Timing of oral anticoagulation in atrial fibrillation patients after acute ischaemic stroke and outcome after 3 months: results of the multicentre Berlin Atrial Fibrillation Registry.

BACKGROUND: Oral anticoagulation (OAC) is key in stroke prevention in patients with atrial fibrillation (AF) but there is uncertainty regarding the optimal timing of OAC (re)initiation after stroke, as recent large randomised controlled trials have methodological weaknesses and excluded stroke patients on therapeutic anticoagulation at stroke onset as well as patients started on a vitamin K antagonist after stroke. The '1-3-6-12 days rule', based on expert consensus and referring to stroke severity, was used in clinical practice to initiate OAC after acute ischaemic stroke or transient ischaemic attack (TIA) since publication in 2013. METHODS: We retrospectively assessed whether compliance to the '1-3-6-12 days rule' was associated with the composite endpoint (recurrent stroke, systemic embolism, myocardial infarction, major bleeding or all-cause death). RESULTS: Among 708 registry patients with known AF before stroke and hospitalisation within 72 hours after stroke, 432 were anticoagulated at stroke onset. OAC was started according to the '1-3-6-12 days rule' in 255 (39.2%) patients. Non-adherence to the '1-3-6-12 days rule' was not associated with the composite endpoint within 3 months in 661 patients who (re-)started on OAC (log-rank test: p=0.74).Results were similar for 521 patients (re)started on a non-vitamin K-dependent OAC. CONCLUSION: (Re)starting OAC after stroke followed the '1-3-6-12 days rule' in about 40% of all patients with AF, and more often in those anticoagulated at stroke onset. Adherence to the '1-3-6-12 days rule' did not reduce the composite clinical endpoint, if OAC was restarted within 3 months of stroke/TIA. TRIAL REGISTRATION NUMBER: NCT02306824.

Prostate Cancer Therapy Cardiotoxicity Map (PROXMAP) for Advanced Disease States: A Systematic Review and Network Meta-analysis with Bayesian Modeling of Treatment Histories.

BACKGROUND AND OBJECTIVE: Recommendations of first-line therapies for metastatic hormone-sensitive (mHSPC), nonmetastatic castrate-resistant (M0CRPC), and metastatic castrate-resistant (mCRPC) prostate cancer do not account for cardiotoxicity due to a lack of clear prior evidence. This manuscript assesses cardiotoxicity of these therapies. METHODS: We searched Ovid Medline, Elsevier Embase, and the Cochrane Library for randomized clinical trials (RCTs) from database inception to January 14, 2024. Network meta-analyses of first-line mHSPC, M0CRPC, and mCRPC therapies were constructed for the five cardiotoxicity metrics defined by the International Cardio-Oncology Society: heart failure, myocarditis, vascular toxicity, hypertension, and arrhythmias. Additional Bayesian network meta-analyses also accounted for prior treatment history. KEY FINDINGS AND LIMITATIONS: Thirteen RCTs (16 292 patients) were included. For mHSPC, androgen deprivation therapy (ADT) plus docetaxel (DTX) plus abiraterone acetate (AA) with prednisone (P) demonstrated a significant increase in hypertension and arrhythmias versus ADT + DTX (risk ratio [RR] 2.85, 95% confidence interval [CI] 1.67-4.89, and RR 2.01, 95% CI 1.17-3.44, respectively); however, no corresponding differences were observed between ADT + DTX plus darolutamide (DAR) and ADT + DTX (RR 1.55, 95% CI 0.73-3.30, and RR 0.94, 95% CI 0.63-1.40, respectively). For mCRPC assuming a history of mHSPC treatment, ADT + AA + P plus olaparib (OLA) demonstrated a statistically significant decrease in hypertension versus ADT + AA + P (RR 0.20, 95% CI 0.16-0.26). M0CRPC results were unremarkable. CONCLUSIONS AND CLINICAL IMPLICATIONS: For mHSPC, ADT + DTX + DAR demonstrates less cardiotoxicity than ADT + DTX + AA + P due to a lower risk of hypertension and arrhythmias from decreased mineralocorticoid excess. In addition, OLA counterintuitively offers decreased hypertension when superimposed on ADT + AA + P for mCRPC treatment after prior androgen deprivation from mHSPC therapy.

Comparing E-Cigarettes and Traditional Cigarettes in Relation to Myocardial Infarction, Arrhythmias, and Sudden Cardiac Death: A Systematic Review and Meta-Analysis.

