Device therapy for patients with atrial fibrillation and heart failure with preserved ejection fraction.

Device therapy is a nonpharmacological approach that presents a crucial advancement for managing patients with atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF). This review investigated the impact of device-based interventions and emphasized their potential for optimizing treatment for this complex patient demographic. Cardiac resynchronization therapy, augmented by atrioventricular node ablation with His-bundle pacing or left bundle-branch pacing, is effective for enhancing cardiac function and establishing atrioventricular synchrony. Cardiac contractility modulation and vagus nerve stimulation represent novel strategies for increasing myocardial contractility and adjusting the autonomic balance. Left ventricular expanders have demonstrated short-term benefits in HFpEF patients but require more investigation for long-term effectiveness and safety, especially in patients with AF. Research gaps regarding complications arising from left ventricular expander implantation need to be addressed. Device-based therapies for heart valve diseases, such as transcatheter aortic valve replacement and transcatheter edge-to-edge repair, show promise for patients with AF and HFpEF, particularly those with mitral or tricuspid regurgitation. Clinical evaluations show that these device therapies lessen AF occurrence, improve exercise tolerance, and boost left ventricular diastolic function. However, additional studies are required to perfect patient selection criteria and ascertain the long-term effectiveness and safety of these interventions. Our review underscores the significant potential of device therapy for improving the outcomes and quality of life for patients with AF and HFpEF.

Pulsed Field Ablation for Atrial Fibrillation: Mechanisms, Advantages, and Limitations.

Pulsed field ablation with irreversible electroporation for the treatment of atrial fibrillation involves tissue-specific and non-thermal energy-induced cell necrosis, which helps avoid complications, such as pulmonary vein stenosis, atrial collateral tissue damage, and extensive atrial structural damage, often encountered with traditional thermal ablation. In existing clinical trials, pulsed field ablation has shown excellent effects on pulmonary vein isolation in patients with paroxysmal and persistent atrial fibrillation. Pulsed field ablation is easy, simple, and quick and can reduce iatrogenic injury. Therefore, the application of pulsed field ablation technology in the treatment of atrial fibrillation has a promising future. Notably, the adjustment of parameters in pulsed field ablation with different ablation catheter systems can strongly affect the area and depth of the necrotic myocardium, which greatly affects the likelihood of atrial fibrillation recurrence and incidence of adverse complications after ablation. In this paper, we review the mechanisms, advantages, and limitations of pulsed field ablation based on the results of a series of previous studies and provide ideas and directions for future research.

Overcoming barriers for left atrial appendage thrombus: a systematic review of left atrial appendage closure.

BACKGROUND: Approximately 90% of intracardial thrombi originate from the left atrial appendage in non-valvular atrial fibrillation patients. Even with anticoagulant therapy, left atrial appendage thrombus (LAAT) still occurs in 8% of patients. While left atrial appendage closure (LAAC) could be a promising alternative, the current consensus considers LAAT a contraindication to LAAC. However, the feasibility and safety of LAAC in patients with LAAT have yet to be determined. METHODS: This systematic review synthesizes published data to explore the feasibility and safety of LAAC for patients with LAAT. RESULTS: This study included a total of 136 patients with LAATs who underwent successful LAAC. The Amulet Amplatzer device was the most frequently utilized device (48.5%). Among these patients, 77 (56.6%) had absolute contraindications to anticoagulation therapy. Cerebral protection devices were utilized by 47 patients (34.6%). Transesophageal echocardiography (TEE) is the primary imaging technique used during the procedure. Warfarin and novel oral anticoagulants were the main anticoagulant medications used prior to the procedure, while dual antiplatelet therapy was primarily used post-procedure. During a mean follow-up period of 13.2 ± 11.5 months, there was 1 case of fatality, 1 case of stroke, 3 major bleeding events, 3 instances of device-related thrombus, and 8 cases of peri-device leakage. CONCLUSIONS: This review highlights the preliminary effectiveness and safety of the LAAC procedure in patients with persistent LAAT. Future large-scale RCTs with varied LAAT characteristics and LAAC device types are essential for evidence-based decision-making in clinical practice.

