Many studies have reported a relationship between various lipids, such as cholesterol, fatty acids, and lipoproteins, and cardiovascular events. Low-density lipoprotein cholesterol (LDL-C) is often cited as a representative marker. However, there is still room for discussion regarding which markers, among other lipids, should take clinical precedence.

This observational study focused on patients without residual stenosis on post-coronary angiography. It was based on blood tests, including lipid profiles at that time, and assessed the association with the subsequent occurrence of major adverse cardiovascular events (MACE, a composite of all-cause mortality, hospitalization due to heart failure, myocardial infarction, stroke, and all revascularizations).

Of the 375 patients analyzed, 134 experienced MACE (median follow-up duration: 1031 days). When comparing the MACE and non-MACE groups, significant differences were observed in lipid markers such as non-high-density lipoprotein cholesterol (non-HDL-C) and remnant-like particle cholesterol (RLP-C) (non-HDL-C; P = 0.003, RLP-C; P < 0.001). Furthermore, the area under the curve for RLP-C was 0.656 (95% CI: 0.598-0.714). Improvement in MACE risk discrimination was observed when LDL-C was replaced with non-HDL-C or RLP-C, in addition to atherosclerosis risk factors (non-HDL-C; net reclassification improvement (NRI) = 0.366, 95% CI: 0.159-0.572, RLP-C; NRI = 0.224, 95% CI: 0.016-0.433).

It is highly likely that non-HDL-C and RLP-C can serve as significant lipid markers for predicting the occurrence of MACE.

Left bundle branch pacing (LBBP) is an emerging physiological pacing technique that expanded in recent reports. The long-term safety and feasibility of LBBP lack adequate evaluation.

The study aimed to evaluate the long-term lead performance and clinical outcomes of LBBP.

We retrospectively enrolled 123 consecutive patients scheduled for LBBP implantation from January to December 2018. The pacing parameters, electrocardiograms, echocardiographic measurements, and complications associated with LBBP were tracked at implant and follow-up.

LBBP was successfully performed in 110 of 123 (89.4%) patients. Left ventricular end-diastolic dimension (LVEDd) and left ventricular ejection fraction (LVEF) improved from baseline in patients with reduced LVEF (n = 29; LVEDd, 55.6 ± 8.1 mm versus 63.4 ± 4.9 mm, P < 0.001; LVEF, 51.6% ± 13.6% versus 33.7% ± 5.5%, P < 0.001) while no significant change was found in patients with preserved LVEF (n = 81; LVEDd, 49.6 ± 12.0 mm versus 51.2 ± 6.0 mm, P = 0.38; LVEF, 65.8% ± 7.9% versus 65.8% ± 7.3%, P = 0.99). In seven patients, LBBP lead protuberance into the LV cavity was observed, with a mean distance between the screw tip and the LV septum of 3.0 ± 0.8 mm (range from 1.8 to 3.9 mm). The LBBP parameters remained stable.

LBBP is a novel physiological, safe, and effective pacing technique for patients with atrioventricular block. Lower BMI, diabetes and thinner interventricular septum (IVS) thickness are associated with mechanical complications.

The tricuspid annulus (TA) is the primary target of tricuspid valve (TV) surgery for tricuspid regurgitation (TR). However, the reference values for TA geometry in the Japanese population is currently unavailable. We aimed to elucidate the geometric reference values of the TA in Japanese individuals using 3-dimensional (3D) echocardiography.

We conducted a prospective study using transthoracic 3D echocardiography on 142 healthy Japanese subjects aged between 20 and 79 years. The tricuspid geometric parameters in the late-diastole and the mid-systole were analyzed using custom 3D software (Realview™).

After excluding 46 subjects with poor images, data from 96 subjects (67.6%) were analyzed. TA area and circumference showed strong correlations with body surface area (BSA) (P < 0.001 for all), while some of these parameters exhibited weak correlations with age. Gender differences in TV geometry were assessed across 3 age groups: 20-39 years (42 subjects), 40-59 years (28 subjects), and 60-79 years (26 subjects). In the youngest subjects (20-39 years), males had a significantly larger TA area and smaller anterior-posterior and medial-lateral diameters (P < 0.001 for all), even after adjusting for BSA, indicating gender differences of TA geometry. These differences diminished with age.