BACKGROUND: The use of electronic cigarettes (e-cigarettes) as a perceived safer alternative to traditional cigarettes has grown rapidly. However, the cardiovascular risks associated with e-cigarettes compared to regular cigarettes remain unclear. OBJECTIVE: To systematically review and compare the cardiovascular outcomes of e-cigarette use versus traditional cigarette use, focusing on the risks of myocardial infarction, arrhythmias, and sudden death. METHODS: A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Peer-reviewed studies published in English were included if they reported cardiovascular outcomes related to e-cigarette or traditional cigarette use. A total of 20 studies were included, covering observational and interventional studies focusing on heart rate variability, myocardial infarction, arrhythmias, and sudden cardiac events. The quality of the evidence was assessed using the GRADE criteria, and data were extracted and analyzed based on the PICOS (Population, Interventions, Comparisons, Outcomes, and Study designs) framework. RESULTS: The systematic review found that both e-cigarettes and traditional cigarettes pose significant cardiovascular risks, with traditional cigarettes linked to a higher incidence of myocardial infarction, arrhythmias, and sudden cardiac death. E-cigarette users also face increased risks of arrhythmias and myocardial infarction compared to non-smokers, primarily due to the constituents of aerosolized e-liquid, including nicotine and flavorings, which contribute to adverse cardiac effects. Regular e-cigarette use, particularly in combination with traditional cigarette use, was associated with a heightened risk of myocardial infarction. Studies also reported heart function abnormalities, such as systolic and diastolic dysfunction, and reduced ejection fractions. Additionally, changes in heart rate variability, heart rate, and blood pressure were observed, indicating both acute and chronic effects of e-cigarettes on cardiovascular autonomic regulation. CONCLUSIONS: While e-cigarettes may present a lower cardiovascular risk compared to traditional cigarettes, they are not without harm. Both products are linked to increased risks of myocardial infarction and arrhythmias, though traditional cigarettes pose a higher overall threat. Given the limitations in the current evidence base, particularly concerning the long-term effects of e-cigarette use, further research is needed to clarify these cardiovascular risks and inform public health guidelines.

Cardiac resynchronization therapy in heart failure based on Strauss criteria for left bundle branch block.

AIMS: The left bundle branch block (LBBB) is a strong predictor of response to cardiac resynchronization therapy (CRT). However, a significant number of patients do not respond to the treatment. The study sought to evaluate the impact of the stricter Strauss criteria for left bundle branch block (St-LBBB) on CRT response, hospitalizations, ventricular arrhythmia (VA) events and mortality. METHODS: This study is a retrospective analysis of prospectively collected data on heart failure (HF) patients with LBBB admitted for CRT implantation. Patients were divided into two groups according to the fulfilment or not of St-LBBB criteria. RESULTS: The study included 82 patients with ischaemic (ICM) and non-ischaemic (NICM) cardiomyopathy [46 (56%) with St-LBBB and 36 (44%) with non-St-LBBB]. Patients with St-LBBB showed higher CRT response rates compared with those with non-St-LBBB (P < 0.01), while the group with NICM exhibited the greatest benefit (P < 0.01). St-LBBB CRT responders displayed significantly lower rates of HF hospitalization (P < 0.0001) compared with the non-St-LBBB group. According to Kaplan-Meier time curves, this was primarily evident in patients with NICM (P < 0.0001). CRT responders displayed significantly fewer VA events (P < 0.001) and lower mortality rates (P < 0.0001) than non-responders. Kaplan-Meier estimates demonstrated a significantly lower incidence of VAs in NICM patients with St-LBBB (P = 0.049) compared with ICM patients with St-LBBB (P = 0.25). Lower mortality rates were observed in CRT responders than non-responders (P < 0.0001), with the group of NICM with St-LBBB criteria exhibiting the greatest benefit (P = 0.0238). CONCLUSIONS: Patients with NICM and St-LBBB present the greatest benefit concerning CRT response, HF hospitalizations, VA events and mortality. Although St-LBBB criteria seem to improve patient selection for CRT, more data are needed to elucidate the role of St-LBBB criteria in this setting.

Electric storm triggered by short-coupled premature ventricular complexes in a young patient with non-obstructive hypertrophic cardiomyopathy.

