Background In nonischemic cardiomyopathy, the clinical relevance of decreased resting myocardial technetium‐99m sestamibi (99mTc‐MIBI) uptake regarding exercise capacity and clinical outcomes remains incompletely understood. We investigated whether decreased 99mTc‐MIBI uptake is associated with impaired exercise capacity and adverse clinical outcomes in nonischemic cardiomyopathy. Methods We retrospectively analyzed 182 patients (mean age 51.4±14.0 years; 27% female) with nonischemic cardiomyopathy and left ventricular ejection fraction <50% who underwent 99mTc‐MIBI scintigraphy and cardiopulmonary exercise testing from 2016 to 2023. Myocardial uptake of 99mTc‐MIBI was evaluated using the summed rest score (SRS). Exercise capacity was assessed by percentage of predicted peak oxygen consumption (PPVO2), with ≤60% defining impairment. Results Seventy‐four patients (41%) had PPVO2 ≤60% and higher SRS (median: 12 versus 8; P < 0.001). Higher SRS remained significantly associated with PPVO2 ≤60% after adjustment for relevant clinical covariates, including brain natriuretic peptide level, left ventricular ejection fraction, and heart failure duration. Over a median follow‐up of 807 days, 23 patients (13%) experienced the composite outcome of all‐cause death, ventricular assist device implantation, or heart transplantation. Higher SRS was associated with composite outcomes after adjusting for PPVO2 ≤60%. Among the 4 groups stratified by median SRS of 9 and PPVO2 of 60%, patients with high SRS and low PPVO2 had the highest incidence of adverse events. Conclusions Decreased myocardial 99mTc‐MIBI uptake was associated with impaired exercise capacity and adverse outcomes in patients with nonischemic cardiomyopathy. Our findings suggest that myocardial injury assessment using 99mTc‐MIBI scintigraphy may provide prognostic information complementary to exercise capacity.

Cardiac allograft vasculopathy (CAV) is a major cause of mortality after heart transplantation, characterized by intimal proliferation-induced coronary stenosis. The first year post-transplantation represents a critical period for CAV development, with most intimal proliferation occurring during this timeframe. This study aimed to investigate the temporal changes in lipid content and its relationship with intimal proliferation during the first year after heart transplantation. Serial three-vessel near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) were performed in 15 heart transplant recipients (38 coronary arteries) at 2 months (baseline) and 12 months (follow-up) following heart transplantation. From baseline to follow-up, the highest lipid-core burden index within a 4 mm segment (maxLCBI4mm) significantly decreased (median: 78.0 [IQR: 6.75 to 196] to 27.5 [IQR: 0 to 122], p = 0.008), while

Background We investigated whether radiomic scores (RadScores), computed from high‐dimensional quantitative features extracted from cardiac magnetic resonance parametric mapping images, can predict left ventricular reverse remodeling (LVRR) in patients with nonischemic dilated cardiomyopathy. Methods This retrospective analysis included 74 patients with nonischemic dilated cardiomyopathy who received optimized medical therapy and underwent cardiac magnetic resonance. LVRR was defined as a left ventricular ejection fraction ≥40% with ≥10% increase at least 180 days after cardiac magnetic resonance. RadScores were calculated for each case as linear combinations of selected radiomic features, with coefficients derived from least absolute shrinkage and selection operator–penalized logistic regression on native longitudinal relaxation time (T1) and extracellular volume (ECV) fraction maps. Predictive performance for LVRR was evaluated using logistic regression and receiver operating characteristic analyses. Results Patients with LVRR (n=31, 42%) had higher T1‐RadScore (0.72±1.52 versus −1.54±2.66; P <0.0001), higher ECV‐RadScore (0.24±0.65 versus −0.16±0.64; P =0.005), lower mean‐ECV (31.5%±3.8% versus 34.9%±6.0%; P =0.004), and lower extent of late gadolinium enhancement (0.19±0.58 versus 2.99±6.5; P =0.047) than those without LVRR. The area under the receiver operating characteristic curve for predicting LVRR was 0.834 (95% CI, 0.716–0.909) for the T1‐RadScore and 0.718 (95% CI, 0.573–0.827) for the ECV‐RadScore. Adding T1‐ and ECV‐RadScore combination to the extent of late gadolinium enhancement model significantly improved the area under the receiver operating characteristic curve from 0.618 to 0.903 ( P <0.0001). Conclusions Radiomic scores extracted from native T1 and ECV maps may enhance LVRR prediction and provide incremental value beyond traditional late gadolinium enhancement assessment in patients with dilated cardiomyopathy.

