BMC Cardiovascular Disorders最新文献

Background: Left ventricular (LV) myocardial contraction patterns can be assessed using LV mechanical dispersion (LVMD), a parameter closely associated with electrical activation patterns. Despite its potential clinical significance, limited research has been conducted on LVMD following myocardial infarction (MI). This study aims to evaluate the predictive value of cardiac magnetic resonance (CMR)-derived LVMD for adverse clinical outcomes and to explore its correlation with myocardial scar heterogeneity.

Methods: We enrolled 181 post-MI patients (median age: 55.7 years; 76.8% male) who underwent CMR examinations. LVMD was calculated using the CMR-feature tracking (CMR-FT) technique, defined as the standard deviation (SD) of the time from the R-wave peak to the negative strain peak across 16 myocardial segments. Entropy was quantified using an algorithm implemented with a generic Python package. The primary composite endpoints included sudden cardiac death (SCD), sustained ventricular arrhythmias (VA), and new-onset heart failure (HF).

Results: Over a median follow-up of 31 months, LVMD and border zone (BZ) entropy demonstrated relatively high accuracy for predicting the primary composite endpoints, with area under the curve (AUC) values of 0.825 and 0.771, respectively. Patients with LVMD above the cut-off value (86.955 ms) were significantly more likely to experience the primary composite endpoints compared to those with lower LVMD values (p < 0.001). Multivariable analysis identified LVMD as an independent predictor of the primary composite endpoints after adjusting for entropy parameters, strain, and left ventricular ejection fraction (LVEF) (hazard ratio [HR]: 1.014; 95% confidence interval [CI]: 1.003-1.024; p = 0.010). A combined prediction model incorporating LVMD, BZ entropy, and LVEF achieved the highest predictive accuracy, with an AUC of 0.871 for the primary composite endpoints. Spearman rank correlation analysis revealed significant linear correlations between LVMD and entropy parameters (p < 0.001 for all).

Conclusions: Myocardial heterogeneity, as assessed by LVMD and BZ entropy, represents reliable and reproducible parameters reflecting cardiac remodeling following MI. LVMD has independent prognostic value, and the combination of LVMD and BZ entropy with the guideline-recommended LVEF as a unified model enhances the accuracy of forecasting the risk of primary combined endpoints in patients after MI.

Background: Systemic light chain amyloidosis is a rare and debilitating disease, especially for which initially presented with digestive tract involvement. Myocardial amyloidosis is highly aggressive with generally poor prognosis and often resulted in missed diagnosis or misdiagnosis with routine examination tools. Multimodality imaging play an important role in diagnosing the amyloidosis effect on multiple organs. Chemoradiotherapy is the mainstay of treatment.

Case presentation: This article presents a rare case of systemic light chain amyloidosis, initially with gastrointestinal symptoms, in a 68-year-old male. He was hospitalized with diarrhea for one year and a half, dysphagia for 4 months, but he had no dyspnea. The transthoracic echocardiogram revealed myocardial hypertrophy of the left ventricle, the hypertrophic heart muscle echoed like "ground glass". The left ventricular ejection fraction (LVEF) detected by Simpson method was 51% and global longitudinal strain (GLS) was -9.00%. But cardiac magnetic resonance showed the patient without gadolinium delayed enhancement. The urinary protein series quantification and the serum free light chain levels were all increased. While the ratio of free κ and free λ was decreased. Hence, the abdominal fat biopsy of the patient was amyloidosis by electronic and immunoelectron microscopy. Organs involved include heart, kidneys, gastrointestinal tract and nervous system, stage III of mayo 2012 model. The patient was treated with Dara-BCD chemotherapy. This case underscores the diagnostic complexity, emphasizing the need for early identification given the grim prognosis associated with systemic AL amyloidosis requiring clinical data, detailed imaging, and histopathological insights. After discharge, the patient became better and followed up in the outpatient.

Conclusions: Systemic light chain amyloidosis can easily be missed diagnosis or misdiagnosis in its early stages, losing the opportunity for initiating earlier treatments to improve potential patient outcomes. Despite advancements in diagnostic biomarkers, this case highlights the potential for missed diagnosis with standard CMR imaging when gadolinium enhancement is negative. The utility of echocardiographic features such as reduced GLS and abnormal ECG findings emerges as critical in early identification of myocardial amyloidosis. The correct diagnosis of this case relied on the comprehensive utilization of multimodal imaging techniques including biopsy.

Background: Qi Li Qiang Xin (QLQX) capsule has a solid theoretical basis and clinical efficacy in the treatment of chronic heart failure; however, the underlying mechanisms remain obscure. This study was designed to determine the effect of the QLQX on the treatment of heart failure and delineate the underlying mechanisms via a nontargeted metabolomics and lipidomics approach.

