Despite increasing interest in remote lifestyle modification, evidence regarding the effectiveness of digital interventions in improving coronary risk factors remains limited. This study presents preliminary findings on a web-app-based remote lifestyle modification program including exercise, diet, and education aimed at managing coronary risk factors in patients following percutaneous coronary intervention (PCI). This single-arm interventional study enrolled 30 patients who had undergone PCI. The intervention protocol included a 5-day comprehensive lifestyle assessment, followed by a 12-week lifestyle modification program delivered through a web-based application. Participants engaged in home-based exercise training, dietary monitoring, and health assessments via the app. Instructors supervised their progress, provided feedback, and facilitated goal-setting for subsequent 2-week periods through a chat-based platform. A total of 24 participants (80%) successfully completed the program, with no adverse events or emergency medical visits related to the intervention. Significant improvements were observed in several clinical parameters, including reductions in systolic blood pressure (P = 0.043), low-density lipoprotein cholesterol (P < 0.001), high-density lipoprotein cholesterol (HDL-C) (P < 0.001), non-HDL-C (P < 0.001), and HbA1c (P = 0.038). There were significant increases in peak VO₂ (P < 0.001), moderate-to-vigorous physical activity (P = 0.012), and the mental component summary score of the SF-36 questionnaire (P = 0.003). Among 14 participants with elevated baseline body mass index, significant weight reduction was achieved (P = 0.008). The web app-based lifestyle modification program was feasible and safely implemented in patients after PCI. The efficacy and cost-effectiveness of asynchronous, technology-supported interventions for the comprehensive management of coronary heart disease should be further investigated in future randomized controlled trials.

Newer-generation drug-eluting stents (DES) that combine ultrathin struts and nanocoating (biodegradable polymer sirolimus-eluting stents, BP-SES) could improve vascular healing in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) over previous DES. However, its time course has not been elucidated.

Patients with STEMI caused by plaque rupture who underwent primary PCI at our institution using BP-SES between June 2018 and August 2020 were eligible. Vascular responses were assessed by frequency-domain optical coherence tomography (OCT), which was serially performed before the final angiography (post-PCI), after 2 weeks (2W-OCT) and 1 year (1Y-OCT).

A total of 24 patients with STEMI were finally assessed. The percentage of uncovered struts declined significantly at 1 year (post-PCI 61.7 ± 20.0%; 1Y-OCT 3.3 ± 3.3%; P < 0.0001). The percentage of malapposed struts also decreased significantly (% malapposed struts: post-PCI; 4.1 ± 3.6%: 1Y-OCT; 1.0 ± 2.3%, P< 0.0001). On the other hand, a total of 9 patients (37.5%) had at least 1 portion (> 3 mm length) of persistent malapposition (16.7%), late acquired malapposition (4.2%), or coronary evagination (16.7%) at 1 year. The site of late acquired malapposition was mostly at the culprit site, while the sites of persistent malapposition and evagination were not. None of the lesions showed signs of stent thrombosis.

In conclusion, BP-SES implanted into culprit plaque ruptures in patients with STEMI showed fast vascular healing in the chronic phase, while subclinical malappositions and evaginations were not rare and showed dynamic changes.

Although anemia is associated with adverse outcomes after acute myocardial infarction (MI), the specific impact of anemia on individual components of the cardiovascular events remains inadequately clarified. This study consisted of 3,229 patients with acute MI from the J-MINUET study. There were 930 patients (28.8%) with anemia, defined as hemoglobin (Hb) levels < 12 g/dL in women and < 13 g/dL in men: 533 (16.5%) with mild anemia (Hb levels 11-12/13 g/dL) and 397 patients (12.3%) with moderate to severe anemia (Hb levels < 11 g/dL). Composite outcomes included all-cause death, admission for heart failure (HF), stroke, and recurrent MI. At 3-year follow-up, the incidence of the composite outcomes was 17.9% in patients with no anemia, 32.3% in those with mild anemia (hazard ratio [HR] 1.95, 95% confidence interval [CI] 1.60-2.38, P < 0.001), and 56.1% in those with moderate to severe anemia (HR 3.91, 95%CI 3.26-4.69, P < 0.001). The impact of anemia was greatest for death, followed by admission for HF and stroke. This effect was more pronounced in patients with moderate to severe anemia. The influence of anemia on recurrent MI was less significant. While chronic kidney disease (CKD) amplified the adverse outcomes of anemia, the impact of anemia and its severity on the incidence of cardiovascular events was consistent regardless of CKD status. In conclusion, the most profound effect of anemia was observed for death, followed by HF and stroke in patients with MI, particularly in moderate to severe anemia, while the association with recurrent MI was less pronounced.