Artificially sweetened beverage consumption and all-cause and cause-specific mortality: an updated systematic review and dose-response meta-analysis of prospective cohort studies.

BACKGROUND: Artificially sweetened beverages (ASB) are consumed globally, but their impact on overall health remains uncertain. We summarized published associations between ASB intake with all-cause and cause-specific mortality. METHODS: We searched Medline, Embase, Web of Science, and Cochrane CENTRAL databases until August 2023. Random effect meta-analysis was conducted to calculate pooled risk ratios (RRs) and 95% confidence intervals (95%CIs) for highest versus lowest categories of ASB consumption in relation to all-cause and cause-specific mortality. Linear and non-linear dose-response analyses were also performed. RESULTS: Our systematic review and meta-analysis included 11 prospective cohort studies. During a median/mean follow-up period of 7.0 to 28.9 years, 235,609 deaths occurred among 2,196,503 participants. Intake of ASB was associated with higher risk of all-cause and CVD mortality with pooled RRs (95%CIs) of highest vs. lowest intake categories of 1.13 (1.06, 1.21) (I2 = 66.3%) for all-cause mortality and 1.26 (1.10, 1.44) (I2 = 52.0%) for CVD mortality. Dose-response analysis revealed a non-linear association of ASB with all-cause mortality (pnon-linearity = 0.01), but a linear positive association with CVD mortality (pnon-linearity = 0.54). No significant association was observed for ASB intake and cancer mortality. Moreover, a secondary meta-analysis demonstrated that replacing 1 serving/day of sugary sweetened beverages (SSB) with ASB was associated with 4-6% lower risk of all-cause and CVD mortality. Per NutriGrade, the evidence quality for associations between ASB intake with all-cause and CVD mortality was moderate. CONCLUSIONS: Higher intake of ASB was associated with higher risk of all-cause and CVD mortality, albeit a lower risk than for SSB. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration no. CRD42022365701.

The effectiveness and safety of temporary transvenous cardiac pacing leads placement into coronary sinus vein in patients with sick sinus syndrome.

BACKGROUND: The temporary pacing lead routinely is placed into right ventricular (RV), which pose a risk of dislocation and cardiac perforation. OBJECTIVE: We aim to evaluate the effectiveness and safety of temporary transvenous cardiac pacing (TTCP) leads placement into the coronary sinus vein (CSV) in patients with sick sinus syndrome (SSS). METHODS: We investigated patients with SSS who underwent TTCP lead placement into the CSV under the guidance of X-ray between January 2013 and May 2023. Patients were randomly divided into two groups: RV group (n = 33) and CSV group (n = 22). The ordinary passive bipolar electrodes were applied in both groups. In RV groups, electrodes were placed into RV. In CSV group, electrodes were placed into CSV. We evaluated the operation duration, fluoroscopic exposure, first-attempt success rate of leads placement, pacing threshold, success rate of leads placement, rate of leads displacement, and complications. RESULTS: Compared with that in RV group, the procedure time, fluoroscopic exposure was significantly prolonged, while the first-attempt success rate of lead placement was obviously increased in CSV group (both p < .05). Compared with that in RV group, the rate of leads displacement is lower in CSV group (both p < .05). There were three patients occurred cardiac perforation in RV group, but no cardiac perforation was reported in CSV group (p > .05). CONCLUSION: TTCP leads placement into the CSV is an effective and safe strategy in patients with SSS. It indicates a high rate of pacing effectiveness with low device replacement and complication rates.

Dietary fruits and vegetables and risk of cardiovascular diseases in elderly Chinese.