Methods: A rat model of heart failure after myocardial infarction (MI) was established via permanent ligation of the anterior descending branch of the left coronary artery. The rats were then randomly divided into the SHAM group, the MI group, the QLQX group (1.3 g/kg/day), and the VAL (valsartan) group (80 mg/kg/day). Cardiac function was measured via echocardiography. The levels of serum NT-proBNP and hs-cTn-I were detected via ELISA. H&E staining and Masson's trichrome staining were used to observe cardiac morphology and myocardial fibrosis. Using the UPLC-QTOF/MS method, metabolomics and lipidomics analyses were performed on the plasma of the rats in each group to identify biomarkers and potential amino acid and lipid therapy mechanisms for heart failure after QLQX administration in rats with heart failure.

Results: QLQX capsule improved the heart f unction of rats with heart failure after myocardial infarction by increasing the LVEF and LVFS, decreasing the LVIDd and LVIDs. QLQX capsule reduce the levels of NT-proBNP and hs-cTn-I, which are markers of heart failure, and improve the myocardial infarction area and degree of myocardial fibrosis. In addition, in the metabolomics analysis, a total of 17 plasma metabolites were significantly different between heart failure rats and normal rats, all of which recovered significantly after QLQX treatment. These metabolites mainly participate in the biosynthesis of unsaturated fatty acids; valine, leucine and isoleucine biosynthesis; phenylalanine, tyrosine and tryptophan biosynthesis; and glycerophospholipid metabolism. Lipid analysis revealed that FA18:2, FA18:3, FA20:5, and FA22:6 in the QLQX group were significantly altered (P < 0.01). The peak area contents of FA18:2, FA18:3, FA20:5, and FA22:6 in the sham surgery group and model group also significantly decreased (P < 0.05).

Conclusion: This study elucidates the therapeutic effect of QLQX on heart failure rats and elucidates its potential mechanisms, which are related mainly to the regulation of amino acid and lipid metabolism in heart failure rats through metabolomics and lipidomics experiments.

Background: Diabetes mellitus (DM) and atrial Fibrillation (AF) are among the most common health issues. They are responsible for the highest rates of morbidity and mortality. The importance of sodium glucose cotransporter-2 inhibitors (SGLT-2is) in treating DM has increased significantly in recent years. In our article, we aimed to evaluate the effect of SGLT-2i on the clinical outcomes of AF patients with DM.

Methods: Our study is a retrospective, observational study. The patients with AF and DM were divided into two groups: those using SGLT-2i or not using SGLT-2i, and 3-year follow-up results were examined. The endpoints of the study were defined as all-cause death, the development of myocardial infarction (MI), major bleeding requiring hospitalization, and an ischemic cerebrovascular event (CVE). Differences between groups according to SGLT-2i use were analyzed.

Results: The study included 485 patients, 205 (42.3%) of whom were male and had an average age of 70.7 ± 9.7 years. A total of 138 of 485 patients (28.5%) received SGLT-2i. All-cause mortality was lower in the group receiving SGLT-2i (p < 0.001). Similarly, a significant reduction in major bleeding events was observed among those who received SGLT-2i treatment (p = 0.009). The incidence of CVEs was lower among SGLT-2i recipients, but the difference was not statistically significant (p = 0.066). SGLT2i usage did not mitigate the risk of MI development (p = 0.317).

Conclusions: In our study, SGLT-2i treatment was associated with a significant reduction in all-cause mortality and major bleeding in diabetic AF patients. Our study provides evidence of the clinical benefit of SGLT-2i in AF patients.

Background: There is little research on cardiorenal anemia syndrome (CRAS) in China. This study was to describe the characteristics of patients with CRAS and to explore risk factors of all-cause death.

Methods: A total of 81,795 patients were hospitalized from August 2012 to August 2021 in the nephrology department and cardiology department, of which 820 patients with CRAS were recruited into this study. The 820 patients were divided into three groups based on New York Heart Association (NYHA) functional class: a NYHA Class II group (n = 124), a NYHA Class III group (n = 492), and a NYHA Class IV group (n = 204). Demographics and laboratory tests were collected and risk factors of all-cause death were analyzed. The primary endpoint of the study was all-cause death.

Results: 820 patients were included, with a median age of 65.00 (51.00-75.00) years and 61.2% were men. The median follow-up was 27.0 (13.0-51.0) months. 416 (50.7%) patients died during follow-up. Age, smoking history, cerebral infarction, NYHA functional class, albumin, serum creatinine (SCr), left ventricular end-diastolic diameter (LVEDD), and left ventricular ejection fraction (LVEF) remained independent predictors of all-cause mortality risk in patients with CRAS (P < 0.05) after adjusting to the potential confounders.

Conclusions: In patients with CRAS, older age, smoking history, and more advanced systolic heart failure and renal failure correlated with worse clinical outcomes at follow-up.