Persistent atrial fibrillation (PerAF) still exhibits less favorable outcomes post-ablation and the efficacy of linear or substrate ablation in addition to pulmonary vein isolation (PVI) remains controversial. The relationship between P-wave morphology and the maintenance of sinus rhythm in PerAF patients who underwent PVI alone remains unknown.

PerAF patients who underwent PVI alone were enrolled. Pvm (mV) was calculated by the square root of the sum of the squared P-wave amplitude in leads II and V6 and one-half of the P-wave amplitudes in V2 in 12-lead electrocardiograms 48 hours post-ablation were analyzed. Pd/Pvm was the ratio of the P-wave duration (ms) to the Pvm. We divided the patients into 2 groups; high and low Pd/Pvm. The cut-off value of the Pd/Pvm was calculated by receiver operating characteristic analysis. The difference in late recurrence of atrial fibrillation (LRAF) between the 2 groups and the relationship between Pd/Pvm and relevant factors were evaluated.

This study population included a total of 451 PerAF patients. The optimal cut-off value for predicting the LRAF was Pd/Pvm = 812.8 ms/mV (AUC = 0.91, sensitivity = 84.6% and specificity = 84.2%). The median follow-up duration was 726 days. LRAF occurred in 169 patients (37.5%). Cox proportional hazards analysis showed that Pd/Pvm was significantly associated with LRAF (P < 0.001). A multiple regression analysis showed that no hypertension, hemoglobin ≥ 14.1 g/dL, and LA diameter < 47 mm were significantly and independently associated with low Pd/Pvm (P = 0.045, P < 0.001 and P = 0.024, respectively).

Pd/Pvm post-ablation was a useful marker for predicting the maintenance of sinus rhythm after PVI alone in PerAF patients.

No reports compared four indices of myocardial work based on aortic valve stenosis (AS) severity. This study aimed to characterize the four myocardial work indices and global longitudinal strain (GLS) in AS with left ventricular ejection fraction (LVEF) > 50%, and to investigate the association of these indices with severe AS.

We measured global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE), and GLS in 154 patients. These indices were compared among three groups: normal, mild-to-moderate, and severe AS.

GWI and GCW were significantly higher in mild-to-moderate and severe AS groups than in normal group. GWW was significantly higher in severe AS group than in normal and mild-to-moderate AS groups. GWE and GLS were significantly lower in severe AS group than in normal and mild-to-moderate AS groups. The ability to discriminate severe AS was examined using receiver operating characteristic analysis, and GWW demonstrated the largest area under the curve. Multivariate logistic regression analysis demonstrated that the four myocardial work indices and GLS were significantly associated with severe AS after adjusting for age, height, and brachial systolic blood pressure.

In conclusions, GWI, GCW, and GWW, were significantly higher, while GWE and GLS were significantly lower in the severe AS group than in the normal group. These findings suggest that the four indices of myocardial work are valuable in detecting the impairment of left ventricular myocardial workload due to severe AS in patients with preserved LVEF.

This study aimed to investigate the association between brain-derived neurotrophic factor (BDNF) levels and the no-reflow phenomenon in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI).

This retrospective study included 100 patients with STEMI from January 2023 to December 2023. Patients were classified into an observation group (slow flow or no-reflow) and a control group (normal flow) based on the post-PCI Thrombolysis in Myocardial Infarction (TIMI) flow grades.

