Cardiac rehabilitation (CR) improves physical function in patients with acute decompensated heart failure (ADHF) and frailty. However, few studies have assessed physical function through multiple measures during hospitalization; moreover, the effect of age remains unclear. This study aimed to evaluate age-specific changes in physical function during the acute-phase treatment period in patients with ADHF. Patients with ADHF hospitalized between June 2018 and June 2023, who were aged ≥ 60 years and underwent CR, were included in the study. Physical function assessments at admission and discharge included grip strength, quadriceps isometric strength, short physical performance battery (SPPB), gait speed, and frailty. Changes in physical function from admission to discharge were assessed. The mean age of the 531 patients was 79.8 ± 9.0 years and 58% were male. Physical function at admission and discharge significantly decreased with age according to all measures. In patients aged ≥ 90 years, quadriceps isometric strength (0.27 ± 0.11 kgf/BW kg) and the SPPB score (4.5 ± 3.6 points) were severely impaired at admission. However, no significant differences were observed in changes in physical function according to age; the improvement in the SPPB score tended to increase with age (+1.7 ± 1.9, +2.3 ± 2.1, +2.2 ± 2.4, and +2.3 ± 1.8, in the 60-69-, 70-79-, 80-89-, and ≥ 90-year age groups, respectively). The improvement in frailty was similar in all groups. Although physical function declined with age, the changes in physical function were similar in patients with ADHF at any age above 60 years who underwent CR.

By ambulatory blood pressure monitoring (ABPM), nocturnal blood pressure (BP) may increase before heart rate (HR), but the details are unknown.Among 102 participants who underwent ABPM, > 90% on hypertension treatment, the averaged BP (HR) data were examined for the time at which the BP (HR) increased significantly above the mean midnight BP (HR) between 3:00 AM - 9:00 AM in all patients and in subgroups divided by clinical variables. Participants were also divided according to the respiratory sinus arrhythmia (RSA) index, which is the ratio of the longest and shortest RR intervals obtained under normal breathing, and the effects of RSA on the nocturnal hemodynamics were examined.The average age of the patients was 70 ± 11 years, and there were 47 (46.1%) males. After midnight, the BP increased and was significantly greater than the midnight BP at 5:00 AM. The time of significant increase in BP was affected by clinical variables and the RSA index; an RSA index < 5% (> 10%) was associated with the earliest (latest) time of BP increase. However, the HR remained unchanged until 7:00 AM or later. According to the ABPM data, a discordant time course between BP and HR and the effect of RSA were evident during the nocturnal period.BP increased earlier than HR toward dawn, and this phenomenon was affected by clinical variables. A low RSA index facilitated the onset of BP increase. The underlying mechanisms and clinical significance of the role of RSA in circulatory regulation remain to be investigated.

There is growing evidence that body nutritional status influences the development of cardiovascular disease, particularly in the elderly population. The Geriatric Nutritional Risk Index (GNRI), as a tool for assessing the nutritional status and nutritional risk of elderly individuals, is applied in clinical practice. This study aimed to elucidate the relationship between GNRI and cardiovascular disease in the elderly and to assess the impact of nutritional status on cardiovascular disease.This study is a cross-sectional study based on the National Health and Nutrition Examination Survey (NHANES) database. The data for this investigation were obtained from the NHANES database from 2007 to 2018, which included 10,277 individuals aged 60 years and older. The relationship between GNRI and cardiovascular disease in the elderly was investigated using weighted multivariable logistic regression models, and smooth fitting curves were drawn to explore their association. In addition, subgroup analyses were used to explore population differences.In this study, after adjusting for all confounding variables, the odds ratio and 95% confidence intervals (CI) of the model were 0.98 (0.96, 1.00), with no statistically significant association. Smooth fitting curves showed a nonlinear correlation between GNRI and cardiovascular disease. We found an inflection point (GNRI = 139.55). Moreover, GNRI was negatively associated with cardiovascular disease in the elderly before the inflection point and not statistically significant after the inflection point.In this large cross-sectional study, we found a nonlinear correlation between GNRI and cardiovascular disease in the general elderly population in the United States.

