the amount of menstrual flow in such women.

In patients with atrial septal defect (ASD), atrial left-to-right shunting causes left atrial (LA) remodeling and dysfunction, leading to atrial fibrillation (AF). In adults with ASD and concomitant AF, LA function should be evaluated after ASD closure plus AF radiofrequency catheter ablation (RFCA).

This multicenter retrospective cohort study included patients who underwent transcatheter ASD closure at one of the four leading hospitals. Patients with a history of AF also underwent preceding RFCA. The association between AF history and LA ejection fraction (EF) (indicating LA global function) at 6-12 months following ASD closure was evaluated. To account for differences in baseline characteristics between patients with and without a history of AF, we conducted the following statistical methods: (1) multivariate regression analysis in the prepropensity score (PS)-matched cohort and (2) univariate comparisons in the PS-matched cohort.

Overall, this study included 231 patients (30 with AF history, 201 without). Multiple regression analysis showed that AF history was independently associated with impaired LAEF (β = −10.425, P < 0.001, model created prior to propensity matching). A one-to-one PS matching (25 pairs) showed that the LAEF at 6-12 months following ASD closure was significantly impaired in patients with ASD and AF history compared to that in patients without history of AF (median LAEF, 37.5% (interquartile range [IQR] 29.4%-48.5%) versus 52.3 [IQR 50.0%-56.6%]; P < 0.001).

LA function was impaired in patients with ASD and a history of AF at 6-12 months after successful transcatheter ASD closure and on maintenance of sinus rhythm by RFCA.

Catheter-directed intra-arterial thrombolysis (CDT) is useful for not only patients with acute limb ischemia but also those with chronic total occlusions (CTOs) of the lower extremity arteries. However, it is difficult to determine whether CTO lesions have significant thrombi, which can be treated by CDT, or not in a clinical setting. Angioscopy can accurately detect thrombi. We investigated the clinical impact of angioscopy guided endovascular therapy following thrombolysis (AGET) for in-stent occlusions (ISOs) in iliac or femoropopliteal arteries.

We performed AGET in 7 patients with ISOs whose occlusion duration was less than 1 year. We performed angioscopy to evaluate the area of the thrombi after a successful wire crossing of an ISO lesion. In addition, we performed biopsies of ISO lesions to confirm whether the angioscopic findings coincided with the histopathological findings at 20 sites. We selectively performed a continuous infusion of urokinase using a fountain infusion catheter for ISO lesions. The next day, we evaluated the lesion flow and performed intervention only at the plaque stenosis site if necessary.

AGET could achieve TIMI 3 flow in all patients, and preserved a 1-year patency in 5 patients (71.4%). The angioscopic findings of thrombi and plaque perfectly coincided with the histopathological findings.

In conclusion, this new endovascular therapy technique, AGET, was observed to be feasible and safe for iliac or femoropopliteal artery ISO lesions.

Ischemic heart disease (IHD) is a prominent global cause of morbidity and death resulting from the narrowing or blockage of cardiac coronary arteries. Exposing isolated cardiac myocytes to hypoxia-reoxygenation (H/R) might be an efficient tool to investigate the etiology and underlying mechanism of myocardial ischemia-reperfusion (I/R) injury. This study found that miR-7015 is upregulated in mouse myocardial tissues after I/R injury and in cardiomyocytes after H/R injury. A model of H/R-induced cardiomyocyte injury was established; miR-7015 overexpression exacerbated while miR-7015 inhibition partially ameliorated H/R-induced cardiomyocyte injury by inhibiting cytokine release, promoting cell viability, and suppressing apoptosis. Bioinformatics and experimental studies have identified nuclear factor-kappa-B-inhibitor alpha (Nfkbia) as a direct downstream target of miR-7015. miR-7015 inhibited Nfkbia expression. Unlike miR-7015 overexpression, Nfkbia overexpression alleviated H/R-induced injury in cardiomyocytes. Moreover, Nfkbia overexpression partially abolished the effects of miR-7015 overexpression on H/R-induced cardiomyocyte injury. In conclusion, the miR-7015/Nfkbia axis modulates cardiomyocyte injury induced by H/R, possibly through the NF-κB signaling.