The observation group exhibited significantly higher BDNF and creatine kinase-MB (CK-MB) levels and significantly lower left ventricular ejection fraction (LVEF) than the control group (P < 0.05). Logistic regression analysis identified diabetes, higher Killip class, lower eGFR, reduced LVEF, multivessel disease, high thrombus burden, elevated B-type natriuretic peptide (BNP), and increased BDNF levels as independent predictors of the no-reflow phenomenon (P < 0.05). Correlation analysis showed that BDNF levels were negatively correlated with TIMI flow grade (r = −0.303, P < 0.01) and LVEF (r = −0.717, P < 0.01) and positively correlated with left ventricular internal dimension in systole (LVIDs; r = 0.509, P < 0.01), STEMI onset time (r = 0.685, P < 0.01), CK-MB (r = 0.689, P < 0.01), TnT (r = 0.708, P < 0.01), and TnI (r = 0.781, P < 0.01).

Higher BDNF levels were significantly associated with impaired myocardial perfusion and reduced cardiac function, as indicated by a lower pre-PCI LVEF. These findings suggest that BDNF may serve as a potential biomarker for the no-reflow phenomenon in patients with STEMI. Further studies are needed to clarify the relationship between BDNF levels and post-PCI recovery of cardiac function.

Artificial intelligence models reportedly detect a low ejection fraction (EF) with chest radiography (CXR) examinations, which traditionally require a transthoracic echocardiogram (TTE) for evaluation. However, whether coupling a CXR model with an electrocardiogram (ECG) model improves the detection performance remains unclear. This study aimed to evaluate various models and fusion strategies for their detection performance.

This study included 7,246 patients who underwent CXR, ECG, and TTE at the University of Tokyo Hospital. Two ECG models were used-a convolutional neural network and masked autoencoder. Two methods for combining CXR and ECG models were tested, early and late fusion. In the early fusion method, the CXR and ECG models were trained simultaneously, whereas in the late fusion method, three ensemble techniques were implemented. The CXR single model achieved an area under the curve (AUC) of 0.798. Both fusion models significantly outperformed the CXR single model. The early fusion model achieved an AUC of 0.937 (P = 0.015), while the late fusion model had an AUC of 0.928 (P = 0.010).

Combining the CXR and ECG models significantly improved detection performance. This approach enables more accurate identification of patients with low EF, a condition typically requiring TTE for diagnosis.

Sarcopenia is an age-dependent skeletal muscle disorder associated with multiple adverse outcomes, including cardiovascular events. This study aimed to clarify the clinical significance of sarcopenia and atrial fibrillation (AF) in heart failure (HF) among elderly individuals.

In total, 130 elderly participants with HF risk factors were included. Body composition, including skeletal muscle mass index (SMI) and the ratio of extracellular water to total body water (ECW/TBW), was assessed using a multifrequency bioelectrical impedance analysis device. Sarcopenia was defined as low SMI with low handgrip strength or slow gait speed. ECW/TBW was higher in patients with HF than in those without. AF was associated with HF. Although sarcopenia by itself was not associated with HF, concomitant sarcopenia and AF was associated with HF. Multiple logistic regression analysis showed that AF accompanied by sarcopenia and high ECW/TBW was associated with HF, independent of other cardiovascular risk factors.

In this study, AF accompanied by sarcopenia and cellular edema increased the prevalence of HF in elderly individuals with cardiovascular risk factors. These data suggest the management of sarcopenia and cellular edema is critical for the prevention of HF in elderly patients with AF.

Changes in the left ventricular ejection fraction (LVEF) of patients with cardiac sarcoidosis (CS) have been reported; however, the prognostic implications remain unknown. This study aimed to investigate the predictive factors for LVEF improvement in patients with CS and the association between LVEF improvement and prognosis. This was a post hoc analysis of the ILLUMINATE-CS registry, a multicenter retrospective study on CS. Patients with a baseline LVEF ≥ 50% were excluded. LVEF improvement was defined as the difference between the baseline and follow-up echocardiographic results. Patients were stratified based on tertiles of LVEF improvement: 1st (≤ 0%, least improved), 2nd (0-9%), and 3rd (> 9%, most improved) tertile groups. The primary outcome was all-cause mortality after follow-up echocardiography. Overall, 188 patients with CS (age: 62.1 ± 10.7 years; male proportion: 42.6%) were analyzed. In the multivariate linear regression analysis, narrower QRS duration, lower baseline LVEF, and no prescription of beta-blockers at baseline were independently associated with greater LVEF improvement. During the median follow-up period of 407 days, 26 deaths occurred. The Kaplan-Meier curves showed a significant difference between the 3 groups (log-rank test, P = 0.002). In the adjusted Cox proportional hazard analysis, the 1st and 2nd tertile groups showed progressively higher mortality rates than the 3rd tertile group. Independent of other variables, LVEF improvement as a continuous variable was associated with a lower mortality rate. Among patients with CS, LVEF improvement was significantly associated with favorable outcomes. LVEF should be monitored if baseline LVEF is decreased.