BACKGROUND:Heterogeneity of heart failure with preserved ejection fraction (HFpEF) results in significant challenges for treatment development. Identifying and characterising distinct HFpEF phenogroups may aid in tailoring therapeutic strategies for these patients. The objective of this study was to assess proteomic patterns of HFpEF phenogroups identified through a machine-learning-based clustering model, with the aim of uncovering specific biological pathways associated with each phenogroup. METHODS:This study represents a post-hoc analysis of the ongoing Prospective mUlticenteR obServational stUdy of patIenTs with Heart Failure with preserved Ejection Fraction (PURSUIT-HFpEF) study, which is a multicentre prospective observational study of hospitalised patients with acute decompensated HFpEF. Of the overall cohort (N=1238), this study analysed 198 patients with HFpEF with available proteomics data. These patients were classified into four phenogroups using the machine-learning-based clustering model. The SomaScan assay V.4.1 was used to measure levels of >7000 plasma proteins, and subsequent pathway analysis was conducted to determine the biological differences among the phenogroups. RESULTS:We identified four distinct phenogroups: Phenogroup 1 ('rhythm trouble'), Phenogroup 2 ('ventricular-arterial uncoupling'), Phenogroup 3 ('low output and systemic congestion') and Phenogroup 4 ('systemic failure'). The proteomics revealed distinct protein expression profiles among the phenogroups, with ribonuclease 4, tax1-binding protein 1, regenerating islet-derived protein 3-gamma and alpha-1-antichymotrypsin being the most significant markers to specific identified phenogroups. Pathway analysis suggested differences in immune response, autonomic activation, cellular homeostasis and tissue repair mechanisms across the phenogroups. CONCLUSIONS:Using a comprehensive plasma proteomics approach, our study identified distinct proteomic profiles of HFpEF phenogroups, which in turn suggest specific underlying biological processes. These profiles suggest the involvement of inflammatory activation, tissue injury and regenerative responses, immune modulation and systemic stress signalling as key components of HFpEF pathophysiology. TRIAL REGISTRATION NUMBER:UMIN-CTR ID: UMIN000021831.

BACKGROUND:In heart failure with preserved ejection fraction (HFpEF), the relationship between N-terminal pro-brain natriuretic peptide (NT-proBNP) levels and echocardiographic parameters and the influence of atrial fibrillation (AF) on the relationship remain poorly understood. METHODS:This study analyzed data from the Prospective mUlticenteR obServational stUdy of patIenTs with HFpEF (PURSUIT HFpEF). Patients hospitalized for acute decompensated HF with a left ventricular ejection fraction (LVEF) ≥ 50% were included. The association between longitudinal NT-proBNP levels and echocardiographic parameters was assessed using linear mixed-effects models, with further stratification by AF status. RESULTS:Of 1238 enrolled patients (median age 83[77, 87] years; 551[45%] male), 617 patients with longitudinal NT-proBNP data available (407 without AF, 210 with AF) were analyzed. In patients without AF, even after covariates adjusted, NT-proBNP levels were positively associated with left ventricular diastolic diameter (β-coefficient: 1.878 ± 0.736, P < 0.001), left ventricular mass index (β-coefficient: 1.467 ± 0.280, P < 0.001), left atrial volume index (β-coefficient: 0.795 ± 0.232, P < 0.001), E/e' (β-coefficient: 1.041 ± 0.214, P < 0.001), and tricuspid regurgitation pressure gradient (TRPG) (β-coefficient: 0.849 ± 0.261, P < 0.001). Conversely, left ventricular ejection fraction was negatively associated (β-coefficient: -1.632 ± 0.607, P < 0.001). However, in patients with AF, most of these parameters except for E/e', TRPG, and interventricular septal thickness at end-diastole had no correlation with NT-proBNP levels. CONCLUSIONS:In HFpEF patients without AF, longitudinal NT-proBNP levels were broadly associated with both structural and functional echocardiographic parameters. Whereas, patients with AF showed limited associations. Notably, E/e' and TRPG remained associated with NT-proBNP irrespective of AF status. TRIAL REGISTRATION:UMIN-CTR ID: UMIN000021831.