Atherosclerosis (ATH) represents a major cause of cardiovascular disease. Long noncoding RNA (LncRNA) myocardin-induced smooth muscle lncRNA, inducer of differentiation (MYOSLID) and microRNA (miR) -29c-3p show substantial roles in ATH. We investigated their regulatory mechanisms on vascular smooth muscle cell (VSMC) proliferation and migration.Angiotensin (Ang) II-induced VSMCs were used for in vitro research. The MYOSLID and miR-29c-3p expression patterns in VSMCs were assessed by reverse transcription-quantitative polymerase chain reaction. MYOSLID was overexpressed, or miR-29c-3p was silenced in VSMCs by cell transfection, followed by proliferation, migration, and apoptosis evaluation. The colocalization of MYOSLID and miR-29c-3p was observed by RNA in situ hybridization. The targeted binding relationship of miR-29c-3p and MYOSLID was verified by dual-luciferase and RNA immunoprecipitation assays. Joint experiments were performed with the overexpressed MYOSLID and miR-29c-3p via cotransfection. An ATH mouse model was established and injected with LV-MYOSLID, with the aortic root atherosclerotic lesion observed by HE staining and the α-SMA expression determined by immunohistochemistry.The MYOSLID expression was decreased, while the miR-29c-3p expression was increased in the Ang II-induced VSMCs, along with the promoted VSMC proliferation, apoptosis, and migration. Meanwhile, the MYOSLID overexpression or miR-29c-3p silencing repressed the Ang II-induced VSMC behaviors. The miR-29c-3p mimics reduced the luciferase activity of the MYOSLID 3'UTR-WT-transfected cells, but had no obvious influence on the MYOSLID 3'UTR-MUT-transfected cells. Overexpressed miR-29c-3p partially nullified the highly expressed MYOSLID-repressed Ang II-induced VSMC apoptosis, proliferation, and migration. The MYOSLID overexpression repressed the miR-29c-3p expression and reduced the atherosclerotic lesion area and the number of α-SMA-positive VSMCs in ATH mice.The MYOSLID overexpression restrained the Ang II-induced VSMC proliferation, migration, and apoptosis by repressing the miR-29c-3p expression, thus retarding the atherosclerotic plaque formation.

Oxidative stress and cardiomyocyte apoptosis are hallmarks of heart failure (HF) development. Plant homeodomain finger protein 8 (PHF8) is a histone demethylase downregulated in failing human hearts. Nevertheless, the potential role of PHF8 in HF remains unclear. Therefore, this study aimed to explore the biological action and molecular mechanism of PHF8 in HF.A rat model of left anterior descending coronary artery (LAD) ligation-induced HF and a cardiomyocyte model of oxygen-glucose deprivation/reperfusion (OGD/R) were developed after gain- or loss-of-function experiments in rats and cardiomyocytes, respectively. Heart function indexes, such as left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction, and left ventricular fractional shortening, were detected. Changes in myocardial tissues were examined by pathological staining. Cardiomyocyte apoptosis and oxidative stress markers, such as malondialdehyde, reactive oxygen species, superoxide dismutase, and catalase, were examined. The relationship between PHF8 and forkhead box A2 (FOXA2) was analyzed by luciferase and chromatin immunoprecipitation-quantitative polymerase chain reaction assays.PHF8 was downregulated in LAD-ligated rats and OGD/R-exposed cardiomyocytes. Following PHF8 upregulation, pathological changes in myocardial tissues and heart dysfunction were improved in LAD-ligated rats. Importantly, cardiomyocyte apoptosis and oxidative stress were diminished in vivo and in vitro upon PHF8 upregulation. Mechanistically, PHF8 increased FOXA2 expression in a histone demethylase-dependent manner. FOXA2 silencing abrogated the protective effect of PHF8 upregulation on cardiomyocytes against OGD/R-induced apoptosis and oxidative stress.PHF8 exerts protective functions against cardiomyocyte apoptosis, oxidative stress, and heart dysfunction in HF, in correlation with FOXA2 upregulation. These results suggest that the PHF8/FOXA2 axis may be a promising therapeutic target to prevent HF.