Pulmonary congestion can be quantitatively assessed using the remote dielectric sensing (ReDS) system, whereas intestinal congestion is evaluated based on the colon wall thickness (CWT) as measured by abdominal computed tomography. However, the relationship between pulmonary and intestinal congestion (i.e., inter-organ congestion) remains poorly understood.

ReDS and CWT values were simultaneously obtained from patients hospitalized for cardiovascular diseases. The association between congestion in these two organs and its prognostic significance for a composite endpoint-including heart failure hospitalization and all-cause mortality-was investigated.

A total of 111 patients (median age: 79 years; 60 males) were analyzed. Patients with high ReDS values and high CWT exhibited a larger left atrial size and lower prescription rates of loop diuretics compared with patients in the Normal group (P < 0.05 for both). Individuals with elevated ReDS values but low CWTs had larger left atrial dimensions, whereas those with high CWTs but low ReDS values had a higher prevalence of chronic kidney disease (P < 0.05 for both). The cumulative incidence of the composite endpoint was significantly stratified by the ReDS values (P = 0.037); in contrast, the CWT values did not demonstrate significant stratification (P = 0.71).

Pulmonary and intestinal congestion reflect distinct pathophysiological processes in patients with cardiovascular diseases. The simultaneous evaluation of ReDS and CWT values may provide valuable insights to guide personalized therapeutic strategies in this patient population.

Although the safety and efficacy of transcatheter atrial septal defect (ASD) closure has been reported in elderly patients, postprocedural outcomes in elderly patients with long-standing persistent atrial fibrillation (AF) have not been fully assessed. The aim of this study was to elucidate the cardiac remodeling process and symptom improvement after transcatheter ASD closure in elderly patients with AF (AF-ASD) compared to those in sinus rhythm (SR-ASD).

We enrolled 52 patients aged > 70 years out of 253 consecutive patients who underwent transcatheter ASD closure. We retrospectively analyzed serial echocardiograms, New York Heart Association (NYHA) functional classification, and plasma brain natriuretic peptide (BNP) levels from baseline to 1 year after the procedure.

With respect to the right-sided chambers, significant reverse remodeling began immediately after the procedure and continued in both groups up to 1 year after the procedure. Left ventricular augmentation was comparable in both groups. Left atrial volume increase was prominent in the AF-ASD group, with a statistically significant difference compared with the SR-ASD group from 2 days to 1 year after the procedure (all P < 0.05). NYHA functional classification improved in both groups. Plasma BNP levels decreased only in the AF-ASD group from baseline to 1 year (median value [interquartile range], 336.2 pg/mL [145.1-491.4] to 173.8 pg/mL [73.6-261.7], P = 0.032).

Transcatheter ASD closure is an effective treatment for heart failure in elderly patients with ASD and long-standing persistent AF.

The optimal management of type A intramural hematoma (IMH) is controversial, particularly in uncomplicated cases. This retrospective analysis assessed how different management approaches (physician-led surgical repair or conservative treatment, patient-led conservative treatment [patients who were recommended by the physician for surgery but selected conservative treatment], and physician-led conservative treatment [patients who were recommended by the physician for conservative treatment]) affect post-treatment mortality in patients with type A IMH. This retrospective study included 79 patients with acute type A IMH who underwent surgical management (n = 17), conservative treatment (n = 18), or patient preference for conservative treatment (n = 44). The analyses included patient demographics, clinical features, length of hospital stay, and post-treatment all-cause mortality. The multivariate Cox regression analysis revealed a trend toward a decreased risk of death with surgery over a median 4-year follow-up that was not significant (surgery versus conservative treatment: hazard ratio [HR] [95% CI] = 0.212 [0.025-1.351], P = 0.156). The risk of death was similar between the two conservative treatment approaches (patient-driven versus physician-driven treatment: HR [95% CI] = 0.915 [0.321-2.666], P = 0.885). The clinicodemographic factors of age (HR [95% CI] = 1.061 [1.006-1.119]), hypertension (HR [95% CI] = 11.747 [1.657-83.285]), hyperlipidemia (HR [95% CI] = 4.837 [1.212-19.314]), and heart disease (HR [95% CI] = 4.739 [1.408-15.873]) increased the risk of death (all P < 0.05). In conclusion, we encourage such patients to undergo early surgical treatment, although conservative treatment may still be a viable option for certain patients. Frequent follow-up with echocardiographic imaging is recommended for type A IMH after surgical or conservative treatment.