BACKGROUND:Diastolic dysfunction is a recognized chronic allograft complication, and a restrictive left ventricular filling pattern is associated with adverse outcomes. However, the underlying pathophysiological mechanisms remain unclear. METHODS AND RESULTS:This study included 32 heart transplant recipients with a normal filling pattern at 1-year after transplantation. Five-year echocardiography classified patients into restrictive (n=12) and non-restrictive (n=20) groups. All patients underwent right heart catheterization and right ventricular endomyocardial biopsy at 1 and 5 years. Bulk RNA sequencing was performed on paired biopsy samples from 10 patients with available tissue. From 1 to 5 years, the restrictive group demonstrated significantly greater increases in pulmonary artery wedge pressure and the E/A and E/e' ratios, with no histopathological evidence of rejection and similar myocardial interstitial fibrosis in the 2 groups (P=0.81). Transcriptome analysis demonstrated that there was significant enrichment of immune and inflammatory pathways, including gene sets annotated as allograft rejection and T cell receptor signaling (Padjusted<0.05), in the restrictive group at 5 years. Temporal analysis revealed that these pathways were downregulated from 1 to 5 years in the non-restrictive group but remained persistently activated in the restrictive group. CONCLUSIONS:The development of a restrictive filling pattern is associated with elevated intracardiac pressures and a persistent immune-related transcriptome signature, despite no histological evidence of rejection.

Background: Low peak oxygen uptake ((V)over dotO(2)), especially <= 14 mL/min/kg, is a strong indicator of poor prognosis in patients with heart failure (HF). However, measuring this parameter is sometimes difficult if the maximal workload is not reached. This study developed a predictive classification model for low peak (V)over dotO(2) in HF patients using machine learning (ML). Methods and Results: We retrospectively analyzed the data for 343 patients with chronic HF and left ventricular ejection fraction <50% who underwent a symptom-limited cardiopulmonary exercise test and extracted 33 variables from their laboratory, echocardiographic, and exercise data up to the submaximal workload. The dataset was randomly divided into training and testing datasets in a 4 : 1 ratio. ML methods, including an exhaustive search for predictor selection, were used, and a support vector machine algorithm was applied for model optimization. We identified 5 important predictors: age, B-type natriuretic peptide, left ventricular end-diastolic diameter, (V)over dotO(2) at rest, and (V)over dotO(2) at respiratory exchange ratio of 1.00. Using these 5 predictors, an optimized predictive model was validated on the testing dataset, yielding an accuracy of 85%, F1 score of 0.81, and area under the receiver operating curve of 0.94 (95% confidence interval: 0.89-1.00). Conclusions: Using readily available parameters, ML methods can enable accurate prediction of low peak (V)over dotO(2) in patients with HF.