Ventricular arrhythmias are commonly associated with hypertrophic cardiomyopathy with and without midventricular obstruction. Although the overall prognosis is relatively good with an annual mortality rate <1%, the propensity to potentially fatal ventricular arrhythmias (ventricular tachycardia) is the most feared complication. Electrical storms are a severe manifestation of ventricular arrhythmias, with poor outcomes. In this report, we present a case of a young patient with non-obstructive hypertrophic cardiomyopathy who presents after a syncopal episode and is found to have an electric storm that is refractory to medical therapy.

Impact on ventricular arrhythmic burden of SGLT2 inhibitors in patients with chronic heart failure evaluated with cardiac implantable electronic device monitoring.

BACKGROUND: Sodium-glucose cotransporter 2 (SGLT2) inhibitors have revolutionized the therapeutic scenario of heart failure, demonstrating favorable effects on mortality and quality of life. Previous studies have yielded conflicting data regarding the effects on ventricular arrhythmias. METHODS: A prospective observational study was conducted to investigate the anti-arrhythmic properties of SGLT2 inhibitors evaluating the intra-patient difference in major adverse arrhythmic cardiac events (MAACE) over a six-month period in patients with chronic heart failure who were undergoing continuous monitoring using a cardiac implantable electronic device. RESULTS: From January 2022 to January 2023, 82 patients [median age 63 years (IQR 15), male 87 %] were enrolled in the study, with a median follow-up of 28 weeks (IQR 5). The rate of MAACE at baseline was 11 %, without relevant differences in the follow up in terms of major and minor arrhythmic events. In patients with an arrhythmic phenotype at baseline, a mild but non statistically significant reduction of MAACE (from 36 % to 28 %, p = 0.727) was observed and a significant decrease of non-sustained ventricular tachycardia (from 68 % to 32 %, p = 0.022). CONCLUSIONS: Our findings suggest potential anti-arrhythmic properties of SGLT2 inhibitors, evident in patients with arrhythmic events before the initiation of the drug.

Cardiac channelopathies in pediatrics: a genetic update.

Cardiac channelopathies are a group of inherited syndromes that can cause malignant arrhythmias and sudden cardiac death, particularly in the pediatric population. Today, a 12-lead electrocardiogram is the most effective tool to diagnose these diseases. Incomplete penetrance and variable expressivity are hallmarks of these syndromes. Some of these malignant entities may remain hidden and only a trigger such as exercise, emotions or fever can unmask the electrical pattern to diagnose the disease. Sudden cardiac death may be the first manifestation of any of these syndromes. The use of complementary tests that allow early diagnosis is strongly recommended, among which we find: pharmacological provocations, exercise tests, and genetic analysis. Genetic testing makes it possible to unravel the origin of the disease, and also identify family members who carry the harmful genetic defect and are therefore at risk. One of the main challenges in this area is the large number of genetic variants of uncertain significance, which prevent effective translation into clinical practice. Early identification of the pediatric population at risk and adequate risk stratification are crucial to adopting personalized preventive measures that reduce the risk of lethal episodes in this population. What is Known: • In the pediatric population, malignant arrhythmias leading to sudden cardiac death are mainly caused by inherited syndromes. • A conclusive genetic diagnosis unravels the origin of the syndrome and allows cascade screening to identify relatives carrying the genetic alteration. What is New: • The use of sequencing technologies allows a broad genetic analysis, helping to unravel new genetic alterations causing inherited arrhythmogenic syndromes. • A periodic reanalysis of genetic variants that currently have an ambiguous role will help discern those that are truly pathogenic.

Prevalence and Associated Factors of Paroxysmal Atrial Fibrillation and Atrial Arrhythmias During Hospitalizations for Exacerbation of COPD.

Purpose: This study aimed to investigate the proportion and risk factors of paroxysmal atrial fibrillation (AF) and atrial arrhythmias (AA) in patients hospitalized for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) in Vietnam. Patients and Methods: A prospective observational study was conducted at two major hospitals in Hanoi, Vietnam, from January 2022 to January 2023. A total of 197 AECOPD patients were recruited. ECG and 24-hour Holter ECG were used to diagnose paroxysmal AF and AA. Results: The prevalence of paroxysmal AF and AA were 15.2% and 72.6%, respectively. Factors associated with a higher likelihood of paroxysmal AF included aging 75 years old and above (aOR = 3.15; 95% CI: 1.28 to 8.48), Premature atrial complex (PAC) with 500 or more (aOR = 3.81; 95% CI: 1.48 to 10.97) and severity of COPD as group C and D (aOR = 3.41; 95% CI: 1.28 to 10.50). For AA, aging 75 years old and above (aOR = 2.25; 95% CI: 1.28 to 5.20), smoking (aOR = 2.10; 95% CI: 1.07 to 4.23) and P wave dispersion (PWD) with 40 milliseconds or more (aOR = 3.04; 95% CI: 1.54 to 6.19) were associated with a higher likelihood of AA. Conclusion: Overall, our findings highlight the associated factors with the paroxysmal AF and AA among AECOPD patients. This underscores the importance of a multifaceted approach to risk assessment and management in this vulnerable population, focusing not only on respiratory symptoms but also on comprehensive cardiovascular evaluation and intervention.