We present reference values for TA geometry by age and gender in a Japanese cohort. BSA may be a suitable metric for indexing the TA parameters. While age-related changes in TA parameters may not be significant, gender differences, particularly in younger individuals, persist even after adjusting for BSA.

Frailty is highly prevalent among patients with aortic stenosis (AS). Nonetheless, the impact of AS severity on frailty remains unclear. This study aimed to clarify the association between AS severity and frailty in this population.

This retrospective study included consecutive patients with AS who were hospitalized as candidates for transcatheter aortic valve implantation (TAVI). The prevalence of frailty, N-terminal pro B-type natriuretic peptide (NT-proBNP) level, gait speed, and geriatric nutritional risk index (GNRI) were compared between patients with severe and those with very severe AS. We employed multiple logistic regression analysis to examine the association between AS severity and frailty.

A total of 137 patients were included. The prevalence of frailty was not significantly different between the severe and very severe AS groups (31% versus 30%). Similarly, no significant differences between the groups were observed for gait speed and GNRI, whereas the NT-proBNP level was significantly higher in the very severe group than in the severe AS group (P < 0.01). In the multiple logistic regression analysis, AS severity was not associated with frailty; however, gait speed and GNRI showed significant association with frailty independently of age, sex, and heart failure (very severe AS: odds ratio [OR] 1.051, 95% confidence interval [CI] 0.439-2.517; low gait speed: OR 5.109, 95% CI 1.556-16.775; malnutrition: OR 2.841, 95% CI 1.145-7.049).

These findings suggest that low-intensity exercise training and nutritional therapy may be necessary in addition to AS treatment for the management of frailty in this population.

Cardiac resynchronization therapy with implantable cardioverter defibrillators (CRT-Ds) are established therapy options for patients suffering from heart failure (HF). Several aspects of HF modification have yet to be described regarding etiology-dependent outcome differences in the long-term.

The Mannheim CArdiac Resynchronization TherApy RetrospeCtive ObservAtioNAl (MARACANA) Registry retrospectively included all patients provided with CRTs in our center from 2013 to 2021. CRT-D recipients (n = 380) were grouped to either ischemic cardiomyopathy (ICM, n = 206) or nonischemic cardiomyopathy (NICM, n = 174). Both groups were compared regarding survival, left ventricular ejection fraction (LVEF), hospitalizations due to HF, intrinsic and paced QRS width, NYHA classification, and several further aspects of HF modification in the long-term (59.1 ± 4.81 months).

Patients with ICM were older (73.3 ± 8.4 versus 67.7 ± 10.8 years) and predominantly male (86.4 versus 74.7%) and presented with higher creatinine values (1.57 ± 0.92 versus 1.31 ± 0.66 mg/dL, each P < 0.05) at baseline. The mean survival for patients with NICM was better (51.9 ± 1.2 versus 54.4 ± 1.1 months, P = 0.03). Improvements in NYHA (2.93 ± 0.4 versus 2.79 ± 0.5-2.19 ± 0.7 versus 1.79 ± 0.7) and LVEF (26.4 ± 6.8 versus 27% ± 6.9% to 35.7 ± 9.6 versus 44 ± 11%, each P < 0.05) were similar for both groups after 5 years. Patients with ICM experienced more hospitalizations due to HF within the first year (odds ratio 1.9, P < 0.05), whereas electrical remodeling was more impressive for NICM (QRS width 157.1 ± 19.4 milliseconds versus intrinsic 116.6 ± 12.7 milliseconds and paced 131.9 ± 21 milliseconds after 5 years, both P < 0.05).