Chronic heart failure (CHF) triggers a cascade of events involving parthanatos and pyroptosis, culminating in cellular malfunction, inflammation, and tissue degeneration. This study aims to inquire into the inherent mechanism of chrysophanol (CHR) in the treatment of CHF.In vitro, we cultured the rat embryonic cardiomyocyte cell line H9c2. Parthanatos was initiated through N-methyl-N'-nitro-N'-nitrosoguanidine (MNNG) induction, followed by treatment with varying concentrations of CHR. The evaluation of parthanatos and pyroptosis in cardiomyocytes was assessed by western blotting. In vivo, the transverse aortic constriction (TAC) model was used to simulate CHF. The hemodynamic indices were performed to evaluate cardiac function in rats. The degree of inflammatory cell infiltration and fibrosis within cardiac tissue was assessed using hematoxylin and eosin staining and Masson's trichrome staining, respectively. Cardiac tissues were obtained and subjected to immunohistochemical analysis to assess PARP-1 expression. Subsequently, dual immunofluorescence staining (caspase-1 and NLRP3) was conducted, aiming to comprehensively evaluate the status of parthanatos and pyroptosis in the cardiac tissues of rats.In contrast to the MNNG or TAC group, the groups administered with CHR exhibited an inhibitory effect on Reactive oxygen species (ROS) expression, as well as parthanatos and pyroptosis proved by cell and animal experiments (P < 0.05). The reduced expression of PAR, PARP-1, AIF, NLRP3, IL-1β, caspase-1, and cleaved-GSDMD compared with the MNNG or TAC group proved it (P < 0.05). Moreover, compared with the TAC group, CHR significantly improved the cardiac histology of TAC rats. These findings collectively suggested the potential of CHR in ameliorating CHF.CHR may mitigate CHF in rats by modulating ROS-mediated parthanatos and pyroptosis.

Esaxerenone, a non-steroidal mineralocorticoid receptor (MR) blocker, exhibits high selectivity for MR. While clinically used as an anti-hypertensive drug, its impact on cardiac remodeling remains poorly understood. This study investigated the effect of esaxerenone on pressure overload-induced cardiac hypertrophy in mice.Eight-week-old C57BL/6 mice underwent either transverse aortic constriction (TAC) or sham surgery. Animals were divided into 2 groups: 0.003% (3.0 mg/kg) Esaxerenone-fed (EX) and normal-fed (CNT) groups (n = 64, Sham/CNT = 12, Sham/EX = 13, TAC/CNT = 18, TAC/EX = 21). Cardiac gene expressions were analyzed using quantitative real-time PCR.Food intake and body weight variations showed no significant differences between CNT and EX groups during the 2-week experimental period. The mortality rate from 24 hours after TAC surgery to the end of the experiment was 30.8% in the CNT group, however, all mice survived following TAC surgery in EX group. CNT group showed a remarkable increase in heart weight/tibial length ratio 2 weeks after TAC compared with the Sham group. The EX group demonstrated a significant decrease in HW/TL following TAC surgery (-23.4%, P = 0.041). Masson's trichrome staining revealed that the TAC/CNT group had a significantly higher proportion of fibrotic area than the Sham/CNT group. However, the TAC/EX group had a slightly lower proportion of fibrotic area than the TAC/CNT group. In cardiac gene expression analysis, ANP and Collagen 3a1 were upregulated in the TAC group but were significantly reduced following treatment with esaxerenone.Esaxerenone attenuates cardiac hypertrophy and hypertrophy-related gene expression, resulting in improved survival in a pressure overload model in mice.