BACKGROUND: Evidence regarding the potential effect of fruit and vegetable consumption on cardiovascular diseases (CVD) was limited and inconsistent among Asian people. METHODS: We prospectively examined associations of fruit and vegetable consumption with the risk of CVD among 9740 participants aged 65 years and older (mean baseline age: 88 years) in the Chinese Longitudinal Healthy Longevity Survey (CLHLS) (2008-2018). Dietary data were collected using a validated food frequency questionnaire. RESULTS: During 37 366 person-years of follow-up, a total of 3738 CVD cases were recorded. After adjusting for demographics, dietary, lifestyle and economical social factors, higher intakes of total fruits and vegetables were associated with lower risk of CVD [comparing with extreme quintiles, hazard ratio and 95% confidence interval: 0.84 (0.74, 0.95)]. The inverse association was mainly driven by vegetable consumption [0.86 (0.77, 0.95)]. Furthermore, the inverse association was stronger for the risk of hypertension [0.84 (0.72, 0.98)]. These associations were consistent across age, sex, body mass index, residence, exercise status, smoking, drinking, meat intake, modified hPDI and health status. CONCLUSIONS: This study suggests higher intakes of total fruits and vegetables are associated with a lower risk of CVD among elderly Chinese people, supporting the current recommendations of increasing fruit and vegetable consumption as part of a healthy diet for the prevention of CVD.

Advances in diagnosis and treatment of mechanical hemolysis following percutaneous interventional for valvular heart diseases. / å¿ƒè„ç“£è†œç— ä»‹å ¥æ²»ç–—æœ¯åŽæœºæ¢°æ€§æº¶è¡€è¯Šç–—è¿›å±•.

Valvular heart disease is one of the common heart diseases in clinical practice, characterized by valve stenosis and/or incomplete closure. At present, drug therapy, surgery, and emerging percutaneous intervention therapy are the main treating methods for heart valve disease. Although the research and development of percutaneous intervention therapy devices is relatively mature, there are still problems such as postoperative mechanical hemolysis. The occurrence of mechanical hemolysis is associated with factors such as excessive shear stress experienced by red blood cells, direct interaction between red blood cells and the heart and valve surfaces, and thrombus formation. Furthermore, the presence of postoperative infection and other hemolytic diseases can also affect the occurrence of mechanical hemolysis. Although most patients are asymptomatic when hemolysis occurs, there are still critical cases. This type of hemolysis can accelerate the deterioration of the condition, and even endanger life in severe cases. Therefore, elucidating the background, pathogenesis, epidemiology, and related clinical research progress of mechanical hemolysis after percutaneous intervention therapy for valvular heart disease is of great significance for guiding the standardized diagnosis and treatment of the disease.

Research progress in the cardiac lymphatic system and myocardial repair after myocardial infarction. / å¿ƒè„æ·‹å·´ç³»ç»Ÿä¸Žå¿ƒè‚Œæ¢—æ­»åŽå¿ƒè‚Œä¿®å¤çš„ç ”ç©¶è¿›å±•.

The lymphatic system of the heart plays an important role in the repair process after myocardial injury and may regulate normal tissue homeostasis and natural regeneration via maintaining fluid homeostasis and controlling the inflammatory response. The lymphatic system in the heart is activated after myocardial injury and is involved in the scarring process of the heart. Recent studies on the lymphatic system and myocardial repair of the heart have developed rapidly, and the mechanisms for lymphangiogenesis and lymphatic endothelial cell secretion have been elucidated by different animal models. A deep understanding of the structural, molecular, and functional characteristics of the lymphatic system of the heart can help develop therapies that target the lymphatic system in the heart. Summarizing the progress in studies on targets related to myocardial repair and the cardiac lymphatic system is helpful to provide potential new targets and strategies for myocardial repair therapy after myocardial infarction.

Rationale and Design of the H-REPLACE Study: Safety and Efficacy of LMWH Versus Rivaroxaban in ChinEse Patients HospitaLized with Acute Coronary SyndromE.