Patients with HF might experience long-term improvements in functional status and left ventricular reverse remodeling following CRT-D, regardless of underlying etiology. Alterations in some aspects of HF modification could be influenced by time- and etiology-associated comorbidities.

The optimal therapeutic approach to facilitate reverse remodeling is desired in patients with systolic heart failure following acute coronary syndrome (ACS). The association between heart rate (HR) and reverse remodeling in this cohort has remained elusive.

Patients with left ventricular ejection fraction (LVEF) < 50% who received echocardiography assessments following ACS were retrospectively included. Theoretically ideal HR was calculated using a previously established formula: 93 - 0.13 × (deceleration time [msec]). Impacts of HR on echocardiographic left ventricular (LV) reverse remodeling during the 2-year observational period were compared between 2 groups stratified by the HR difference between theoretically ideal and actual values: optimal HR group (HR difference ≤ 10 bpm) versus sub-optimal HR group (HR difference > 10 bpm).

A total of 27 patients (median 72 years old, 23 males) were included. There were no significant differences in the baseline characteristics including maximum serum creatinine kinase level and the dose of beta-blocker between the 2 groups. LV ejection fraction increased significantly only in the optimal HR group at follow-up (from 42% to 54%; P = 0.001). The optimal HR group exhibited a more pronounced decrease in LV end-diastolic diameter (from 57 to 52 mm) compared to the sub-optimal HR group (from 58 to 56 mm).

Optimal HR, which was calculated using a previously proposed formula, was associated with more substantial post-infarct LV reverse remodeling. The implications of aggressive HR modulation targeting theoretically ideal HR among those with systolic heart failure following ACS are the focus of our investigation here.

Acute heart failure is an important cause of unplanned hospitalizations and poses a significant burden through increased mortality and frequent hospitalizations. Heart failure with preserved ejection fraction (HFpEF) presents as a diverse condition characterized by complex cardiovascular and non-cardiovascular pathology. This study aimed to identify distinct clinical phenotypes in acute decompensated HFpEF (ADHF) using cluster analysis and assess their prognostic significance. We applied a latent class analysis to 1,281 ADHF patients admitted to a single cardiac intensive care unit between 2008 and 2022 with a left ventricular ejection fraction ≥ 50%. We used 83 factors obtained at hospitalization. We evaluated the association between phenogroups and clinical outcomes using either Cox regression model or Fine-Gray competing risk model. We identified 4 phenogroups: Phenogroup 1 (n = 133, 10%) included younger patients with metabolic disorders and a low level of B-type natriuretic peptide (BNP); Phenogroup 2 (n = 346, 27%) had systemic congestion and high BNP levels; Phenogroup 3 (n = 514, 40%) had multiple comorbidities and vascular disorders; Phenogroup 4 (n = 288, 22%) included older patients with bradyarrhythmia and atrial fibrillation. After adjusting for age, sex, and Get with the Guidelines-Heart Failure risk score, Phenogroup 2 had the highest risk of all-cause death and cardiac death. In conclusion, we identified 4 clinically relevant phenogroups of ADHF patients, each associated with different adverse outcomes. Phenotyping may provide a better understanding of the underlying mechanisms involved in the heterogeneity of ADHF and decompensation. Furthermore, it may facilitate the search for phenotype-specific therapeutic strategies.

This study aims to evaluate the comparative efficacy and safety of the combination of recombinant human brain natriuretic peptide (rhBNP) and sacubitril/valsartan in the sequential treatment of senile patients with acute heart failure (AHF).

The study objects were a total of 136 senile patients over 60 years old with AHF admitted to the Department of Cardiology of Anji County People's Hospital of Huzhou from August 2022 to August 2023. Using the envelope method, the patients were divided into three groups: the standard treatment group (45 patients who underwent hydragogue, digoxin, valsartan, and beta-blockers), the rhBNP group (46 patients were performed with basic treatment for AHF combined with rhBNP), and the sequential treatment group (45 patients received the basic treatment for AHF combined with rhBNP followed by sacubitril/valsartan). The clinical effects, cardiac function, safety, and prognosis among the three groups were compared.