Maternal overnutrition correlates with detrimental outcomes in offspring. However, the specific effects of gestational exposure to a high-fat diet (HFD) on fetal development remain unclear. This study aimed to elucidate the developmental phenotypes of neonatal organs and cardiomyocytes of mice exposed to gestational HFD, revealing growth retardation and a notable reduction in cardiomyocyte cell cycle activity. In this study, an HFD model was used to investigate the effects of maternal HFD on offspring development. Defective development was observed in the offspring, and severe restriction of cell proliferation was noted in the neonatal organs as a result of maternal HFD. Based on this evidence, we detected a reduction in cardiomyocyte proliferation in offspring exposed to maternal HFD. Moreover, RNA sequencing analysis revealed that HFD diminished fatty acid metabolism, enhanced the inflammatory response, and upregulated the transcription of genes involved in Tp53-regulated cell cycle arrest in postnatal day 0 (P0) cardiomyocytes. Furthermore, our results showed that the effects of the maternal diet during gestation are profound and normal lactation and feeding after delivery cannot help adult offspring recover from defective heart development. These findings highlight the diverse pathways affected by maternal HFD, particularly implicating a potential TP53-dependent mechanism contributing to cardiac defects in offspring.

Myocardial infarction (MI) is a cardiovascular condition that leads to increased morbidity and mortality, impacting the quality of life of individuals. Aloperine (ALO), derived from Sophora alopecuroides L, has been recognized for its beneficial effects in treating various diseases by showcasing therapeutic properties. However, the precise protective mechanisms of ALO on hypoxia/reoxygenation (H/R) -induced damage in cardiomyocytes in vitro remain unclear. In this study, it was manifested that cell proliferation was weakened after H/R treatment, but this impact was offset after ALO treatment. Furthermore, cell apoptosis was heightened after H/R treatment, but this phenomenon was neutralized after ALO treatment. ALO relieved inflammation in H/R-treated H9C2 rat cardiomyoblast cells. Moreover, ALO strengthened autophagy in H/R-triggered H9C2 rat cardiomyoblast cells through enhancing the LC3II/LC3I level and the LC3B fluorescence intensity. Lastly, it was testified that ALO can rescue the weakened autophagy, the heightened cell apoptosis, and the augmented inflammation after CC treatment in H/R-mediated H9C2 rat cardiomyoblast cells. In conclusion, ALO regulated inflammation, apoptosis, and autophagy through AMPK/Nrf2 pathway in H9C2 rat cardiomyoblast cells after excessive hypoxia. This study suggested that ALO may be an underlying drug for MI therapy.

The prevalence of atrial fibrillation (AF) increases with age and treatment with catheter ablation is performed frequently. Catheter ablation may have a lower rate of success and a higher rate of complications in older patients.We compared the characteristics, success rates, and complications of catheter ablation in patients with AF categorized into late old-aged (≥ 75 years, n = 148), early old-aged (65-74 years), n = 129), and middle-aged (< 65 years, n = 91) groups. Effects of catheter ablation on cardiac function in the left ventricle (LV) and left atrium (LA), and plasma B-type natriuretic peptide levels were evaluated at baseline and 1 year.AF ablation was successfully performed in older patients and the recurrence rate did not differ between groups (late old-aged: 29.7%, early old-aged: 15.5%, middle-aged: 23.1%). Procedural complications did not statistically differ among the groups (late old-aged: 9.5%, early old-aged: 6.2%, middle-aged: 3.3%). The LA volume index was greater in the late old-aged patients than in the other 2 groups. As comorbidities, hypertension and history of heart failure and stroke were more common in late old-aged patients. At 1 year after ablation, the LV ejection fraction, the LA volume index, and LA emptying fraction were improved, even in late old-aged patients. Plasma B-type natriuretic peptide levels were reduced in both the late old-aged and early-old-aged groups.Our findings indicate that AF ablation in late old-aged patients is effective, particularly with regard to LA structure and function, and the complication rate is similar to that in middle-aged patients.