BACKGROUND: Acute coronary syndrome (ACS) is a serious and life-threatening condition. Anticoagulation during the acute phase of ACS is effective in reducing ischemic events. The most widely used parenteral anticoagulation agent in ACS patients is enoxaparin. Rivaroxaban is a novel oral anticoagulant with potent anti-Xa activity, which might be an attractive alternative drug to enoxaparin. In fact, rivaroxaban was consistently shown to be non-inferior to enoxaparin therapy in terms of reduction of recurrent venous thromboembolism events. OBJECTIVE: This prospective, randomized, open-label, active-controlled, multicenter study is designed to compare the safety and efficacy of rivaroxaban versus enoxaparin in patients with ACS, who missed the primary reperfusion therapy window and before selective revascularization. METHODS AND RESULTS: Up to 2055 participants receiving background treatment of aspirin plus clopidogrel or ticagrelor will be randomly assigned to either oral rivaroxaban 2.5 mg twice daily or rivaroxaban 5 mg twice daily or subcutaneous enoxaparin 1 mg/kg twice daily until hospital discharge for a maximum of 8 days or 12 h before revascularization therapy. The primary safety endpoint is the International Society on Thrombosis and Hemostasis definition of bleeding events [minor, clinically relevant non-major and major bleeding]. The primary efficacy endpoint is a composite of major adverse cardiac events (MACE), including cardiac death, myocardial infarction, re-revascularization or stroke, and major bleeding events. Secondary endpoints include cardiac-related rehospitalization and all-cause death. Patients will be followed for 12 months after randomization. CONCLUSIONS: The H-REPLACE trial offers an opportunity to assess clinical outcomes of rivaroxaban versus enoxaparin during the acute phase of ACS and may provide an alternative anticoagulation strategy for ACS patients, who missed the primary reperfusion therapy window and before selective revascularization. TRIAL REGISTRATION: ClinicalTrials.gov; NCT03363035.

Advances in extracardiac mechanisms for heart failure with preserved ejection fraction. / å°„è¡€åˆ†æ•°ä¿ç•™çš„å¿ƒåŠ›è¡°ç«­å¿ƒè„å¤–æœºåˆ¶ç ”ç©¶è¿›å±•.

Heart failure with preserved ejection fraction (HFpEF) is a syndrome with highly heterogeneous clinical symptoms, and its incidence has been increasing in recent years. Compared with heart failure with reduced ejection fraction (HFrEF), HFpEF has a worse prognosis. Traditional therapies targeting the internal mechanisms of the heart show limited or inefficacy on HFpEF, and new therapeutic targets for HFpEF are expected to be found by focusing on the extracardiac mechanisms. Recent studies have shown that cardiopulmonary pathophysiological interaction exacerbates the progression of HFpEF. Hypertension, systemic vascular injury, and inflammatory response lead to coronary microvascular dysfunction, myocardial hypertrophy, and coronary microvascular remodeling. Acute kidney injury affects myocardial energy production, induces oxidative stress and catabolism of myocardial protein, which leads to myocardial dysfunction. Liver fibrosis mediates heart injury by abnormal protein deposition and inflammatory factors production. Skeletal muscle interacts with the sympathetic nervous system by metabolic signals. It also produces muscle factors, jointly affecting cardiac function. Metabolic syndrome, gut microbiota dysbiosis, immune system diseases, and iron deficiency promote the occurrence and development of HFpEF through metabolic changes, oxidative stress, and inflammatory responses. Therefore, the research on the extracardiac mechanisms of HFpEF has certain implications for model construction, mechanism research, and treatment strategy formulation.

Circulating Endothelial Progenitor Cells Are Preserved in Female Mice Exposed to Ambient Fine Particulate Matter Independent of Estrogen.