This study aims to explore the underlying mechanisms of how Pioglitazone (Pio) affects myocardial ischemia-reperfusion (I/R) injury. In this study, after pretreatment of Pio, the pathologic change of myocardial tissues was measured via hematoxylin and eosin staining. The release of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and nitric oxide (NO) were measured. The cardiomyocyte apoptosis was detected via TUNEL assay and flow cytometry assay. The mitochondrial membrane potential (ΔΨm) was estimated using the JC-1 probe. The release of cytochrome c in mitochondria and the translocation of cytochrome c in the cytosol were measured using western blot. Additionally, apoptosis-associated molecules and NOD-like receptor pyrin domain containing-3 (NLRP3)/caspase-1 pathway-related molecules were measured using western blot, quantitative real-time-polymerase chain reaction, and immunofluorescence staining. Results showed that the pretreatment of Pio significantly decreased myocardial tissue damage. Pio pretreatment inhibited the release of creatine kinase and LDH but promoted NO release in serum and H9c2 cell supernatants. Moreover, the pretreatment of Pio notably alleviated cardiomyocyte apoptosis. Pio pretreatment also maintained the mitochondrial membrane potential and prevented cytochrome c release in H/R-induced cardiomyocytes. Additionally, we confirmed that Pio pretreatment inhibited cardiomyocyte apoptosis via repressing the NLRP3/caspase-1 pathway. In conclusion, our study demonstrated that Pio could inhibit myocardial I/R injury and cardiomyocyte apoptosis by inhibiting the activation of the NLRP3/caspase-1 signaling pathway.

Forsythiaside, one of the main bioactive components of Chinese medicine Lian Qiao, exerts antioxidant, anti-bacterial, and anti-inflammatory effects. To date, the mechanism of Forsythiaside in cardiomyocyte injury remains unclear. However, the antioxidant effects of Forsythiaside on cardiac cells are currently unknown. This study investigated the effect and mechanism of Forsythiaside on oxidative stress in H9c2 cardiomyocytes. H9c2 cells were treated with H₂O₂ and Forsythiaside and then transfected with small-interfering RNA against nuclear factor erythroid 2-related factor 2 (siNrf2). Cell viability, apoptosis, accumulation of reactive oxygen species (ROS), and mitochondrial membrane potential were measured using methyl thiazolyl tetrazolium (MTT), terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, fluorescent probe 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA), and rhodamine 123, respectively. The levels of oxidative stress-related markers were determined using their respective detection kits. Furthermore, the levels of apoptosis- and Nrf2 pathway-related molecules were determined via Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Forsythiaside had no obvious toxicity on H9c2 cells. H₂O₂ suppressed the viability, and reduced the levels of mitochondrial membrane potential, B-cell lymphoma-2 (Bcl-2), glutathione peroxidase (GSH-Px) and catalase (CAT) and superoxide dismutase (SOD), while promoted apoptosis, ROS accumulation, and elevated the levels of cleaved caspase 3, BCL2-Associated X (Bax) and malondialdehyde (MDA) in H9c2 cells. Contrarily, Forsythiaside reversed the aforementioned effects. H₂O₂ advanced the levels of cytoplasm Nrf2, heme oxygenase-1 (HO-1), and nucleus Nrf2 in H9c2 cells, whereas Forsythiaside enhanced these effects. SiNrf2 reversed the functions of H₂O₂ or Forsythiaside in cell viability, MDA, SOD, GSH-Px, CAT, Nrf2, and HO-1 in H9c2 cells, whereas Forsythiaside reversed the aforementioned effects of siNrf2. In sum, Forsythiaside protected H9c2 cells from oxidative stress and apoptosis induced by H₂O₂ by activating the Nrf2/HO-1 pathway.