The prognosis of patients with aortic aneurysm (AA) and cardiovascular comorbidities remains suboptimal compared to that of the general population, highlighting the need for reliable mortality biomarkers. Apolipoprotein A2 (ApoA2) is a structural and functional component of high-density lipoprotein cholesterol (HDL-C), but its relevance to all-cause mortality remains unclear. Therefore, we investigated the prognostic value of ApoA2 in patients with AA after surgical repair. ApoA2 levels were measured in 203 consecutive patients with AA who were successfully treated with surgical repair. The primary focus was the predictive value of ApoA2 levels for mortality events. During a median follow-up of 3.5 years, mortality events were observed in 32 patients (15.8 %). Patients with mortality events had lower ApoA2 levels than the survivors [22.0 (19.0, 25.0) mg/dL versus 25.0 (22.0, 29.0) mg/dL, P < 0.001]. ApoA2 was inversely correlated with age, BNP, C-reactive protein (CRP), and fibrinogen levels and positively correlated with eGFR. Multivariate Cox analysis identified ApoA2 (HR 0.92, 95% CI 0.86-0.99), eGFR < 60 mL/minute/1.73 m² (HR 3.49, 95% CI 1.49-8.20), COPD (HR 2.63, 95% CI, 1.07-6.49), and thoracic AA (HR 2.54, 95% CI 1.25-5.18) as independent mortality predictors. Moreover, the addition of ApoA2 levels significantly improved the discriminative ability of the baseline risk factors in predicting mortality (AUC 0.79 versus 0.73, P = 0.04). Therefore, ApoA2 is a potential biomarker for predicting long-term mortality in patients with AA following surgical repair, and may contribute to improved risk stratification in this high-risk population.

Cardiac rehabilitation (CR) is a comprehensive intervention aimed at improving recovery, reducing mortality, and enhancing the quality of life in myocardial infarction patients. Despite its proven benefits, its global implementation remains inconsistent, warranting further exploration of research trends and challenges. This study explores hot topics and frontiers in research on cardiac rehabilitation after myocardial infarction over the past 23 years. We aim to map the development trajectory of this field and provide references for related research. Literature on cardiac rehabilitation of myocardial infarction patients from 2000 to 2023 was gathered from the Web of Science core database. VOSviewer and CiteSpace were used to create knowledge maps of authors, institutions, and countries. We used Scimago Graphica to create a world map of publications by country. A total of 9,471 papers on cardiac rehabilitation after myocardial infarction were identified. We found a gradual increase in the annual number of publications over the years. The United States produced the highest number of publications, with significant contributions from higher education institutions, which engaged in extensive collaborations. Recent research hotspots and frontiers include physical activity, secondary prevention, risk management, quality of life, mortality, depression, management, high-intensity interval training (HIIT), systematic reviews, resistance exercise, position papers, and barriers to rehabilitation. Over the past 23 years, the annual global publication output on cardiac rehabilitation of myocardial infarction patients has steadily increased. However, the implementation of cardiac rehabilitation continues to face challenges worldwide. Experts from around the world need to make concerted efforts to conduct more in-depth clinical studies of the research hotspots and frontiers identified in this paper. This is vital to ongoing improvements in the quality of cardiac rehabilitation after myocardial infarction.