In the sequential treatment group, the duration of clinical symptom remission, the duration of hospitalization, and the improvement rate of New York Heart Association classification at discharge were (2.27 ± 0.76) days, (6.99 ± 1.96) days, and 93.3%, which were better than those in the rhBNP group ([2.58 ± 0.94] days, [7.43 ± 2.78] days, and 78.3%) and the standard treatment group ([2.89 ± 0.71] days, [8.82 ± 2.89] days, and 71.1%); the P value among all groups was lower than 0.05. In terms of cardiac function and myocardial injury, the sequential treatment group was superior to the standard treatment group and rhBNP group. The incidence of adverse reactions in the standard treatment group, the rhBNP group, and the sequential treatment group was 37.8%, 34.8%, and 26.7%, respectively, P = 0.510. In the sequential treatment group, the rate of heart failure readmitted within 6 months after discharge was 28.9% and no death occurred, which was lower than those in the rhBNP (34.8%) and the standard treatment group (35.6%).

Sequential treatment with rhBNP and sacubitril/valsartan could significantly improve the clinical symptoms of elderly patients with AHF, enhance cardiac function, and reduce myocardial damage, which could also improve the prognosis.

Isolated cardiac sarcoidosis (iCS) is increasingly recognized; however, its prognosis and the efficacy of immunosuppressive therapy remain undetermined. We aimed to compare the prognosis of iCS and systemic sarcoidosis including cardiac involvement (sCS) under immunosuppressive therapy.

We retrospectively reviewed the clinical data of 42 patients with sCS and 30 patients with iCS diagnosed at Kyushu University Hospital from 2004 through 2022. We compared the characteristics and the rate of adverse cardiac events including cardiac death, fatal ventricular tachyarrhythmia, and heart failure hospitalization between the 2 groups. The median follow-up time was 1535 [interquartile range, 630-2555] days, without a significant difference between the groups. There were no significant differences in gender, NYHA class, or left ventricular ejection fraction. Immunosuppressive agents were administered in 86% of sCS and in 73% of iCS patients (P = 0.191). When analyzed only with patients receiving immunosuppressive therapy (sCS, n = 36; iCS, n = 21), the cardiac event-free survival was significantly lower in iCS than sCS (37% versus 79%, P = 0.002). Myocardial LGE content at the initial diagnosis was comparable in both groups. The disease activity was serially evaluated in 26 sCS and 16 iCS patients by quantitative measures of FDG-PET including cardiac metabolic volume and total lesion glycolysis, representing 3-dimensional distribution and intensity of inflammation in the entire heart. Although iCS patients had lower baseline disease activity than sCS patients, immunosuppressive therapy did not attenuate disease activity in iCS in contrast to sCS.

iCS showed a poorer response to immunosuppressive therapy and a worse cardiac prognosis compared to sCS despite lower baseline disease activity.

Balance dysfunction in older patients compromises independence and increases the risk of falls and disability. Arterial stiffness, an important parameter of atherosclerosis, can affect peripheral organs, including the brain, causing balance disorders. The cardio-ankle vascular index (CAVI), measured independently of blood pressure, has attracted attention as an indicator of arterial stiffness. However, the association between balance dysfunction and CAVI in patients with heart failure remains unclear. We investigated the association between the Short Physical Performance Battery (SPPB) score and CAVI in older patients with heart failure.

We investigated heart failure patients from our cardiac rehabilitation database between 2017 and 2022. Physical function, body composition, and CAVI were measured the day before discharge. Body composition was assessed using bioelectrical impedance analysis. Physical function was determined by assessing handgrip strength, 6-minute walk distance, and SPPB. Sarcopenia was classified according to the Asian Working Group for Sarcopenia 2019 guidelines, defining sarcopenia as an SPPB total score ≤ 9.