MiR-6870-3p acts as a crucial regulator of gene expression at the posttranscriptional level and participates in immune responses. However, the roles of miR-6870-3p and its target genes and their underlying mechanisms in the inflammatory responses of epicardial adipose tissues (EATs) are unknown.

MiRNA microarray was used to collect the miRNA expression profiles of EATs from five patients with coronary artery disease (CAD) and four individuals without CAD (n-CAD). Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to examine the expression of miR-6870-3p in the EATs. The mRNA and protein expression levels of Tollip and the key genes of the Toll-like receptor 4 (TLR4) signaling pathway were examined by qRT-PCR and Western blot analysis. The levels of inflammatory factors in the cell supernatant were measured by enzyme-linked immunosorbent assay (ELISA). We used a dual-luciferase reporter assay to validate the target gene of miR-6870-3p. The protein expression levels of c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NF-κB) were measured by Western blot analysis.

Our results showed that miR-6870-3p was higher in the CAD EATs than in the n-CAD EATs. MiR-6870-3p was positively correlated with TLR4, interleukin (IL)-6, JNK, NF-κB (p65), and tumor necrosis factor (TNF)-α in the CAD EAT samples. Lipopolysaccharide (LPS) treatment upregulated the miR-6870-3p expression and downregulated the Tollip expression in the macrophages. When the macrophages were stimulated with LPS, MiR-6870-3p upregulation also aggravated the production of proinflammatory cytokines. The result of the luciferase reporter assays confirmed that miR-6870-3p directly targets Tollip. Moreover, miR-6870-3p upregulation in the macrophages resulted in the activation of the JNK/NF-κB pathway.

Our study showed that miR-6870-3p regulates human EAT inflammation by targeting the Tollip-mediated JNK and NF-κB signaling pathways.

The role of endothelial injury and inflammation in atherosclerosis has been well established. miRNAs have been found to be key regulators in the development of atherosclerosis. Here we investigated whether miR-32-5p and its predicted target gene axin interactor, dorsalization associated (AIDA) are involved in endothelial injury and inflammation. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (oxLDL) to induce endothelial injury and inflammation. AIDA was predicted to be a target gene of miR-32-5p using TargetScan software. Cell viability, migration, and angiogenesis were evaluated using Cell Counting Kit-8, wound-healing, and tube formation assays, respectively. The expression of inflammatory factors was detected using quantitative PCR, enzyme-linked immunosorbent assay, and western blot. We found that miR-32-5p expression was significantly decreased, whereas AIDA expression was significantly increased in oxLDL-treated HUVECs and the increased AIDA expression was reversed by the up-regulation of miR-32-5p. Moreover, both miR-32-5p mimic and knockdown of AIDA enhanced cell viability, promoted cell migration and angiogenesis and suppressed the expression of inflammatory factors including IL-1β, IL-6, TNF-α, ICAM-1, and VCAM-1 in oxLDL-induced HUVECs. Furthermore, miR-32-5p was verified to directly target AIDA using dual-luciferase reporter assay. Overall, these findings suggest that miR-32-5p/AIDA signal plays an important role in oxLDL-induced endothelial injury and inflammation. This study provides new insights into novel molecular mechanisms of endothelial dysfunction and atherosclerosis.

Left ventricular dilatation (LVD) and left ventricular hypertrophy (LVH) are risk factors for heart failure, and their detection improves heart failure screening. This study aimed to investigate the ability of deep learning to detect LVD and LVH from a 12-lead electrocardiogram (ECG). Using ECG and echocardiographic data, we developed deep learning and machine learning models to detect LVD and LVH. We also examined conventional ECG criteria for the diagnosis of LVH. We calculated the area under the receiver operating characteristic (AUROC) curve, sensitivity, specificity, and accuracy of each model and compared the performance of the models. We analyzed data for 18,954 patients (mean age (standard deviation): 64.2 (16.5) years, men: 56.7%). For the detection of LVD, the value (95% confidence interval) of the AUROC was 0.810 (0.801-0.819) for the deep learning model, and this was significantly higher than that of the logistic regression and random forest methods (P < 0.001). The AUROCs for the logistic regression and random forest methods (machine learning models) were 0.770 (0.761-0.779) and 0.757 (0.747-0.767), respectively. For the detection of LVH, the AUROC was 0.784 (0.777-0.791) for the deep learning model, and this was significantly higher than that of the logistic regression and random forest methods and conventional ECG criteria (P < 0.001). The AUROCs for the logistic regression and random forest methods were 0.758 (0.751-0.765) and 0.716 (0.708-0.724), respectively. This study suggests that deep learning is a useful method to detect LVD and LVH from 12-lead ECGs.

