International heart journal最新文献

The effectiveness of ischemic postconditioning (iPoC) in patients with ST-elevation myocardial infarction (STEMI) without ischemic preconditioning has not been determined. Therefore, we investigated the impact of iPoC and its potential mechanism related to heat shock protein 72 (HSP72) induction on myocardial salvage in patients with STEMI without prodromal angina (PA).

We retrospectively analyzed data from 102 patients with STEMI with successful reperfusion among 323 consecutive patients with acute coronary syndrome. Among these, 55 patients with iPoC (iPoC (+) ) underwent 4 cycles of 60-second inflation and 30-second deflation of the angioplasty balloon. Both the iPoC (+) and iPoC (-) groups were divided into 2 further subgroups: patients with PA (PA (+) ) and those without (PA (-) ). We analyzed HSP72 levels in neutrophils, which were measured until 48 hours after reperfusion. I-123 β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) scintigraphy was performed within a week of reperfusion therapy. In 64% of patients, thallium-201 (TL) scintigraphy was performed 6-8 months after STEMI onset.

Using BMIPP and TL, in the PA (-) subgroups, the iPoC (+) group had a significantly greater myocardial salvage ratio than the iPoC (-) group. iPoC was identified as an independent predictor of the myocardial salvage ratio. The HSP72 increase ratio was significantly elevated in the iPoC (+) PA (-) group. Importantly, the myocardial salvage effect in patients without PA was significantly correlated with the HSP72 increase ratio, which was greater in patients with iPoC.

These results suggest the potential impact of iPoC via HSP72 induction on myocardial salvage; however, the effects may be limited to patients with STEMI without PA.

Treatment with enhanced external counterpulsation (EECP) or cardiac rehabilitation (CR) benefits patients with coronary heart disease; this paper intends to explore the feasibility of EECP combined with CR in patients with nonobstructive coronary heart disease (NOCAD) and coronary microcirculation disorders (CMD).

In January 2021-2022 month June our income NOCAD patients as the research object, the line of cardiac magnetic resonance (CMR), myocardial perfusion reserve (MPR) < 2.0 coronary microcirculation disorders (CMD, 80 cases). Random indicator method 80 CMD patients divided into two groups, 40 cases in each. Usual treatment group: conventional drugs and CR therapy. EECP treatment group: on the basis of standard treatment group, employ EECP therapy. Comparing the two groups before and after the treatment curative effect cardiac function index, endothelial unction index, adverse cardiovascular events, etc.

After EECP treatment, the treatment group showed a higher effective rate compared to the usual treatment group (P < 0.05). EECP group curative effect, left ventricular ejection fraction,plasma NO and vascular endothelial growth factor levels higher than the usual group, the incidence of adverse cardiovascular events is lower than the usual group. The difference was statistically significant (P < 0.05).

EECP combined with cardiac rehabilitation in patients with CMD symptoms has better effect and safety and provides reference for treatment of CMD patients.

Cardiopulmonary resuscitation (CPR) is essential for the survival of cardiac arrest patients, but it can cause severe traumatic complications. In the catheterization laboratory, various physical constraints complicate the appropriate performance of CPR. However, we are not aware of reports of CPR complications in this setting. Here, we report a case of coronary artery perforation (CAP) caused by manual CPR in the catheterization laboratory. The patient, a 68-year-old woman, initially underwent successful percutaneous coronary intervention (PCI) for unstable angina. Back in the ward, the patient experienced acute stent thrombosis, which resulted in cardiac arrest, and another PCI was performed under ongoing manual CPR. Although revascularization was successful, sudden CAP occurred, leading to cardiac tamponade. Despite extensive treatment efforts, the patient died 18 hours later.

Initially, the compression site of CPR was on the midline of the sternum; however, the compression site shifted to the left, to just above the left anterior descending artery, by the time that CAP was detected via angiography. This corresponded to the area where rib fractures were observed upon computed tomography, suggesting the possibility of traumatic CAP due to manual CPR. The physical constraints in the catheterization laboratory can lead to an inappropriate CPR technique and severe traumatic complications.

This study aimed to explore the relationship between the trajectory of the triglyceride-glucose (TyG) index and the occurrence of major adverse cardiovascular and cerebrovascular events (MACCE) in patients with atrial fibrillation (AF).

This prospective study included 1979 patients with AF, who were initially selected from the Kailuan study. Patients of AF were split into four groups according to the value of TyG index. The clinical endpoint was MACCE, including myocardial infarction and ischemic stroke. Cox proportional hazard models were employed to examine the hazard ratio (HR) and 95% confidence interval (CI) for MACCE in various trajectory groups.