Males have a higher risk for cardiovascular diseases (CVDs) than females. Ambient fine particulate matter (PM) exposure increases CVD risk with increased reactive oxygen species (ROS) production and oxidative stress. Endothelial progenitor cells (EPCs) are important to vascular structure and function and can contribute to the development of CVDs. The aims of the present study were to determine if sex differences exist in the effect of PM exposure on circulating EPCs in mice and, if so, whether oxidative stress plays a role. Male and female C57BL/6 mice (8-10 weeks old) were exposed to PM or a vehicle control for six weeks. ELISA analysis showed that PM exposure substantially increased the serum levels of IL-6 and IL-1ß in both males and females, but the concentrations were significantly higher in males. PM exposure only increased the serum levels of TNF-α in males. Flow cytometry analysis demonstrated that ROS production was significantly increased by PM treatment in males but not in females. Similarly, the level of circulating EPCs (CD34+/CD133+ and Sca-1+/Flk-1+) was significantly decreased by PM treatment in males but not in females. Antioxidants N-acetylcysteine (NAC) effectively prevented PM exposure-induced ROS and inflammatory cytokine production and restored circulating EPC levels in male mice. In sharp contrast, circulating EPC levels remained unchanged in female mice with PM exposure, an effect that was not altered by ovariectomy. In conclusion, PM exposure selectively decreased the circulating EPC population in male mice via increased oxidative stress without a significant impact on circulating EPCs in females independent of estrogen.

Osteoprotegerin promotes intimal hyperplasia and contributes to in-stent restenosis: Role of an αVß3/FAK dependent YAP pathway.

OBJECTIVE: Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are related to in-stent-restenosis (ISR) following percutaneous coronary intervention (PCI). Osteoprotegerin (OPG) has been implicated in various vascular diseases. However, the effects of OPG on ISR and the underlying mechanism remained elusive. We here investigated the association between OPG and ISR, and to demonstrate the role and potential mechanisms of OPG in neointimal hyperplasia. APPROACH AND RESULTS: From 2962 patients who received coronary angiography and follow-up coronary angiography at approximately one year, 291 patients were diagnosed with ISR, and another 291 gender- and age- matched patients without ISR were selected as controls. Serum OPG levels were significantly increased in patients with ISR. Multivariable logistic regression analysis indicated that OPG level was independently associated with the increased risk of ISR. In a mouse femoral artery wire injury model, upregulated OPG was evidenced in vascular tissue after injury. OPG deletion attenuated the vascular injury-induced neointimal hyperplasia and related gene expression in mice. OPG promoted neointimal hyperplasia and human aortic smooth muscle cell (hASMC) proliferation and migration through activation of yes-associated protein (YAP), a major downstream effector of the Hippo signaling pathway, whereas knockdown or inhibition of YAP in hASMCs blunted OPG-induced above effects. Moreover, we found that OPG, as a ligand for integrin αVß3, mediated phosphorylation of focal adhesion kinase (FAK) and actin cytoskeleton reorganization, resulting in YAP dephosphorylation in hASMCs. OPG-dependent YAP and VSMC activation was prevented by treatment with αVß3-blocking antibodies and inhibitors of FAK and actin stress fibers. CONCLUSIONS: Increased serum OPG levels are associated with increased risk of ISR following PCI and OPG could promote neointimal hyperplasia in response to injury through integrin αVß3 mediated FAK and YAP activation, indicating OPG/YAP inhibition might serve as an attractive novel target for the prevention of ISR after PCI.

Metformin regulates adiponectin signalling in epicardial adipose tissue and reduces atrial fibrillation vulnerability.

Epicardial adipose tissue (EAT) remodelling is closely related to the pathogenesis of atrial fibrillation (AF). We investigated whether metformin (MET) prevents AF-dependent EAT remodelling and AF vulnerability in dogs. A canine AF model was developed by 6-week rapid atrial pacing (RAP), and electrophysiological parameters were measured. Effective refractory periods (ERP) were decreased in the left and right atrial appendages as well as in the left atrium (LA) and right atrium (RA). MET attenuated the RAP-induced increase in ERP dispersion, cumulative window of vulnerability, AF inducibility and AF duration. RAP increased reactive oxygen species (ROS) production and nuclear factor kappa-B (NF-κB) phosphorylation; up-regulated interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and transforming growth factor-ß1 (TGF-ß1) levels in LA and EAT; decreased peroxisome proliferator-activated receptor gamma (PPARγ) and adiponectin (APN) expression in EAT and was accompanied by atrial fibrosis and adipose infiltration. MET reversed these alterations. In vitro, lipopolysaccharide (LPS) exposure increased IL-6, TNF-α and TGF-ß1 expression and decreased PPARγ/APN expression in 3T3-L1 adipocytes, which were all reversed after MET administration. Indirect coculture of HL-1 cells with LPS-stimulated 3T3-L1 conditioned medium (CM) significantly increased IL-6, TNF-α and TGF-ß1 expression and decreased SERCA2a and p-PLN expression, while LPS + MET CM and APN treatment alleviated the inflammatory response and sarcoplasmic reticulum Ca2+ handling dysfunction. MET attenuated the RAP-induced increase in AF vulnerability, remodelling of atria and EAT adipokines production profiles. APN may play a key role in the prevention of AF-dependent EAT remodelling and AF vulnerability by MET.