The deformability of red blood cells (RBCs) is essential for peripheral circulation and RBC survival and is reportedly altered in several diseases. However, its detail in iron-deficiency (ID) anemia remains poorly understood. We investigated the association between ID and RBC deformability in 120 participants classified into four groups according to their ferritin and hemoglobin levels: non-ID/non-anemia (n = 61), ID/non-anemia (n = 32), ID/anemia (n = 15), and non-ID/anemia (n = 12). In the analysis using the established on-chip deformability checker, the normalized transit velocity of RBCs through the peripheral-vessel constriction models was significantly higher in the ID/anemia group than in the other groups. The RBC deformability index (RDI), derived from the normalized transit velocity and degree of RBC deformation, was highest in the ID/anemia group, followed by the ID/non-anemia group. The RDI was negatively correlated with log(10) ferritin levels (r = -0.66, p < 0.01), even after adjusting for hemoglobin levels. Lower log(10) ferritin levels correlated with thinner, more oval-shaped RBCs and lower internal viscosity. These RBC characteristics were significantly associated with a higher RDI. These results suggest that, among several known determinants of RBC deformability, RBC morphology and internal viscosity are altered in ID, resulting in higher deformability.

This cross-sectional pilot study investigated the clinical characteristics of anti-centromere antibody (ACA)-positive patients with below-the-knee arterial disease. Sixteen ACA-positive patients (mean age 69 ± 10 years; 94% women) underwent contrast-enhanced computed tomography evaluation, with arterial damage scored using the Global Limb Anatomic Staging System. Lower extremity arterial disease (LEAD) was defined as a below-the-knee arterial score ≥ 1 or > 50% stenosis in above-the-knee lesions. Eight patients were categorized into the LEAD group (below-the-knee arterial damage score 12 ± 6). The LEAD group showed significantly higher serum IgG1 levels (1029 ± 484 vs. 531 ± 72 mg/dL, p < 0.001) and a higher prevalence of diastolic dysfunction (62% vs. 0%, p = 0.026) compared to the non-LEAD group. Patients with diastolic dysfunction had significantly higher serum IgG1 levels than those without (1190 ± 559 vs. 593 ± 139 mg/dL, p = 0.008). These findings suggest associations between elevated serum IgG1 levels, below-the-knee arterial disease, and left ventricular diastolic dysfunction in ACA-positive patients.

In catheter ablation for outflow tract premature ventricular contraction (PVC), electrical mapping of the aortic sinus cusp (ASC) provides critical information for identifying the origin of the PVC. The OCTARAY™ (Biosense Webster, Diamond Bar, CA, USA), a multispline 48-polar electrode catheter with TRUEref™ technology, fits the shape of the ASC and enables detailed and prompt high-resolution ASC mapping without inducing PVCs due to mechanical stimulation. We present a case of successful catheter ablation for two similar PVCs from the ASC based on activation and voltage mapping using TRUEref™ technology. High-resolution mapping could be helpful for the visual assessment of the detailed wavefront propagations of PVC. Learning objective:In catheter ablation for outflow tract premature ventricular contraction (PVC), mapping the aortic sinus cusp is useful to identify the origin; however, it is sometimes challenging with a conventional electrode catheter. High-resolution mapping using OCTARAY™ might be helpful for detailed assessment of outflow tract PVC.

Background:A4-wave amplitude (A4-amplitude) is a crucial factor determining the percentage of atrioventricular synchrony (%AVS) in a mechanical sensing-based VDD leadless pacemaker (VDD-LP). We hypothesized that 12-lead electrocardiographic (ECG) parameters related to right atrial (RA) excitation could predict A4-amplitude. Objectives:We aimed to investigate the relationship between A4-amplitude and 12-lead ECG parameters reflecting RA excitation and assess its predictive power for achieving an appropriate A4-amplitude associated with high %AVS. Methods:This single-center, retrospective, observational study enrolled consecutive patients undergoing VDD-LP implantation. The relationship between A4-amplitude and the positive peak amplitude of the P wave in lead II (P2), the positive peak amplitude of the P wave in lead V1 (V1P), and the sum of P2 and V1P (V1PP2) were assessed. Results:Of the 67 patients undergoing VDD-LP implantation, 46 without atrial fibrillation bradycardia were enrolled. They had a data set of manual atrial mechanical sensing tests and 12-lead ECG. Among P2, V1P, and V1PP2, only V1PP2 was correlated with A4-amplitude (R 2=0.10; P=.029). In 30 patients in VDD pacing mode, the median %AVS was 67.8%. The A4-amplitude cutoff for %AVS ≥ 67.8% was 3.2 m/s2 (area under the curve [AUC] 0.81; P=.002). For A4-amplitude ≥ 3.2 m/s2, V1PP2 had moderate predictive power (AUC 0.72; P=.007). In 30 patients without sick sinus syndrome, the predictive power of V1PP2 for A4-amplitude ≥ 3.2 m/s2 was increased (AUC 0.80; cutoff value 110 μV; sensitivity 83%; specificity 71%; P=.011). Conclusion:V1PP2, reflecting RA excitation, was related to A4-amplitude and had moderate predictive power. Notably, its predictive power increased when limited to patients without sick sinus syndrome. V1PP2 is a simple ECG predictor of A4-amplitude.