We retrospectively analyzed major cardiovascular events (MACE), a composite of cardiac death, nonfatal myocardial infarction, unplanned revascularization, heart failure leading to hospitalization, and stroke during a 3-year follow-up of patients with hemodialysis at the dialysis center of our general hospital that can treat comprehensive diseases. Moreover, we conducted an exploratory study that focuses on the risk factor for MACE in patients with hemodialysis.

A total of 132 patients with hemodialysis at our dialysis center as of June 2017 were included in the study. Data on event incidence, including death and various clinical indicators, were collected in the electronic medical record for three years until June 2020. Between June 2017 and June 2020, of the 132 patients with hemodialysis, 31 patients experienced MACE (10 cardiovascular deaths, 3 nonfatal myocardial infarction, 11 unplanned revascularizations, 5 heart failure leading to hospitalization, and 2 stroke). The patients with MACE had a lower body mass index (BMI), longer duration of dialysis with more preexisting gastrointestinal (GI) bleeding, and took more aspirin compared to the MACE-free patients. Malnutrition markers (serum total protein, serum albumin, and serum total cholesterol) were similar in both groups. In a univariate analysis for MACE, the odds ratio was significantly higher for BMI < 18.5, duration of hemodialysis, and history of GI bleeding. Multivariable-adjusted odds ratios for MACE were significantly higher for BMI < 18.5.

In conclusion, BMI < 18.5 without malnutrition may be an independent risk factor for MACE in patients with hemodialysis.

The Senning operation used to be widely performed for an intracardiac repair in a complete transposition of the great arteries. During the long-term follow-up, supraventricular tachycardia (SVT) is often observed because of the complex suture lines. The typical mechanism of a Senning-related SVT is cavo-tricuspid isthmus-dependent atrial flutter. On rare occasions, complex SVTs (e.g., biatrial tachycardia (BiAT)) whose diagnosis and treatment are challenging, may occur. We report a rare case of a BiAT following a Senning operation that was successfully ablated from the superior vena cava, and the local activation time histogram module (CARTO3 V7 module [Biosense Webster, Irvine, CA, USA]) was crucial for analyzing the complex circuit.

The feasibility and safety of left bundle branch area pacing (LBBAP) used in pediatric patients with atrioventricular block (AVB) have not been well demonstrated. Currently, only several case reports for pediatric patients have been published since the advent of LBBAP, with 3 months to 1 year follow-up. Here, we present a case of LBBAP in a 6-year-old child with a high-degree AVB secondary to the transcatheter device closure of congenital ventricular septal defect. No procedure-related complications were observed, and the electrical parameters were stable at 2-year follow-up. Additionally, we performed a systematic literature review on pediatric patients with LBBAP. Fifteen cases were retrieved after systematically searching PubMed and Embase databases. No complications have been reported among these published cases. In conclusion, consistent with previous cases, our case with 2-year follow-up has demonstrated that LBBAP may be an alternative pacing modality from a very early age. However, given the limited evidence, the long-term outcomes of LBBAP in pediatric patients should be further investigated.