Although several observational studies have suggested an association between plasma homocysteine (Hcy), vitamin B12, and folate levels and aortic diseases, including aortic dissection (AD), thoracic aortic aneurysm (TAA), and abdominal aortic aneurysm (AAA), the causality remains unclear. The aortic diameter was also included in the analysis. Therefore, this study employed Mendelian randomization (MR) analysis to investigate the effects of plasma Hcy, vitamin B12, and folate levels on aortic diseases. Single-nucleotide polymorphisms (SNPs) associated with Hcy, vitamin B12, and folate were obtained from reliable genome-wide association studies. Data for AD, TAA, and AAA were obtained from the Finnish database. We conducted a two-sample MR analysis using the following methods: inverse variance weighted, weighted median, MR-Egger, simple mode, weighted mode, and Bayesian weighted MR. Heterogeneity and pleiotropy were assessed using the Cochran's Q test and the MR-Egger test, respectively. In addition, leave-one-out and Steiger filtering analyses were performed to test the stability of MR findings. Our MR results demonstrated no significant causal association between Hcy, vitamin B12, and folate levels and aortic diseases or aortic diameter (P > 0.05). The Cochran's Q test and MR-Egger test indicated no heterogeneity or pleiotropy (P > 0.05). The leave-one-out and Steiger filtering analyses confirmed the robustness of the MR results. The MR analysis underscored that no direct genetic predisposition promotes elevated Hcy and decreased vitamin B12 or folate levels in the development of aortic diseases. This study found that plasma Hcy, vitamin B12, and folate levels had no effect on aortic diseases or aortic diameter. Therefore, vitamin B12 or folate supplementation to lower Hcy levels may not be effective in preventing aortic diseases.

Myocardial fibrosis (MF) is closely related to various cardiovascular diseases, especially heart failure. However, the mechanisms related to the treatment of MF are not entirely clear. Therefore, this study investigated the effects of miR-411-5p and HCN1 on MF alleviation.

RT-qPCR and Western blotting were used to determine Ang II-induced fibrosis of H9c2 cells and alterations in miR-411-5p and HCN1 expression. CCK-8, EdU staining, Transwell assay, immunofluorescence staining, and Western blot were used to determine the effects of the corresponding transfectants on H9c2 cell viability, cell proliferation, migration, and fibrosis. Meanwhile, the dual-luciferase report, RNA binding protein immunoprecipitation assay, RT-qPCR, and Western blot were collectively employed to investigate the targetability between miR-411-5p and HCN1.

In this study, the optimal concentration of Ang II used to establish fibrosis of H9c2 cells was 10 ng/mL, under which the expression level of miR-411-5p was downregulated but the expression level of HCN1 was upregulated. Enhanced miR-411-5p or HCN1 silencing downregulated the elevation of cell viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs caused by Ang II. MiR-411-5p inhibitors reversed the decline in the viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs induced by sh-HCN1 transfection. In addition, miR-411-5p targets and negatively regulates HCN1 expression.

In conclusion, miR-411-5p alleviated Ang II-induced fibrosis of H9c2 cells and primary CFs by inhibiting HCN1.

Cardiomyocyte apoptosis is the underlying pathogenic factor of myocardial ischemia-reperfusion injury (MIRI). Long non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) plays a crucial role in cell apoptosis regulation. In this study, we investigated the mechanism of lncRNA NORAD in promoting MIRI via the miR-144-3p/trinucleotide repeat-containing gene 6a (TNRC6A) axis.

H9C2 cells were induced by oxygen-glucose deprivation/reperfusion (OGD/R) in vitro, and then treated with oe-NORAD, si-NORAD, miR-144-3p inhibitor, and oe-TNRC6A. Meanwhile, an MIRI rat model was established and treated with sh-NORAD. The expression of NORAD, miR-144-3p, TNRC6A, apoptosis proteins, and inflammatory factors (tumor necrosis factor-α [TNF-α] and interleukin [IL]-6) was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot, and enzyme-linked immunosorbent assay. Cell viability and apoptosis were assessed using Cell Counting Kit-8 and flow cytometry. Echocardiography, 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining were used to evaluate cardiac function, pathological changes in myocardial tissues, and myocardial apoptosis. Additionally, the potential binding sites of miR-144-3p with NORAD and TNRC6A were predicted using the StarBase database and then validated by the dual-luciferase reporter gene assay.

NORAD expression, cell apoptosis, and TNF-α and IL-6 levels were augmented, whereas miR-144-3p expression and cell viability were diminished in OGD/R-exposed cells. NORAD knockdown impeded OGD/R-induced cardiomyocyte apoptosis and inflammatory responses. Repression of miR-144-3p or TNRC6A overexpression partially offset the inhibitory effect of NORAD knockdown on OGD/R-induced cardiomyocyte apoptosis. In vivo tests confirmed that NORAD knockdown reduced MIRI in rats.