Exploring SCN5A Variants Associated with Atrial Fibrillation in Atrial Cardiomyocytes Derived from hiPSCs: A Characterization Study.

BACKGROUND: Atrial fibrillation (AF) poses a major risk for heart failure, myocardial infarction, and stroke. Several studies have linked SCN5A variants to AF, but their precise mechanistic contribution remains unclear. Human induced pluripotent stem cells (hiPSCs) provide a promising platform for modeling SCN5A-linked AF variants and their functional alterations. OBJECTIVE: The purpose of this study was to assess the electrophysiological impact of three AF-linked SCN5A variants, K1493R, M1875T and N1986K identified in three unrelated individuals. METHODS: CRISPR-Cas9 was used to generate a new hiPSC line in which NaV1.5 was knocked-out. Following differentiation into specific atrial cardiomyocyte by using retinoic acid, the adult WT and SCN5A variants were introduced into the NaV1.5 KO line through transfection. Subsequent analysis including molecular biology, optical mapping, and electrophysiology were performed. RESULTS: The absence of NaV1.5 channels altered the expression of key cardiac genes. NaV1.5 KO hiPSC-aCMs displayed slower conduction velocities, altered action potential (AP) parameters, and impaired calcium transient propagation. The transfection of the WT channel restored sodium current density and AP characteristics. Among the AF variants, one induced a loss-of-function (N1986K) while the other two induced a gain-of-function in NaV1.5 channel activity. Cellular excitability alterations, and early afterdepolarizations were observed in AF variants. CONCLUSION: Our findings suggest that distinct alterations in NaV1.5 channel properties may trigger atrial hyperexcitability and arrhythmogenic activity in AF. Our KO model offers an innovative approach for investigating SCN5A variants in a human cardiac environment.

Phenogroups and Their Prognosis of Acute Decompensated Heart Failure with Preserved Ejection Fraction.

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.

Bilateral paramedian thalamic infarction in the setting of uncontrolled atrial fibrillation with rapid ventricular response.

This case report outlines the first reported case of bilateral paramedian thalamic infarct, likely stemming from a rare artery of Percheron (AOP) variant, secondary to uncontrolled atrial fibrillation with rapid ventricular response. We underscore the importance of considering hypoperfusion due to decreased cerebral perfusion as a potential mechanism in cryptogenic AOP infarcts, challenging the conventional association with embolic etiology. This report contributes to the limited literature on AOP infarctions, emphasizing the need for heightened awareness among healthcare providers for diverse clinical presentations and potential etiologies to improve diagnosis and management, ultimately enhancing patient outcomes.

IRS2 Signaling Protects Against Stress-Induced Arrhythmia by Maintaining Ca2+ Homeostasis.