Several autoantigens related to inflammatory myopathy have been identified. Antimitochondrial antibody M2 (AMA-M2) is known as one of the serologic hallmarks of primary biliary cholangitis (PBC). There have been several reports on the association between AMA-M2 and various types of inflammatory myopathy, including cardiomyopathy. We report a case of a 58-year-old man with decompensated heart failure who also had PBC and skeletal inflammatory myopathy. Endomyocardial biopsy revealed severe fibrotic replacement of the myocardium without massive inflammatory infiltration, which was pathologically similar to what happens in dilated cardiomyopathy (DCM). Although the potential relationship between chronic autoimmune inflammation and DCM has been discussed, the concept of the inflammatory DCM has not yet been established. When we see elevated liver enzymes, and which is not simply due to congestive hepatopathy, we should consider the coexisting disease such as PBC.

Hypertrophic cardiomyopathy is a common cardiac complication in mitochondrial disorders, and the morbidity rate in neonatal cases is up to 40%. The mortality rate within 3 months for neonatal-onset mitochondrial cardiomyopathy is known to be high because there is currently no established treatment.

We report the case of a male infant with neonatal-onset mitochondrial disorder presenting lactic acidosis and hypertrophic cardiomyopathy. Genetic analysis of the patient revealed recurrent m.13513G>A, p.Asp393Asn in mitochondrially encoded NADH dehydrogenase 5 gene (MT-ND5). Low-dose propranolol was initially administered for cardiomyopathy; however, he developed hypertrophic obstructive cardiomyopathy (HOCM) at 3 months of age. To reduce the risk of hypoglycemia associated with high-dose propranolol, cibenzoline, a class Ia antiarrhythmic drug, was added at a dose of 2.5 mg/kg/day and increased weekly to 7.5 mg/kg/day with monitoring of the blood concentration of cibenzoline. Left ventricular outflow tract stenosis (LVOTS) dramatically improved from 5.4 to 1.3 m/second in LVOTS peak velocity after 6 weeks, without notable adverse effects. The plasma N-terminal pro-brain natriuretic peptide level decreased from 65,854 to 10,044 pg/mL. Furthermore, myocardial hypertrophy also improved, as the left ventricular mass index decreased from 173.1 to 108.9 g/m² after 3 months of the treatment.

The administration of cibenzoline, in conjunction with low-dose propranolol, may serve an effective treatment for HOCM in infantile patients with mitochondrial disorders.

Sleep-disordered breathing is one of the complications commonly seen in patients with adult congenital heart disease (ACHD) due to multiple causes including complex underlying cardiac defects, cardiomegaly, previous thoracotomies, obesity, scoliosis, and paralysis of the diaphragm. It is often hard to determine its main cause and predict the efficacy of each treatment in its management. We herein report a 30-year-old woman after biventricular repair of pulmonary atresia with intact ventricular septum diagnosed as sleep-related hypoventilation disorder. Simultaneous treatment targeting obesity, paralysis of the diaphragm, and cardiomegaly followed by respiratory muscle reinforcement through non-invasive ventilation resolved her sleep-related hypoventilation disorder. Such management for each factor responsible for the hypoventilation is expected to provide synergetic therapeutic efficacy and increase daily activity in a patient with ACHD.

Long-term complications after the Fontan procedure are important concerns for patients with pediatric and adult congenital heart disease. Although thrombocytopenia due to portal hypertension and hypersplenism is a well-known complication of the Fontan circulation, few studies have reported on its management. Herein we describe a young adult Fontan patient with thrombocytopenia and a splenic artery aneurysm caused by conduit stenosis. The patient required conduit replacement due to high venous pressure. We performed partial splenic artery embolization (PSE) and embolization of the aneurysm preoperatively to reduce the risk of bleeding, resulting in successful subsequent cardiac surgery. Preoperative evaluation of the splenic artery aneurysm was informative, and PSE was a safe and effective treatment option for thrombocytopenia to avoid bleeding during open-heart surgery in this patient.