Metformin regulates lipid metabolism in a canine model of atrial fibrillation through AMPK/PPAR-α/VLCAD pathway.

BACKGROUND: Atrial lipid metabolic remodeling is critical for the process of atrial fibrillation (AF). Abnormal Fatty acid (FA) metabolism in cardiomyocytes is involved in the pathogenesis of AF. MET (Metformin), an AMPK (AMP-activated protein kinase) activator, has been found to be associated with a decreased risk of AF in patients with type 2 diabetes. However, the specific mechanism remains unknown. METHODS: Fifteen mongrel dogs were divided into three groups: SR, ARP (pacing with 800 beats/min for 6 h), ARP plus MET (treated with MET (100 mg/kg/day) for two weeks before pacing). We assessed metabolic factors, speed limiting enzymes circulating biochemical metabolites (substrates and products), atrial electrophysiology and accumulation of lipid droplets. RESULTS: The expression of AMPK increased in the ARP group and significantly increased in the MET+ARP group comparing to the SR group. In the ARP group, the expressions of PPARα、PGC-1α and VLCAD were down-regulated, while the concentration of free fatty acid and triglyceride and the lipid deposition in LAA (left atrial appendage) increased. Moreover, AERP and AERPd have also been found abnormally in this process. Pretreatment with MET before receiving ARP reversed the alterations aforementioned. CONCLUSIONS: The FA metabolism in LAA is altered in the ARP group, mainly characterized by the abnormal expression of the rate-limiting enzyme. Metformin reduces lipid accumulation and promotes ß-oxidation of FA in AF models partially through AMPK/PPAR-α/VLCAD pathway. Our study indicates that MET may inhibit the FA lipid metabolic remodeling in AF.

Stiff Left Atrial Syndrome: A Complication Undergoing Radiofrequency Catheter Ablation for Atrial Fibrillation.

Radiofrequency catheter ablation for atrial fibrillation is an effective approach for treating atrial fibrillation. Its complications have attracted much attention, of which the stiff left atrial syndrome is a recently discovered complication that has not been completely understood. This study aims to investigate the concept, pathologic basis, clinical characteristics, predictors, and treatment protocols of the stiff left atrial syndrome after radiofrequency ablation for atrial fibrillation.

Enhancing myocardial function with cardiac contractility modulation: potential and challenges.

Cardiac contractility modulation (CCM) offers a novel therapeutic avenue for heart failure patients, particularly those unresponsive to cardiac resynchronization therapy within specific QRS duration ranges. This review elucidates CCM's mechanistic underpinnings, its impact on myocardial function, and utility across patient demographics. However, CCM is limited by insufficient data on mortality and hospitalization rate reductions, as well as the need for specialized device implantation skills. While prevailing research has concentrated on left ventricular effects, a knowledge gap persists for other patient subsets. Future inquiries should address combinatory treatment strategies, extended usage and the impact of atrial fibrillation on device implantation. Such expanded studies could refine therapeutic outcomes and widen the scope of beneficiaries.

Ruxolitinib as a CaMKII inhibitor for treatment of cardiac arrhythmias: Applications and prospects.