Among the 205 consecutive hospitalized patients aged ≥ 65 years (mean, 77.0 years; male, 140; female, 65), 45.0% had sarcopenia. CAVI was significantly higher in patients with sarcopenia than in those without (10.4 [9.5, 11.4] versus 9.8 [8.9, 10.8], respectively). Age, 6-minute walk distance, SPPB tandem time, 4-m walk time, 5 repetition sit-to-stand time, and SPPB score were significantly associated with CAVI, with tandem being an independent CAVI determinant (β = -0.142, P = 0.047).

These results suggest an association between arterial stiffness and SPPB score in older patients with heart failure.

This study aimed to evaluate the safety and necessity of antithrombotic drugs for acute type B aortic dissection (TBAD) treated with thoracic endovascular aortic repair (TEVAR).

The patients of acute TBAD treated with TEVAR were retrospectively enrolled from January 2007 to October 2022 in General Hospital of Northern Theater Command. The primary outcomes such as mortality and aortic adverse events [stroke, paraplegia, limb ischemia, organ failure (renal and intestinal tract), endoleak, redissection, aortic rupture, reintervention, and mortality] were recorded and evaluated at 1 month (early term) and 18 months (late term).

The 697 patients of TBAD treated with TEVAR were divided into the antithrombotic (AT) group (n = 208) and nonantithrombotic (NAT) group (n = 489). The incidence of early mortality, early aortic adverse events, and the 18 months of cumulative freedom from all-cause mortality and aortic adverse events were not significantly different between the AT and NAT groups (2.4% versus 1.4%, 2.9% versus 4.5%, 94.7% versus 96.5% and 88.4% versus 89.9%, respectively). Log-rank tests also indicated that there were no significant differences. In multivariate Cox regression models, only pleural effusion, partially thrombosed of false lumen, maximum diameter of false lumen, and branch involvement were independent predictors of mortality, whereas the systolic blood pressure (SBP), pleural effusion, partially thrombosed of false lumen, true lumen compression, maximum diameter of false lumen, branch involvement were independent predictors of adverse aortic events.

The antithrombotic drug for acute TBAD treated with TEVAR does not influence the mortality and aortic events in the early and late terms.

Despite establishing conventional risk factors and preventive medicine for cardiovascular diseases (CVD), there remains a notable lack of research for identifying social determinants of health (SDOH). The aim of this study was to identify the SDOH domains contributing to health inequities perceived by Japanese CVD citizens. An online survey was conducted among 2,083 Japanese CVD patients from November 7 to 13, 2023, to assess their perceptions of 19 social determinants of health (SDOH) domains and their impact on health inequities. Using the 5-point Likert scale, a high level of agreement was defined as over 50% selecting "Agree" or "Strongly Agree." The "Health inequity perception score (HIPS)" was calculated by assigning 1 point for 'Agree' and 2 points for 'Strongly Agree.' Additionally, patient factors that defined a group with HIPS above the median were also evaluated. High agreement was noted in 7 out of 19 domains: "Employment" (61%), "Food Insecurity" and "Environmental Condition" (each at 60%), "Poverty" (58%), "Early Childhood Development and Education" (57%), "Housing Instability and Quality" (56%), and "Access to Health Service" (52%). Young age, high annual income, high educational level, and living alone were significantly associated with high HIPS. This study highlights that several SDOH factors commonly acknowledged in Western contexts are also recognized as contributors to health inequities among Japanese CVD patients.

Accurate prediction of echocardiographic parameters is essential for diagnosis and treatment of cardiac disease, especially for segmentation of the left ventricle to obtain measurements such as left ventricular ejection fraction and volume. However, manually outlining left ventricle on echocardiographic images is a time-consuming and physician experience-dependent task. Therefore, it is crucial to develop an accurate and efficient automatic segmentation tool. Therefore, we aimed to explore a model to perform echocardiography of left ventricle segmentation by combining transformer and convolutional neural networks (CNN).