BACKGROUND:Percutaneous coronary intervention (PCI) is a good option for patients with ischemic cardiomyopathy (ICM) at high operative risk. However, evidence shows little benefit of PCI, potentially due to heterogeneity in ICM. Here, we applied latent class analysis (LCA) to clinical data to characterize ICM phenotypes based on clinical features and to assess differences in clinical outcomes. METHODS AND RESULTS:LCA was performed on data from 492 patients with a left ventricular (LV) ejection fraction <50% who underwent PCI. Primary outcomes included all-cause mortality and heart failure (HF) hospitalization. The optimal number of clinical phenotypes was 3. Phenotype 1 (n=101) was characterized by severe chronic kidney disease and a high frequency of hemodialysis. Phenotype 2 (n=192) included men with early-onset ICM, a high frequency of lifestyle-related diseases, and a high body mass index. Phenotype 3 (n=199) included older adults with a high prevalence of atrial fibrillation, moderate/severe mitral regurgitation, and high B-type natriuretic peptide levels. The risk of combined all-cause mortality and HF hospitalization was significantly lower for Phenotype 2 than the other phenotypes. LV reverse remodeling (LVRR) was associated with a lower incidence of the primary outcome in Phenotype 3, but not in the other phenotypes. CONCLUSIONS:We identified differences in clinical outcomes and LVRR across clinical ICM phenotypes after PCI, suggesting distinct underlying mechanisms across ICM phenotypes that may benefit from targeted treatments.

Background: The clinical course of cardiac sarcoidosis is typically subacute, and fulminant cases requiring mechanical circulatory support are rare. Here, we report the case of a patient with pathologically diagnosed cardiac sarcoidosis who presented with fulminant myocarditis and whose cardiac function was improved by aggressive immunosuppressive therapy based on the treatment of giant cell myocarditis. Case Presentation: A 55-year-old woman presented with progressive dyspnoea and nausea that persisted for 1 month and was eventually diagnosed with acute heart failure. Echocardiography showed a reduced left ventricular ejection fraction with thinning of the basal septal wall. During hospitalisation, she experienced ventricular tachycardia and fibrillation attacks, and bradycardia due to a complete atrioventricular block and sinus dysfunction was observed after starting amiodarone. Subsequently, she underwent intra-aortic balloon pump insertion in addition to inotropic agent administration; however, venoarterial extracorporeal membrane oxygenation and Impella 5.0 were needed because biventricular dysfunction progressed. We diagnosed our patient with cardiac sarcoidosis based on the pathological findings revealing inflammatory cell infiltration, including giant cells with extensive fibrosis and granulomas. However, the possibility of giant cell myocarditis could not be ruled out because of the fulminant clinical course; therefore, aggressive immunosuppressive therapy with corticosteroids and cyclosporine was started. Her cardiac function improved, and all mechanical circulatory support and inotropic agents were discontinued. Conclusion: Cardiac sarcoidosis is difficult to differentiate from giant cell myocarditis because they have many similarities in terms of myocardial histopathology and clinical manifestations. While whether the two diagnoses are parts of a single-disease continuum remains debatable, aggressive combination immunosuppressive therapy may contribute to favourable outcomes.