Highly expressed NORAD promoted cardiomyocyte apoptosis and inflammatory responses. However, NORAD knockdown suppressed cardiomyocyte apoptosis to reduce MIRI through the miR-144-3p/TNRC6A axis.

Heart failure is associated with poor quality of life and mortality, and the prevalence of heart failure is increasing together with aging of the population. Approximately 50% of patients with heart failure present as HFpEF, and the survival of HFpEF patients is as poor as that of HFrEF patients. Furthermore, therapies for HFpEF are limited and are not proven to improve prognosis, except for SGLT2 inhibitors. HFpEF is more prevalent in women and the risk of HFpEF increases more drastically with aging in women than men. HFpEF is a syndrome with multiple comorbidities, and modeling HFpEF in animal models has been attempted by reproducing major comorbidities highly associated with human HFpEF. In order to elucidate the female-specific mechanisms of HFpEF, we established a new mouse model by applying additional stressors on the basis of obesity and post-menopausal model. Ovariectomy or epinephrine injection was added to a high-fat diet-induced obesity model. Ovariectomy exacerbates obesity and serial epinephrine injections ameliorate obesity. Exercise tolerance in treadmill testing was inversely correlated with body weight, and was reduced more than expected based on body weight in mice that underwent ovariectomy and epinephrine injection (OVX + Epi group). In a pressure-volume analysis, the end-diastolic pressure at afterload increase was significantly high in OVX + Epi mice, which is considered to reflect left ventricular diastolic dysfunction. In conclusion, this study demonstrated that epinephrine and depletion of female sex hormone by ovariectomy reproduce the pathology of obesity-induced cardiac phenotype, which might represent an early phase of HFpEF conditions.

DNA damage is strongly associated with myocardial infarction (MI), but its role in post-MI cardiac remodeling remains unclear. In this study, we investigated the effects of DNA double-strand breaks (DSBs), the most severe form of DNA damage, on cardiac remodeling using Ku80^+/− mice, which exhibit diminished expression of this key DSB repair protein. Ku80-deficient mice exhibited a worse prognosis, lower cardiac function, and a larger infarct size after MI than wild-type (WT) mice. Ku80-deficient mice also displayed persistent DSBs 2 weeks post-MI. Notably, Ku80-deficient mice had reduced anti-inflammatory M2 macrophage infiltration despite exhibiting no significant differences in bone marrow-derived macrophage polarization. In addition, the mRNA levels of interleukin-10 (IL-10), an anti-inflammatory cytokine essential for M2 macrophage polarization and infiltration, were significantly lower in Ku80-deficient hearts than in WT hearts both at baseline and after MI. In situ analysis revealed that cells near the ischemic border zone - likely cardiomyocytes -serve as the major sources of IL-10. In vitro studies using HL-1 murine cardiac cells confirmed that chemical hypoxia induces IL-10 expression, whereas preexisting DSBs blunt this response. Together, these findings suggest that DSB accumulation hinders cardiac repair after MI, potentially because of insufficient IL-10 expression in cardiomyocytes, thereby disturbing M2 macrophage recruitment. Targeting DNA damage pathways or enhancing IL-10 signaling in cardiomyocytes could represent a new therapeutic strategy to improve cardiac repair after MI.

The pharmacological blockade of mineralocorticoid receptors (MR) is a potential therapeutic approach to reduce cardiovascular complications. Recent studies suggest that MR blockers affect several extrarenal tissues, including vascular function. We investigated the effects of a novel non-steroidal selective MR blocker, esaxerenone, on vascular function and atherogenesis.

Esaxerenone (3 mg/kg/day) was orally administered for 20 weeks or vehicle for 8 weeks to apolipoprotein E-deficient (ApoE^-/-) mice fed a Western-type diet to investigate the effects on atherogenesis or vascular dysfunction. Human umbilical vein endothelial cells (HUVEC) were used to perform in vitro experiments.