ResNet-50 was used in CNN branch. The encoder-decoder architecture was used for transformer branch, which was fused to the corresponding feature maps of the CNN branches. Fusion module was used to effectively combine feature information from the CNN and transformer. Bridge attention used to increase sensitivity and prediction accuracy of model. The entire network was trained end-to-end using the binary cross-entropy with logits loss L.

In this work, we propose an automatic left ventricular (LV) segmentation model based on Transformer and CNN that efficiently captures global dependencies and spatial details and create a fusion module using CBAM that fuses Transformer and CNN features. In addition, attention is also computed using multi-level fusion features to obtain the final attention segmentation map. The model was trained and evaluated on a large cardiac image dataset, EchoNet-Dynamic, with test dice coefficient of 92.4%.

The results show that our model can better segment left ventricle. We also tested our model on clinical patient ultrasound images, and visualization results proved effectiveness of the model.

Left atrial appendage (LAA) closure can prevent stroke in high-risk patients with atrial fibrillation.

A bioabsorbable LAA occluder made of degradable polymer materials, such as polydioxanone (PDO) and poly-L-lactic acid (PLA), and nitinol wire was used. Occluders were successfully implanted in 18 Chinese rural dogs, 2 of which died within 48 hours after operation due to pericardial tamponade and hemorrhage, respectively. Follow-up observation was performed after transcatheter LAA closure. New tissue was found on the surface of the occluder 2 months after operation. No adjacent structures such as the mitral valve and the left superior pulmonary vein were affected by the occluder discs. Hematoxylin and eosin (HE) staining was performed at 3 months after operation, which showed intact intimal structure on the occluder surface, and unabsorbed PDO and PLA were observed. Scanning electron microscopy showed irregular arrangement of endothelial cells. New endothelial tissue was observed to completely cover the occluder at 6 months after operation. Most PDOs were replaced by fibrous connective tissue, and scanning electron microscopy showed regularly arranged endothelial cells. Pathological examination at 12 months showed only a small remnant of PDO. The gross specimens of the liver, spleen, and kidneys and pathological examination did not indicate thromboembolism.

The bioabsorbable LAA occluder made of PDO, PLA, and nitinol wire was safe and effective for the occlusion of LAA in dogs. The surface of the occluder was endothelialized half a year after operation. The absorbable materials of the occluder were degraded after 1 year.

Cardiac rupture is a fatal complication following myocardial infarction (MI) and there are currently no effective pharmacological strategies for preventing this condition. In this study, we investigated the effect of colchicine on post-infarct cardiac rupture in mice and its underlying mechanisms.

We induced MI in mice by permanently ligating the left anterior descending artery. Oral colchicine or vehicle was administered at a dose of 0.1 mg/kg/day from day 1 to day 7 after MI. Cultured neonatal cardiomyocytes and fibroblasts were exposed to normoxia or anoxia and treated with colchicine.

Colchicine significantly improved the survival rate (colchicine, n = 46: 82.6% versus vehicle, n = 42: 61.9%, P < 0.05) at 1 week after MI. Histological analysis revealed colchicine significantly reduced the infarct size and the number of macrophages around the infarct area. Colchicine decreased apoptosis in the myocardium of the border zone and cultured cardiomyocytes and fibroblasts as assessed by TUNEL assay. Colchicine also attenuated the activation of p53 and decreased the expression of cleaved-caspase 3 and bax, as assessed by Western blotting.

Colchicine prevents cardiac rupture via inhibition of apoptosis, which is attributable to the downregulation of p53 activity. Our findings suggest that colchicine may be a prospective preventive medicine for cardiac rupture, however, large clinical trials are required.

In addition to its antihypertensive and diuretic effects, hydrochlorothiazide also demonstrates additional cardioprotective properties; however, the existence of a synergistic interaction between dapagliflozin and hydrochlorothiazide remains unclear.