Saddle pulmonary thromboembolism (PTE) is defined as a thromboembolism straddling the bifurcation of the main pulmonary artery trunk and it is rarely seen in extremely low birth weight infants (ELBWI). Saddle PTE is a critical disease that requires urgent treatment. However, the treatment guidelines for ELBWI are not established. We present the case of a 1-day-old preterm infant (gestational age 23 weeks) who showed sudden desaturation and pulmonary hypertension due to saddle PTE. A thrombus was observed in the bifurcation of the pulmonary artery. The blood flow to the pulmonary artery on the left side was interrupted, and the right side showed severe stenosis. Since the patient was an ELBWI in the acute phase, we decided to use recombinant tissue plasminogen activator (rt-PA) and administered a maintenance dose (0.08 mg/kg/hour), instead of the loading dose. After using rt-PA, the thrombus dissolved in 8 hours without adverse events. This case suggests that starting with a maintenance dose of rt-PA may be an effective treatment option for saddle PTE in ELBWI in the acute phase under the high risk of bleeding.

Some patients with aortic arch aneurysm are ineligible for open repair because of excessive perioperative risk, and others may not be suited for total endovascular repair due to anatomic constraints. We herein report a case of aortic arch aneurysm in a 94-year-old woman. The patient underwent hybrid aortic arch repair consisting of total arch debranching using bilateral femoral artery inflow and thoracic endovascular aortic repair. The patient was discharged without complications and is in good condition with dependent ambulation at 14 months of follow-up. Although a careful selection of cases is highly recommended, the use of the femoral artery inflow for arch debranching is considered to be a viable rescue option for high-risk patients.

Stabilization of aortic vulnerable plaques has not been fully elucidated. Non-obstructive general angioscopy (NOGA) is a novel method for the detailed evaluation of atheromatous plaques in the aortic intimal wall. A 57-year-old man presenting with acute myocardial infarction underwent percutaneous coronary intervention (PCI). NOGA was performed for the evaluation of aortic atherosclerosis, and vulnerable puff-chandelier plaques in the aortic arch were identified. After a strictly controlled low-density lipoprotein cholesterol lowering therapy with a strong statin for 8 months after the primary PCI, NOGA revealed stabilized aortic plaques in the same lesions. Therefore, NOGA may be helpful in evaluating the effects of lipid-lowering therapy on aortic plaque stabilization.

Myocardial ischemia/reperfusion (I/R) injury can bring about more cardiomyocyte death and aggravate cardiac dysfunction, but its pathogenesis remains unclear. This study aimed to investigate the role of long intergenic noncoding RNA-p21 (LincRNA-p21) in myocardial I/R injury and its underlying mechanism. Mice were subjected to myocardial I/R injury by ligation and release of the left anterior descending artery, and HL-1 cardiomyocytes were treated with hydrogen peroxide. Infarct area, cardiac function, and cardiomyocyte apoptosis were determined. Consequently, LincRNA-p21 was found to significantly be elevated both in the reperfused hearts and H₂O₂-treated cardiomyocytes. Moreover, genetic inhibition of LincRNA-p21 brought about reduced infarct area and improved cardiac function in mice subjected to myocardial I/R injury. LincRNA-p21 knockdown was also demonstrated to inhibit cardiomyocyte apoptosis both in vivo and in vitro. Notably, LincRNA-p21 silencing increased the expression of microRNA-466i-5p (miR-466i-5p) and suppressed the expression of nuclear receptor subfamily 4 group A member 2 (Nr4a2). Mechanically, LincRNA-p21 downregulated and directly interacted with miR-466i-5p, while application of miR-466i-5p inhibitor promoted cardiomyocyte apoptosis that was improved by LincRNA-p21 inhibition. Furthermore, Nr4a2 upregulation caused by LincRNA-p21 overexpression was partially reversed by miR-466i-5p mimics. Thus, LincRNA-p21 positively regulated the expression of Nr4a2, through sponging miR-466i-5p, promoting cardiomyocyte apoptosis in myocardial I/R injury. The current study revealed a novel LincRNA-p21/miR-466i-5p/Nr4a2 pathway for myocardial I/R injury, indicating that LincRNA-p21 may serve as a potential target for future therapy.