Administration of esaxerenone for 20 weeks suppressed the development of atherosclerotic plaques in the aortic arch compared with the vehicle group (P < 0.001) without alteration of blood pressure. In addition, esaxerenone significantly reduced the expression of intercellular cell adhesion molecule-1, macrophage infiltration, and lipid deposition as determined by immunohistochemical analysis. Moreover, phosphorylation of eNOS^Ser1177 and Akt were increased in the aorta of esaxerenone-treated mice. Administration of esaxerenone for 8 weeks attenuated Western-type diet-induced endothelial dysfunction, accompanied by a decrease in expression of ICAM-1 and phosphorylation of JNK in the descending aorta. In an ex vivo vascular reactivity assay using ApoE^-/- aortic rings, esaxerenone diminished aldosterone-induced endothelial dysfunction. In an in vitro experiment, aldosterone decreased the phosphorylation of eNOS^Ser1177 and increased the phosphorylation of eNOS^Thr495 in a dose-dependent manner, which were attenuated by esaxerenone in HUVECs.

Esaxerenone ameliorated hyperlipidemia-induced atherosclerotic plaque progression and vascular dysfunction in ApoE^-/- mice, suggesting that esaxerenone is a promising therapeutic approach for cardiovascular complications.

A novel telemonitoring system utilizing contactless sensor technologies combined with automated overnight respiratory stability time (RST) analysis has emerged as a sensitive and specific indicator of worsening heart failure (HF), enabling early clinical exacerbation identification. However, the correlation between the RST trajectory and other clinical parameters, as well as targeted therapeutic strategies for improving RST in patients experiencing acute decompensated HF, remains unclear. Herein, we present two cases of hospitalized patients with HF and reduced left ventricular ejection fraction, which were successfully managed through clinical interventions monitored by integrated RST parameters. A significant recovery in RST was observed following the improvement of congestion and hypoperfusion. Further research is warranted to validate the clinical efficacy of RST-directed therapeutic approaches in the management of HF.

Evidence for pregnancy in patients with drug-induced cardiomyopathy is limited, presenting significant challenges in medication management for such cases.

A 28-year-old female patient developed severe heart failure due to doxorubicin-induced cardiomyopathy following treatment for extraosseous Ewing's sarcoma. After a decade of heart failure management, the patient successfully achieved a safe pregnancy and delivery.

This report describes how we reduced and discontinued cardioprotective drugs for heart failure and prompted an evaluation of her ability to tolerate an increased circulating plasma volume through a saline stress test, followed by infertility treatment.

In preterm infants with large ventricular septal defects (VSD), severe chronic lung disease (CLD), and pulmonary hypertension (PH), hemodynamic instability may occur after open-heart surgery. The selection of first pulmonary artery banding or one stage VSD closure is a clinical issue. At present, no guidelines exist to support decision-making in this unique population. This study reports the case of a preterm infant with a gestational age of 23 weeks and 4 days, a birth weight of 540 g, and elevated immunoglobulin-M levels, who was successfully treated with pulmonary artery banding and subsequently VSD closure. Before pulmonary artery banding, the pulmonary-to-systemic blood flow ratio was 2.5 and pulmonary vascular resistance was 2.6 U·m² under general anesthesia with FiO₂ = 0.6. However, pulmonary artery banding preceded considering the severe CLD and the risk of PH crisis after cardiopulmonary bypass. In a review of the literature on preterm infants with VSD with CLD and PH, only five infants, including the one in this case, were found. One infant underwent pulmonary artery banding first and survived, and three infants underwent one-stage VSD closure, after which one died (trisomy 21) due to a postoperative PH crisis. Three of the five cases underwent tracheostomy. The selection of first pulmonary artery banding or one-stage VSD closure needs to be carefully considered on a case-by-case basis, taking into consideration the severity of the VSD with CLD and PH. A future registry study will be needed to review these cases and clarify the outcome of the two strategies.

Several errors (shown with underlines) in the following list appeared in Table IV on page 973 in the article "Lifestyle Habits of Patients with Acute Myocardial Infarction and Specificity by Age Group" by Keiko Matsuzaki, Nobuko Fukushima, Chizuru Saito, Daiki Hagiwara, Hiroaki Nishikawa, Yousuke Katsuda, and Shin-ichiro Miura (Vol. 65 No.6, 969-977, 2024).