Acute coronary syndrome (ACS) is a rare complication of infective endocarditis (IE) and is associated with high mortality. Typically, coronary artery occlusion is a complication of bacterial autologous valve IE. We present the case of a 74-year-old woman with a history of aortic valve replacement for aortic stenosis who was receiving immunosuppressive therapy for rheumatoid arthritis. Upon admission, she was diagnosed with ST-elevation myocardial infarction (STEMI), and coronary angiography (CAG) revealed complete occlusion in the terminal branches of the left circumflex coronary artery (LCX #12 and #14). On day 3 of admission, three-dimensional transesophageal echocardiography (3D-TEE) was performed, and vegetation was detected, leading to IE diagnosis.The patient underwent prosthetic valve replacement on day 4. Subsequent blood cultures grew Candida albicans, and histopathological examination using Grocott staining confirmed the presence of Grocott-positive fungi within the vegetation, leading to a definitive diagnosis of prosthetic valve endocarditis (PVE) caused by Candida albicans; this management resulted in favorable outcomes. The present case suggests that fungal PVE can also complicate STEMI, and real-time 3D-TEE was instrumental in diagnosing and accurately assessing the vegetation in this condition.

Several errors (shown with underlines) in the following list appeared in the article "Phenogroups and Their Prognosis of Acute Decompensated Heart Failure with Preserved Ejection Fraction" by Taro Makino, Yuya Ishihara, Masahide Harada, Yoshihiro Sobue, Eiichi Watanabe, Yukio Ozaki, Hideo Izawa (Vol. 65 No.5, 841-848, 2024).

Atherosclerotic diseases, like coronary artery disease (CAD), are recognized to be associated with oxidative stress and inflammation. Sestrin2 is a stress-inducible protein that has anti-oxidant and anti-inflammatory properties. We previously reported that plasma sestrin2 levels were high in patients with CAD. However, no study has shown their prognostic value in patients with CAD. We investigated the association between plasma sestrin2 levels and major adverse cardiovascular events (MACE) (cardiovascular death, myocardial infarction, unstable angina, coronary revascularization, heart failure, or stroke) in 320 patients undergoing coronary angiography, of whom 191 had CAD. During a mean follow-up of 7.0 ± 4.2 years, 58 patients had MACE. Plasma sestrin2 levels were higher in patients with CAD than without CAD (median 16.4 versus 14.2 ng/mL, P < 0.05). Notably, patients with MACE had higher sestrin2 levels (19.5 versus 14.9 ng/mL) and more often had sestrin2 > 15.0 ng/mL (79% versus 49%) than those without MACE (P < 0.001). Kaplan-Meier analysis showed lower event-free survival in patients with sestrin2 > 15.0 ng/mL than in those with ≤ 15.0 ng/mL (P < 0.001). In multivariate Cox hazards analysis, sestrin2 level (> 15.0 ng/mL) was a significant predictor of MACE (hazard ratio: 2.44; 95%CI: 1.28-4.67), independent of CAD and atherosclerotic risk factors. Moreover, among 191 patients with CAD, sestrin2 level was also a significant predictor of MACE (hazard ratio: 2.51; 95%CI: 1.28-4.82), independent of the severity of CAD and coronary revascularization. Thus, high plasma levels of sestrin2 at baseline angiography were found to be associated with an increased risk of cardiovascular events in patients with CAD and patients undergoing coronary angiography.

Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by progressive obliteration of pulmonary arteries. Dysregulated bone morphogenetic protein (BMP) signaling pathway contributes to the development of PAH, and pulmonary vasodilators including endothelin receptor antagonists, phosphodiesterase 5 inhibitors, prostaglandins and soluble guanylate cyclase stimulators, dramatically improve the long-term prognosis. However, there still exist refractory patients who require continuous catecholamine support or lung transplantation, and the development of new treatment strategies targeting molecular mechanisms of PAH is highly anticipated. Sotatercept, a first-in-class activin signaling inhibitor, has recently been approved for the treatment of PAH, and it targets and restores an imbalance in activin-growth differentiation factor and BMP pathway signaling. In addition, treatment strategies targeting peroxisome proliferator-activated receptor-γ signaling, inflammatory and immune systems, DNA damage response and cellular senescence, and growth factor receptors including vascular endothelial growth factor and platelet-derived growth factor receptors, are being devised. In this review, we briefly summarize the recent advances in basic research paving the way for the development of more effective treatments for PAH and their potential in clinical therapeutic applications.