To establish a rat model of heart failure for investigating the effects and mechanisms of dapagliflozin in combination with hydrochlorothiazide during early intervention, H9c2 cells were cultured to validate their in vitro efficacy. The combination group exhibits a synergistic improvement in hemodynamics, ejection fraction, and a reduction in plasma B-type natriuretic peptide concentration. This combination effectively decreases collagen volume fraction and the expression of collagen I and III, p47phox, p67phox, NF-κB p65, Bax, and caspase-3. The combination group demonstrates a synergistic effect in enhancing cardiac function, attenuating oxidative stress and inflammation. The in vitro effects of the combination were demonstrated in H9c2 cardiomyocytes. In addition, the combination exhibits a more pronounced inhibitory effect on NHE1 expression. The expression of NHE1 in H9c2 cells is inhibited by hydrochlorothiazide, thereby alleviating the consequences of NHE1 overexpression. The results of molecular docking and kinetic simulations indicate a strong binding affinity (−6.1 kcal/mol) between hydrochlorothiazide and NHE1, resulting in the formation of a stable conformation. This may elucidate the underlying mechanism responsible for the synergistic effects of drugs.

The combination of dapagliflozin and hydrochlorothiazide has synergistic effects on improving cardiac function, oxidative stress, and inflammation in rats with heart failure. Hydrochlorothiazide binds to and inhibits the expression of NHE1, thereby enhancing dapagliflozin's inhibitory effect on NHE activity. This mechanism potentially elucidates its enhanced cardioprotective effects.

Pulmonary arterial hypertension is a progressive heart and lung disease that is caused by irreversible pulmonary vascular remodeling. Sinomenine hydrochloride is an alkaloid that is extracted from sinomenium acutum, which has strong anti-inflammatory effects. In this study, male rats were injected with monocrotaline, and endothelial cells were exposed to hypoxia for 24 hours to induce pulmonary arterial hypertension. Apoptosis, inflammation, and oxidative stress pathways were observed the in lungs and cells. Sinomenine hydrochloride repressed the increased right ventricular systolic pressure and attenuated the right ventricular hypertrophy and pulmonary artery remodeling in model rats. It reversed the expression of BCL2 and BAX and prevented the apoptosis of endothelial cells. Additionally, it increased the contents of IKBα and NRF2. P65, P-P65, TNFα, IL1β, and IL6 levels in the lungs decreased by it. Malondialdehyde contents decreased, and the superoxide dismutase and glutathione peroxidase activity and HO-1 level increased in the treatment group. In vivo, it promoted apoptosis of pulmonary artery endothelial cells. Moreover, by activating PPAR-γ, sinomenine hydrochloride attains the above effects. These data suggested that sinomenine hydrochloride could protect endothelial cells, restrain inflammation and oxidative stress, and enhance pulmonary vascular remodeling.

Right ventricular dysfunction is a key clinical issue for the viability of donation-after-circulatory-death (DCD) heart transplantation. DCD hearts with volume overload have the potential to exhibit aggravated right ventricular dysfunction following heart transplantation. The c-jun/c-fos mRNAs are genes that immediately respond to myocardial cell stretch. We assessed myocardial cell stretch during asphyxia-induced cardiac arrest by measuring c-jun/c-fos mRNA expression levels. The trachea was dissected and ligated to initiate asphyxiation in anesthetized Wistar rats under paralyzed ventilation. The hearts were harvested at 4 time points: 0, 15, 30, and 45 minutes after the termination of ventilation. Free walls of the right and left ventricles and the interventricular septum were sectioned. Total RNA was extracted from these tissues, and cDNA was synthesized using reverse transcription. The c-jun/c-fos mRNA expression levels were quantified using the droplet digital polymerase chain reaction method. In the left ventricle, c-jun/c-fos expression levels rapidly increased at 15 minutes, but the expression levels returned to the baseline level at 30 minutes after tracheal ligation. In contrast, in the right ventricle, c-jun/c-fos expression levels gradually increased and peaked 30 minutes after tracheal ligation. Myocardial cell stretching in the right ventricle is prolonged after asphyxia-induced cardiac arrest compared to that in the left ventricle, which may lead to right ventricular dysfunction after DCD heart transplantation.