The mean age of all patients with AF was 67.65 ± 11.15 years, and 1752 (88.53%) were male. Over a median follow-up duration of 5.31 years, in total 227 MACCE were recorded. MACCE cumulative incidence in Quartile 4 (26.96%) was significantly higher than those in other quartiles (P = 0.023). Multivariate Cox proportional hazards regression analysis showed that a higher TyG index (Quartile 4) was significantly and positively linked to MACCE in patients with AF (P = 0.023, HR: 2.103; 95% CI: 1.107-3.994).

The evaluated TyG index is significantly associated with an increased risk of MACCE in patients with AF.

Cardiomyocyte lipotoxicity and ferroptosis are the key to the development of diabetic cardiomyopathy (DCM). Perilipin 5 (PLIN5) is perceived as a significant target of DCM. This study aimed to focus on the role and mechanism of PLIN5 on lipotoxicity and ferroptosis in DCM.

Following transfection, mouse cardiomyocytes HL-1 were induced by 0.1 mM palmitic acid (PA) to set up lipotoxic cardiomyocyte models. The cell viability and lipid accumulation were evaluated by cell counting kit-8 assay and Oil red O staining, respectively. Ferrous ion (Fe²⁺), glutathione (GSH), malondialdehyde (MDA), and reactive oxygen species (ROS) levels were determined to verify the effects of PLIN5 or Pirin (PIR) on ferroptosis. Quantitative real-time reverse transcription polymerase chain reaction or Western blot was performed for quantitative analysis.

PLIN5 overexpression promoted the viability, GSH level, and expression of GPX4/PIR/intracellular P65, yet suppressed lipid accumulation, level of Fe²⁺/MDA/ROS, and expression of interleukin (IL) -1β/IL-18/intranuclear P65 in PA-stimulated HL-1 cells. PIR silencing counteracted the roles of PLIN5 overexpression in PA-stimulated HL-1 cells.

PLIN5 suppresses lipotoxicity and ferroptosis in cardiomyocyte via modulating PIR/NF-κB axis, hinting its potential as a therapeutic target in DCM.

Pericardial effusion (PE) presentation varies from an incidental finding to a life-threatening situation; thus, its etiology and clinical course remain unknown. The aim of the present study was to retrospectively investigate these factors.

We analyzed 171 patients (0.4%) who presented with PE among 34,873 patients who underwent echocardiography between 2011 and 2021 at our hospital. Clinical and prognostic information was retrieved from electronic medical records. The primary endpoints were all-cause death, hospitalization due to heart failure (HF), and other cardiovascular events such as cardiovascular death, acute coronary syndrome, elective percutaneous coronary intervention, and stroke.

The etiologies of PE were as follows: idiopathic (32%), HF-related (18%), iatrogenic (11%), cardiac surgery-related (10%), radiation therapy-related (9%), malignancy (8%), pericarditis/myocarditis (8%), myocardial infarction-related (2%), and acute aortic dissection (2%). Patients with idiopathic/HF etiology were more likely to be older than the others.

During a mean follow-up period of 2.5 years, all-cause death occurred in 21 patients (12.3%), cardiovascular events in 10 patients (5.8%), and hospitalization for HF in 24 patients (14.0%). All-cause death was frequently observed in patients with malignancy (44% per person-year). Cardiovascular events were mostly observed in patients with radiation therapy-related and malignancy (8.6% and 7.3% per person-year, respectively).

The annual incidence of hospitalization for HF was the highest in patients with HF-related (25.1% per person-year), followed by radiation therapy-related (10.4% per person-year).

This retrospective study is the first, to the best of our knowledge, to reveal the contemporary prevalence of PE, its cause, and outcome in patients who visited a cardiovascular hospital in an urban area of Japan.

Myocardial fibrosis is a pathological feature of doxorubicin-induced chronic cardiotoxicity that severely affects the prognosis of oncology patients. However, the specific cellular and molecular mediators driving doxorubicin-induced cardiac fibrosis, and the relative impact of different cell populations on cardiac fibrosis, remain unclear.

This study aimed to explore the mechanism of doxorubicin-induced cardiotoxicity and myocardial fibrosis and to find potential therapeutic targets. Single-cell RNA sequencing was used to analyze the transcriptome of non-cardiomyocytes from normal and doxorubicin-induced chronic cardiotoxicity in mouse model heart tissue.

We established a mouse model of doxorubicin-induced cardiotoxicity with a well-defined fibrotic phenotype. Analysis of single-cell sequencing results showed that fibroblasts were the major origin of extracellular matrix in doxorubicin-induced myocardial fibrosis. Further resolution of fibroblast subclusters showed that resting fibroblasts were converted to matrifibrocytes and then to myofibroblasts to participate in the myocardial remodeling process in response to doxorubicin treatment. Ctsb expression was significantly upregulated in fibroblasts after doxorubicin-induced.