In patients diagnosed with ST-segment elevation myocardial infarction (STEMI), despite exhibiting normal patency in the culprit arteries following percutaneous coronary intervention (PCI), coronary microvessels do not recover adequately, leading to microvascular dysfunction (MVD). Limited data are available regarding microcirculation assessed through invasive measures during the midterm period. This study aimed to investigate the assessment of MVD in STEMI patients using the index of microvascular resistance (IMR) during the midterm period.We prospectively evaluated 41 patients with STEMI who underwent PCI. IMR was measured by placing a coronary pressure wire with intravenous adenosine at 1 week as the acute phase and at 6 months after primary PCI as the midterm period. An improvement in IMR was observed from baseline to follow-up, with values changing from 30.00 (15.00-45.50) to 19.00 (10.50-30.50) (P = 0.020). The degree of MVD significantly decreased during follow-up (from 61.0% to 34.1%, McNemar's test: P = 0.016). Compared to patients with normal microcirculation, those with MVD (IMR > 25) at midterm follow-up exhibited significantly elevated levels of brain natriuretic peptide (180.25 [68.25-370.65] pg/mL versus 75.90 [18.70-169.70] pg/mL, P = 0.043) and prolonged symptom-onset-to-balloon time (727.00 [213.50-1170.00] minutes versus 186.00 [125.00-316.00] minutes, P = 0.002).These findings indicate that the extent of MVD 6 months post-PCI has significantly diminished compared to discharge levels and is associated with symptom-onset-to-balloon time. Therefore, MVD in patients with STEMI can potentially improve in the midterm under specific circumstances.

This study aimed to explore the clinical efficacy of Ginkgo biloba combined with Nicorandil in patients with heart failure who have a mild decrease in ejection fraction (HFmrEF).A total of 316 patients with HFmrEF were selected and randomly assigned to either a control group or a combination of the Ginkgo biloba and Nicorandil group, each group consisting of 158 patients. The control group received standard secondary preventive treatment, while patients in the combination group received oral Ginkgo biloba and Nicorandil based on stable conventional treatment. Both groups were treated continuously for six months. The age, sex, body mass index (BMI), New York Heart Association cardiac function classification, history of coronary heart disease, hypertension, diabetes, atrial fibrillation, smoking, left ventricular ejection fractions (LVEF), heart rate, glycosylated hemoglobin (HbA1c), and combined drug use of the patients in the two groups were recorded. The efficacy endpoints were BMI, heart rate, blood lipid levels, fasting blood glucose, renal function, HbA1c, N-terminal pro-brain natriuretic peptide (NT-proBNP), LVEF, cardiopulmonary exercise testing parameters, 6-minute walking distance (6MWD), and the Kansas City Cardiomyopathy Questionnaire (KCCQ) score after six months of treatment. The incidence of adverse reactions in the two groups was recorded.After six months of treatment, the BMI, heart rate, NT-proBNP, low-density lipoprotein cholesterol, triglyceride, creatinine, fasting blood glucose, and HbA1c levels of patients in the Ginkgo biloba combined with Nicorandil group were lower than those in the control group (P < 0.05). The LVEF, high-density lipoprotein cholesterol, VO2peak, oxygen uptake efficiency slope, 6MWD, and KCCQ scores were higher in the Ginkgo biloba combined with Nicorandil group than in the control group (P < 0.05). There was no statistically significant difference between the two groups of patients (P > 0.05) in the incidence of hypotension, hypoglycemia, hypokalemia, headache, and hospitalization due to worsening heart failure.Ginkgo biloba combined with Nicorandil can effectively improve heart function, blood lipid levels, blood glucose levels, renal function, exercise tolerance, and health-related quality of life in patients with HFmrEF. Because there were no significant adverse reactions, they can be safely used.