Excessive neointimal hyperplasia (NIH) of coronary vessels in patients is the main cause of restenosis (RS) after percutaneous coronary intervention (PCI). This study aimed to identify the regulatory genes related to NIH in a rat carotid artery balloon injury model.

We established a rat model and performed RNA sequencing to identify differentially expressed long non-coding RNAs (DElncRNAs) and differentially expressed message RNAs (DEmRNAs). Immune cells were analyzed using a murine Microenvironment Cell Population counter. The Pearson correlation between DEmRNAs, DElncRNAs, and immune cells was analyzed, followed by function enrichment analysis. Core DEmRNA was identified using Cytoscape. Next, a core lncRNAs-mRNAs-immune cell regulatory network was constructed. NIH-related gene sets from the Gene Expression Omnibus and GeneCards databases were used for validation.

A total of 2,165 DEmRNAs and 705 DElncRNAs were identified in rat carotid artery tissue. Four key immune cells were screened out, including mast cells, vessels, endothelial cells, and fibroblasts. Based on the Pearson correlation between DEmRNAs, DElncRNAs and 4 key immune cells, 246 DEmRNAs and 93 DElncRNAs were obtained. DEmRNAs that interact with lncRNAs were mainly involved in the cell cycle, MAPK signaling pathway, and PI3K-Akt signaling pathway. A core lncRNA-mRNA-immune cell regulatory network was constructed, including 9 mRNAs, 4 lncRNAs, and fibroblasts. External datasets validation confirmed the significant correlation of both these mRNAs and lncRNAs with NIH.

In this study, an lncRNA-mRNA-immune cell regulatory network related to NIH was constructed, which provided clues for exploring the potential mechanism of RS in cardiovascular diseases.

Acute myocardial infarction (MI) and stroke occurring simultaneously in one patient is a rare clinical event. These medical emergencies involve many diagnostic and treatment challenges due to different causes, treatment modalities, and shifting priorities. Presence and exacerbation of bronchiectasis has been considered as a risk factor for atherosclerotic cardiovascular and cerebrovascular diseases and can trigger a cardioembolic stroke. We describe a case of a 59-year-old male patient with bronchiectasis who was treated at our tertiary care center due to concurrent MI and stroke.

Whether transfemoral transcatheter aortic valve replacement (TAVR) can be accomplished in patients with a bicuspid aortic valve (AV) and previous type A aortic dissection remains rarely addressed. We report such a case in whom transfemoral TAVR was smoothly performed employing an extraordinary long sheath to bypass the dissected aortic segment, yet at the cost of perioperative left temporoparietal infarction owing to no suitable cerebral embolic protection device available in the presence of a remaining dissection in the aortic arch. Thus, for such patients, transfemoral TAVR is still feasible but novel embolic protection devices of distinct designs should be developed to avoid perioperative cerebral embolism.

Tracheobronchial or esophageal fistula after aortic surgery has been reported sporadically in the literature, however, reports of an aortopulmonary fistula associated with a post-operative aortic pseudoaneurysm are rare. We experienced a case of refractory heart failure due to an aortopulmonary fistula associated with a post-operative aortic pseudoaneurysm. A 60-year-old man who had undergone aortic surgery 2 years earlier was hospitalized for congestive heart failure. He was diagnosed with refractory heart failure after 10 days of diuretic therapy failed to improve his condition. He underwent a contrast-enhanced computed tomography (CT) scan and was suspected to have pulmonary artery perforation of an aortic pseudoaneurysm at the anastomotic site of the ascending aortic surgery. Transesophageal echocardiography showed shunt blood flow from the aortic aneurysm into the right pulmonary artery, leading to a definitive diagnosis of aortopulmonary fistula with post-operative aortic pseudoaneurysm. Computed tomography angiography is commonly used to diagnose an aortic fistula; however, diagnosis is often difficult because of the subtle imaging findings. We highlight the usefulness of transesophageal echocardiography in providing a definitive diagnosis and detailed morphologic information on this pathophysiology.