BACKGROUND:Atrial tachycardia (AT) during acute heart failure with reduced left ventricular ejection fraction (LVEF) can worsen hemodynamics. Antiarrhythmic drugs are limited by negative inotropic effects. CASE SUMMARY:A 55-year-old man with idiopathic dilated cardiomyopathy was admitted with worsening heart failure under sustained AT. His LVEF had declined to 12%. Multiple ATs caused resistance to inotropes and diuretics. Repeated electrical cardioversion with intravenous amiodarone failed owing to recurrent ATs triggered by premature atrial contractions, leading to cardiogenic shock. Intravenous nifekalant and digoxin were administered for rhythm and rate control. After electrical cardioversion, premature atrial contractions no longer induced AT. Continuous nifekalant maintained sinus rhythm, allowing recovery from shock without mechanical support. Catheter ablation, cardiac resynchronization therapy, and oral sotalol achieved long-term rhythm control. The patient was discharged on day 96. DISCUSSION:Nifekalant, a selective delayed rectifier potassium current blocker, prolongs refractoriness with minimal inotropic effect, stabilizing rhythm and bridging to definitive therapy. TAKE-HOME MESSAGE:Nifekalant may be effective for refractory AT in patients with severely reduced LVEF and hemodynamic instability.

Cardiac sympathetic hyperactivity may be implicated in the pathogenesis of Takotsubo syndrome (TTS). With complete denervation of a transplanted heart, the recipient heart is less susceptible to sympathetic hyperactivity. We report a rare case of recurrent TTS in a heart transplant recipient from a donor with TTS. Iodine-123 meta-iodobenzylguanidine (123I-MIBG) scintigraphy results for evaluating sympathetic activity are presented. A 46-year-old woman underwent heart transplantation for dilated phase of hypertrophic cardiomyopathy following recurrent cerebral haemorrhage complications after left ventricular assist device therapy 2 years prior. The donor heart exhibited a transient mildly reduced left ventricular ejection fraction suggestive of TTS. Four years post-transplantation, she was admitted with difficulty breathing, and echocardiography showed decreased biventricular apical wall motion. During her treatment course, wall motion improved spontaneously, and giant negative T waves were observed on electrocardiography (ECG). Coronary computed tomography and endomyocardial biopsy findings were normal, and a diagnosis of TTS was made. Approximately 5 years post-transplantation, she was readmitted with difficulty breathing, and echocardiography showed akinesis of the mid-to-apical biventricular wall. Wall motion normalized within a few days, and ECG showed typical giant negative T waves, consistent with TTS. 123I-MIBG scintigraphy taken prior to discharge and 6 months later showed minimal myocardial uptake in the basal anterior wall, indicating insufficient sympathetic reinnervation. Recurrent TTS in a denervated heart suggests the possibility of other underlying mechanisms besides cardiac sympathetic hyperactivity. This case highlights potential TTS development in transplant recipients from donors with TTS, underlining the need for close monitoring.