Recent studies have highlighted the critical role of calcium/calmodulin-dependent protein kinase II (CaMKII) overactivation in the pathogenesis of various cardiac arrhythmias. Ruxolitinib, a Janus kinase inhibitor widely used for the treatment of myelofibrosis and acute graft-vs-host disease, has expanded its research horizons to include its potential as a CaMKII inhibitor in the treatment of cardiac arrhythmias. This article reviews the basic pharmacologic properties of ruxolitinib and delves into the role of CaMKII in cardiac arrhythmias, including its structural fundamentals, activation mechanisms, and association with arrhythmic conditions. Furthermore, the current state of CaMKII inhibitor research is discussed, with a special focus on the advances and clinical potential of ruxolitinib in this field. Studies indicate that ruxolitinib effectively inhibits CaMKII activity and has therapeutic potential against cardiac arrhythmias in animal models and at the cellular level. In addition, we address the critical issues that need to be resolved before the clinical application of ruxolitinib in arrhythmia treatment, including dosage concerns, long-term inhibitory effects, potential impacts on the nervous system, and efficacy across different types of arrhythmias. Future research directions involve further exploration of the clinical application potential of ruxolitinib, particularly in diseases such as heart failure, hypertrophic cardiomyopathy, dilated cardiomyopathy, and ischemic arrhythmias. In summary, the efficacy, low toxicity, and safety profile of ruxolitinib as a CaMKII inhibitor in the treatment of cardiac arrhythmias suggest a promising future for its development as a therapeutic drug in this domain.

GLP-1 receptor agonists and myocardial metabolism in atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Many medical conditions, including hypertension, diabetes, obesity, sleep apnea, and heart failure (HF), increase the risk for AF. Cardiomyocytes have unique metabolic characteristics to maintain adenosine triphosphate production. Significant changes occur in myocardial metabolism in AF. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have been used to control blood glucose fluctuations and weight in the treatment of type 2 diabetes mellitus (T2DM) and obesity. GLP-1RAs have also been shown to reduce oxidative stress, inflammation, autonomic nervous system modulation, and mitochondrial function. This article reviews the changes in metabolic characteristics in cardiomyocytes in AF. Although the clinical trial outcomes are unsatisfactory, the findings demonstrate that GLP-1 RAs can improve myocardial metabolism in the presence of various risk factors, lowering the incidence of AF.

Subarachnoid haemorrhage-induced reversible cardiac dysfunction: time course and potential mechanisms.

AIMS: Cardiac dysfunction is commonly observed in patients with subarachnoid haemorrhage (SAH). However, the specific timeline of cardiac remodelling and the underlying mechanisms responsible for this effect following SAH remain unknown. This study aims to explore the impact of SAH on cardiac dysfunction and its potential mechanisms over time. METHODS AND RESULTS: In Protocol 1, we investigated cardiac function and potential mechanisms in a Sprague-Dawley rat model of SAH at six time points (baseline and Days 1, 3, 7, 14, and 28) while exploring the underlying mechanisms. Our assessments included the haemodynamic profile, echocardiography, and the concentrations of plasma biomarkers at various time points post-SAH. We determined neuropeptide Y (NPY) 1-5 receptor protein expression levels through western blotting. In Protocol 2, we administered an NPY1 receptor antagonist to evaluate the effects of cardiac dysfunction induced by SAH on Day 3. In Protocol 1, SAH gradually provoked cardiac systolic dysfunction during the acute phase, reaching its peak on Day 3 without concurrent alterations in wall thickness. However, no significant changes were observed from Days 14 to 28 compared with Day 0. The changes in cardiac dysfunction were consistent with myocardial injury, inflammatory biomarkers, and NPY levels. SAH resulted in a heightened heart rate and systolic blood pressure, correlating with elevated epinephrine and norepinephrine levels. In Protocol 2, the administration of the NPY1 receptor antagonist effectively ameliorated cardiac dysfunction. CONCLUSIONS: SAH induces transient cardiac dysfunction in the acute phase, and the underlying mechanisms for this response involve the NPY-NPY1 receptor pathway, otherwise known as catecholamines.