In conventional radiofrequency ablation for symptomatic paroxysmal atrial fibrillation, there are concerns regarding the risk of esophageal thermal injury (ETI), such as esophageal ulcers and left atrioesophageal fistulas. While the incidence of ETI is generally considered low with cryoballoon ablation, some cases of esophageal ulcers and gastric hypoperistalsis have been reported. In this report, we present the case of a 77-year-old male patient with atrial fibrillation after esophageal surgery who had successfully undergone cryoballoon ablation without esophageal complications, despite the close proximity of the left atrium and gastric tube. Cryoballoon ablation achieved pulmonary vein isolation without complications in the upper alimentary tract.

The psoas muscle area (PMA) and rectus femoris muscle area (RFMA) have been used to estimate whole-body muscle mass in elderly patients. However, it is unclear whether combining these measurements can improve the predictive ability of traditional risk factors for adverse clinical events in elderly patients with aortic valve stenosis (AVS). We analyzed data from 153 patients with AVS who underwent transcatheter aortic valve replacement (TAVR), and measured PMA and RFMA using computed tomography (CT) before the procedure. This study assessed a composite of adverse clinical events including all-cause death and heart failure (HF) requiring hospitalization for up to 3 years after TAVR. During the follow-up period, 31 patients experienced adverse clinical events (19 died, and 12 had HF). The multivariate Cox hazards analysis demonstrated that patients exhibiting lower PMA (males with < 3.36 cm/m and females with < 2.52 cm) and lower RFMA (males with < 3.26 cm/m and females with < 3.15 cm/m) had a higher probability of experiencing adverse clinical events compared to those with higher PMA and RFMA values, whether in combination or alone (P < 0.05). Additionally, net reclassification improvement (NRI) and integrated discrimination improvement (IDI) analyses showed that the combination of lower PMA and RFMA had a greater incremental effect on the predictive value of clinical risk factors for adverse clinical events. Therefore, the combined measurement of skeletal muscles using CT scans may be a valuable tool for assessing the risk of AVS in elderly patients undergoing TAVR.

Very late stent thrombosis (VLST) is a rare but critical complication of stent placement. In this report, we present 2 VLST cases diagnosed with neoatherosclerosis by detecting cholesterol crystals (CCs) via the filter paper rinse method. In terms of differentiating between neoatherosclerosis and stent thrombosis. There was no visible thrombus observed on thrombus aspiration. Examination of the blood sample obtained from the thrombus aspiration using the filter paper rinse method showed the presence of CCs under polarized light microscopy, thus, diagnosing VLST caused by neoatherosclerosis. Diagnosis of neoatherosclerosis would provide a rationale for intensive lipid-lowering therapy.

Previous studies have reported the efficacy and safety of therapeutic angiogenesis through bone marrow-derived mononuclear cell (BM-MNC) implantation in patients with no-option chronic limb-threatening ischemia (CLTI) from atherosclerotic lower extremity artery disease (LEAD). However, uncertain clinical prognostic factors impact treatment outcomes. This study aimed to elucidate the long-term outcomes of patients with atherosclerotic LEAD-derived no-option CLTI after BM-MNC implantation and to identify prognostic factors.In this retrospective, single-center, observational study, the primary endpoints included the long-term prognosis of BM-MNC implantation and factors influencing 1-year outcomes. A total of 92 limbs in 84 patients were analyzed in the final cohort (mean age: 67 years; male, 65%). The 5- and 10-year overall survival rates were 50.0% and 31.0%, respectively, while the 5- and 10-year amputation-free survival rates were 37.6% and 23.3%, respectively. Multivariate logistic analysis linked all-cause mortality to age ≥ 70 years, hemodialysis, smoking, and a controlling nutrition status score ≥ 5. Major amputation or mortality was associated with male sex, hemodialysis, and C-reactive protein levels ≥ 3.0 mg/dL. No adverse events were associated with therapeutic angiogenesis.These findings endorse the feasibility and safety of BM-MNC implantation for patients with no-option CLTI due to atherosclerotic LEAD. Moreover, the study highlights the significance of several prognostic factors, including advanced age, hemodialysis, smoking, and inflammatory markers, in influencing the long-term outcomes of this treatment.