Background: Ventricular separation is a multipart, extensive disease of the heart that hinders the electrical conduction of the cardiac system ventricular muscle, causing a bidirectional conduction block. The occurrence of ventricular separation suggests that the myocardium is in a state of severe ischemia, and the prognosis is generally poor. Herein, we present arescue case in which the extremely rare phenomenon of ventricular separation developed and was documented in realtime.

Case presentation: An 82-year-old man with syncope presented to the emergency departmentin a critical condition with no vital signs and was immediately treated via endotracheal intubation, mechanical ventilation, and cardiopulmonary resuscitation.The patient's electrocardiogram (ECG) showed two completely independent waveforms that were excited at their respective frequencies without interfering with one another, with the overall ECG resembling a third-degree atrioventricular block. A review of a previous ECG showed findings mimicking a first-degree atrioventricular block.Based on the patient's clinical manifestations, the ECG diagnoses were sinus arrest, ventricular escape rhythm, and ventricular separation. The patient was declared dead 30 min after rescue attempts failed.The ECG was variable in this case, and the original conduction-related ventricular wave showed complete separation that could easily have been misdiagnosed as an atrioventricular block. Since the patient was in a critical condition and his vital signs had disappeared, the ECG diagnoses supported ventricular separation.

Conclusions: Ventricular separation is not a static condition, and as observed in this case, it can manifest a number of dynamic changes. Therefore, it is imperative to study this uncommon phenomenon in order to gain an improved understanding of the electrocardiac system.

Background: Heart failure (HF) is a syndrome with complex etiology and high mortality in the world. Macrophage-related inflammation is involved in HF development. O-GlcNAcylation is a post-translational modification that affects pathological processes. This study aimed to investigate the role of O-GlcNAcylation in HF, especially its effect on macrophage polarization.

Methods: Raw264.7 cells were treated with lipopolysaccharide (LPS) to induce pro-inflammatory macrophages. HF mice were generated by transverse aortic constriction (TAC). After knockdown of OGT or overexpressing IRF1, macrophage polarization was evaluated using quantitative real-time polymerase chain reaction and flow cytometry. Underlying mechanism was analyzed using bioinformatic analysis, co-immunoprecipitation (co-IP), IP, and western blotting.

Results: The results showed that O-GlcNAcylation and OGT levels were high in LPS-treated Raw264.7 cells. OGT knockdown inhibited pro-inflammatory macrophage polarization and promoted anti-inflammatory macrophage polarization caused by LPS, and alleviated TAC-induced cardiac dysfunction and fibrosis. Mechanistically, OGT silence suppressed O-GlcNAcylation of IRF1 at Ser (S)283 site. IRF1 overexpression reversed macrophage polarization modulated by OGT knockdown.

Conclusion: Silencing of OGT promotes macrophage polarization from pro-inflammatory to anti-inflammatory phenotype to alleviate HF through O-GlcNAcylation of IRF1. The findings suggest that O-GlcNAcylation has the potential to treat HF.

Objective: To screen Myocardial ischemia-reperfusion Injury in mice. adenosine monophate-activatedprotein kinase (AMPK) -related differentially expressed circularRNA (circRNA) in MIRI model, Ampk-related circRNA network was drawn to provide possible ideas for the prevention and treatment of MIRI.

Methods: The mouse MIRI model was constructed by ligation of the left anterior descending artery. After the model was successfully established, the related indicators of cardiac function were detected, and high-throughput sequencing was performed on the myocardial tissue of the mice.

Results: MIRI model was successfully constructed, and two AMPK related differentially expressed loops (novel_circ_043550 and novel_circ_035243) were screened out. A circRNA-miRNA-mRNA network consisting of 2 circRNA, 28 microRNA(miRNA) and 229 messengerRNA (mRNA) was constructed.

Conclusions: This study reveals the differential expression of several AMPK-related circRNAs in MIRI in mice, and the AMPK-related circRNA regulatory network is constructed, suggesting that AMPK-related circRNA may have potential clinical application prospects as a potential molecular marker and therapeutic target for MIRI.

Premature ventricular contractions (PVCs) are a common finding in patients with surgically repaired congenital heart defects including transposition of the great arteries (D-TGA). While often asymptomatic, PVCs can sometimes lead to palpitations, dyspnea, and hemodynamic compromise, requiring therapeutic intervention. The arterial switch operation is the preferred treatment for D-TGA, but these patients have a 2% incidence of ventricular arrhythmias and 1% incidence of sudden cardiac death post-operatively. Though radio-frequency ablation is an effective option for treating outflow ventricular arrhythmias, little data is available on its use in the post-arterial switch D-TGA population. This case report describes a successful catheter ablation of frequent PVCs originating from the left ventricular summit region in a 9-year-old child with a history of arterial switch repair for D-TGA and frequent monomorphic PVCs, highlighting the challenges and considerations in managing ventricular arrhythmias in this complex anatomical setting.