This study provides a comprehensive map of the non-cardiomyocyte landscape at high resolution, reveals multiple cell populations contributing to pathological remodeling of the cardiac extracellular matrix, and identifies major cellular sources of myofibroblasts and dynamic gene-expression changes in fibroblast activation. Finally, we used this strategy to detect potential therapeutic targets and identified Ctsb as a specific target for fibroblasts in doxorubicin-induced myocardial fibrosis.

Deficiency of vitamin B₁ (VB1), an essential micronutrient, causes heart failure (HF). A recent randomized controlled trial failed to show any improvement in HF prognosis after short-term VB1 supplementation. In the current study, we investigated the efficacy of long-term maintenance of normal blood VB1 levels in preventing adverse outcomes in patients with HF.

This study included 88 consecutive patients with HF who received guideline-directed medical therapy at Arida Municipal Hospital. The patients were divided into 3 groups: a control group with normal VB1 levels and no VB1 supplementation (normal group, n = 25), and those presenting with VB1 deficiency, who either required short-term VB1 supplementation (short-term supplementation group, n = 25), or long-term maintenance of normal blood VB1 levels (long-term maintenance group, n = 38). The time to the first appearance of composite outcomes, including cardiovascular death and hospitalization for HF, was compared between the 3 groups.

VB1 deficiency was observed in 63 (72%) patients. The Kaplan-Meier curve showed that the long-term maintenance group had better outcomes than the other 2 groups. In the multivariate analysis, long-term maintenance of normal blood VB1 levels and age were independent predictors of composite outcomes.

VB1 deficiency is frequently observed, and the long-term maintenance of normal blood VB1 levels may result in better outcomes in patients with HF. Our results suggest that the detection of VB1 deficiency and long-term restoration of VB1 levels may be part of the overall therapeutic strategy for HF.

The presence of epicardial connections (ECs) between the pulmonary veins (PVs) and atrium may contribute to atrial fibrillation (AF) recurrence. This study aimed to determine the impact of sleep-disordered breathing (SDB) on the presence of ECs and the interplay between SDB and ECs on AF recurrence.

We retrospectively reviewed 400 consecutive non-valvular AF patients. Among them, 235 patients exhibiting a 3% oxygen desaturation index (ODI) of ≥ 10 events/hour underwent polysomnography to evaluate the SDB severity, measured by the apnea-hypopnea index (AHI). To facilitate the ablation of AF and ECs, a high-density mapping catheter (HDMC) was employed. AF recurrence was evaluated over a 12-month period post-AF ablation.

The key findings included: 1) 63% of AF patients with ECs had SDB with an AHI ≥ 20 events/hour. 2) Despite achieving complete PV isolations and precise EC ablation using an HDMC, SDB presence was associated with an increased AF recurrence. 3) Continuous positive airway pressure therapy for SDB improved AF recurrence among the AF patients with both ECs and SDB (57% versus 73%; P = 0.016). 4) AHI (odds ratio [OR] = 1.91, ≥ 28.4 events/hour) and left atrial volume (LAV) (OR = 1.42, ≥ 128.3 mL) were independent predictors of the presence of ECs, and AHI (OR = 1.44, ≥ 27.8 events/hour) was an independent predictor of the presence of AF recurrence.

It is essential for physicians to recognise the potential complexity of ECs and SDB in AF patients. Thus, screening and treating SDB in AF patients presenting with ECs might play a pivotal role in suppressing AF recurrence.

Inflammation plays a pathophysiological role in atherosclerosis and its clinical consequences. In addition to glycemic control, glucagon-like peptide-1 receptor agonists (GLP-1RAs) are of wide concern for cardioprotective effects. The structure, half-life, homology, and clinical efficacy of GLP-1RAs exhibit remarkable disparity. Several studies have compared the disparities in anti-inflammatory effects between daily and weekly GLP-1RAs. This study aimed to compare the similarities and differences between liraglutide and dulaglutide in terms of inhibiting atherosclerotic inflammation and improving co-cultured endothelial cell function. The expression of inflammation markers was examined by immunofluorescence, Western blotting, and real-time PCR. The tube-forming ability of endothelial cells was tested on Matrigel. The results verify that 10/50/100 nmol/L liraglutide and 100 nmol/L dulaglutide markedly suppressed the expression of inflammatory factors in LPS-induced atherosclerosis after 24 and 72 hours, respectively. Moreover, they promoted the polarization of M1 macrophages toward the M2 phenotype and improved the function of co-cultured endothelial cells. Both liraglutide and dulaglutide ameliorate atherosclerosis development. The difference between the two resided in the extended intervention duration required to observe the effect of dulaglutide, and liraglutide demonstrated a superior dose-dependent manner. We provide a potential strategy to understand the dynamics of drug action and possible timing administration.