BackgroundElevated resting energy expenditure (REE) promotes cachexia, worsening prognosis in patients with advanced heart failure (HF). However, adequate assessment of energy balance is challenging because of unvalidated common prediction methods and unestablished determinants of REE, resulting in a lack of biomarkers for predicting insufficient energy intake.ObjectiveThis cross-sectional study aimed to evaluate REE in patients with advanced HF and explore biomarkers for insufficient energy intake.MethodsWe measured REE by indirect calorimetry and calculated the total energy expenditure (TEE) of 72 hospitalized patients with advanced-stage HF. We compared these values with commonly-used formulas and analyzed the associations between REE per body weight (REEBW) and parameters related to hemodynamics and HF severity. In 17 of 72 patients, plasma amino acid (AA) and 24-h urinary AA concentrations were measured to analyze their correlations with energy balance, the ratio of caloric intake to REE.ResultsResting energy expenditure and TEE values were significantly higher than the predicted values. The mean REEBW was 25 kcal/kg/day, while that for the underweight (<18.5 kg/m2) was 28 kcal/kg/day. We found a significant negative correlation between REEBW and body mass index (BMI), but no significant correlation between REEBW and HF-related parameters. The difference between TEE and predicted TEE using the European Society for Clinical Nutrition and Metabolism formula was most significant in the underweight patients because of underestimation, whereas TEE and pTEE using our modified formula with coefficients by BMI categories did not differ. There was a significant correlation between energy balance and urinary histidine and its metabolite 3-methylhistidine excretion, but no significant correlation with serum albumin and other AA concentrations.ConclusionUnderweight patients with advanced HF require more energy per weight than the predicted value. Our proposed formula for pTEE in each BMI category may be useful in clinical practice to avoid underestimation of daily energy requirements. Inadequate energy intake, even with such an approach, may be identified by decreased urinary essential AA levels.

AIMS:Electron microscopy reveals microstructural alterations in cardiomyocyte nuclei and myofilaments in non-ischaemic cardiomyopathy (NICM), particularly in dilated cardiomyopathy (DCM). Nevertheless, the correlation between such observations and clinical outcomes, including prognosis and left ventricular reverse remodelling (LVRR), remains unclear. This study aimed to examine the association between electron microscopic findings and outcomes in patients with NICM. METHODS:In this multicentre, prospective, observational study, 170 patients with NICM with reduced ejection fraction (EF) < 40%, scheduled for diagnostic endomyocardial biopsy and optimization of medical therapies, were enrolled. Electron microscopic findings of cardiomyocytes such as discontinuous or continuous nuclear envelopes and injured or preserved myofilaments were evaluated. Data on cardiac events (cardiac death or left ventricular assist device implantation) and LVRR, defined as achieving an EF > 35% with a 10% unit absolute increase, were collected 1 year post-biopsy. RESULTS:A total of 148 patients were finally analysed. Discontinuous nuclear envelopes and myofilament injuries were observed in 17 (11%) and 46 (31%) patients with NICM, respectively. The incidence of cardiac events at 1 year did not differ between groups with discontinuous and continuous nuclear envelopes [12% vs. 6%, odds ratio (OR): 2.05, 95% confidential interval (CI): 0.40-10.6, P = 0.391], whereas the LVRR rate was significantly lower in the discontinuous group than in the continuous group (24% vs. 52%, OR: 0.29, 95% CI: 0.08-0.92, P = 0.036). The incidences of cardiac events and LVRR at 1 year differed between the injured and preserved myofilament groups (15% vs. 3%, OR: 6.64, 95% CI: 1.32-33.5, P = 0.022; 15% vs. 64%, OR: 0.10, 95% CI: 0.04-0.25, P < 0.001, respectively). These associations between electron microscopic findings and clinical outcomes persisted, even in patients who were finally diagnosed with DCM. CONCLUSIONS:Discontinuous nuclear envelopes were associated with a reduced LVRR rate, whereas injured myofilaments were correlated with higher 1 year cardiac events and a decreased LVRR. Evaluation of electron microscopic images in diagnostic endomyocardial biopsy can facilitate risk stratification of NICM or DCM with reduced EF.

A male patient in his 60s with advanced heart failure and a HeartMate3 left ventricular assist device (LVAD) was admitted to our hospital for the sixth time in one year due to recurrent small-bowel bleeding. Nine months after admission, conservative treatment failed to achieve stable hemostasis. Gastroenterologists and surgeons performed double-balloon enteroscopy with mini-laparotomy and achieved complete hemostasis with endoscopic clipping and surgical suturing from the serosal side to multiple bleeding sites. The patient was discharged without any signs of rebleeding. In conclusion, our method represents an effective strategy for managing challenging SBB cases in patients with LVAD.