BACKGROUND: The docking protein IRS2 (insulin receptor substrate protein-2) is an important mediator of insulin signaling and may also regulate other signaling pathways. Murine hearts with cardiomyocyte-restricted deletion of IRS2 (cIRS2-KO) are more susceptible to pressure overload-induced cardiac dysfunction, implying a critical protective role of IRS2 in cardiac adaptation to stress through mechanisms that are not fully understood. There is limited evidence regarding the function of IRS2 beyond metabolic homeostasis regulation, particularly in the context of cardiac disease. METHODS: A retrospective analysis of an electronic medical record database was conducted to identify patients with IRS2 variants and assess their risk of cardiac arrhythmias. Arrhythmia susceptibility was examined in cIRS2-KO mice. The underlying mechanisms were investigated using confocal calcium imaging of ex vivo whole hearts and isolated cardiomyocytes to assess calcium handling, Western blotting to analyze the involved signaling pathways, and pharmacological and genetic interventions to rescue arrhythmias in cIRS2-KO mice. RESULTS: The retrospective analysis identified patients with IRS2 variants of uncertain significance with a potential association to an increased risk of cardiac arrhythmias compared with matched controls. cIRS2-KO hearts were found to be prone to catecholamine-sensitive ventricular tachycardia and reperfusion ventricular tachycardia. Confocal calcium imaging of ex vivo whole hearts and single isolated cardiomyocytes from cIRS2-KO hearts revealed decreased Ca²+ transient amplitudes, increased spontaneous Ca²+ sparks, and reduced sarcoplasmic reticulum Ca²+ content during sympathetic stress, indicating sarcoplasmic reticulum dysfunction. We identified that overactivation of the AKT1/NOS3 (nitric oxide synthase 3)/CaMKII (Ca2+/calmodulin-dependent protein kinase II)/RyR2 (type 2 ryanodine receptor) signaling pathway led to calcium mishandling and catecholamine-sensitive ventricular tachycardia in cIRS2-KO hearts. Pharmacological AKT inhibition or genetic stabilization of RyR2 rescued catecholamine-sensitive ventricular tachycardia in cIRS2-KO mice. CONCLUSIONS: Cardiac IRS2 inhibits sympathetic stress-induced AKT/NOS3/CaMKII/RyR2 overactivation and calcium-dependent arrhythmogenesis. This novel IRS2 signaling axis, essential for maintaining cardiac calcium homeostasis under stress, presents a promising target for developing new antiarrhythmic therapies.

Cardiac Arrhythmias and Their Management: An In-Depth Review of Current Practices and Emerging Therapies.

Cardiac arrhythmias encompass a range of conditions characterized by abnormal heart rhythms, affecting millions globally and significantly contributing to morbidity and mortality. This review provides a comprehensive analysis of the current practices and emerging therapies in managing cardiac arrhythmias, covering their definition, classification, epidemiology, and the critical importance of effective management. It explores the pathophysiology underlying various arrhythmias, including the mechanisms of arrhythmogenesis, such as re-entry, automaticity, and triggered activity. The review details the latest diagnostic tools, including ECG, Holter monitoring, and electrophysiological studies, and discusses the clinical presentation of different arrhythmias, from supraventricular to ventricular types and bradyarrhythmias. We examine current pharmacological and non-pharmacological treatment strategies, such as antiarrhythmic drugs, catheter ablation, and device therapy, highlighting their efficacy and limitations. Furthermore, the review delves into emerging therapies, including advanced catheter ablation techniques, novel antiarrhythmic agents, gene therapy, and innovative device technologies like leadless pacemakers and subcutaneous implantable cardioverter-defibrillators (ICDs). Special considerations for managing arrhythmias in diverse populations, including pediatrics, the elderly, and pregnant women, are discussed. Additionally, the review explores future directions in arrhythmia management, emphasizing personalized medicine, artificial intelligence applications, and the integration of advanced technologies in diagnosis and treatment. By synthesizing current knowledge and prospects, this review aims to enhance understanding and promote advancements in the field, ultimately improving patient outcomes with cardiac arrhythmias.

Study on the mechanisms and Pharmacodynamic substances of Lian-Gui-Ning-Xin-Tang on Arrhythmia Therapy based on Pharmacodynamic-Pharmacokinetic associations.

Background: The Chinese herbal compound Lian-Gui-Ning-Xin-Tang (LGNXT), composed of 9 herbs, has a significant antiarrhythmic effect. Previous studies have confirmed that preventing intracellular Ca2+ overload and maintaining intracellular Ca2+ homeostasis may be the important antiarrhythmic mechanisms of LGNXT. Recent studies are focused on elucidating the mechanisms and pharmacodynamic substances of LGNXT. Purpose: 1) To investigate the antiarrhythmic mechanisms of LGNXT; 2) to explore the association of pharmacodynamics (PD) and pharmacokinetics (PK) of the potential pharmacodynamic substances in LGNXT to further verify the mechanisms of action. Methods: First, pharmacodynamic studies were conducted to determine the effect of LGNXT in arrhythmia at the electrophysiological, molecular, and tissue levels, and the "effect-time" relationship of LGNXT was further proposed. Next, an HPLC-MS/MS method was established to identify the "dose-time" relationship of the 9 potential compounds. Combining the "effect-time" and "dose-time" curves, the active ingredients closely related to the inhibition of inflammation, oxidative stress, and energy metabolism were identified to further verify the mechanisms and pharmacodynamic substances of LGNXT. Results: Pretreatment with LGNXT could delay the occurrence of arrhythmias and reduce their duration and severity. LGNXT exerted antiarrhythmic effects by inhibiting MDA, LPO, IL-6, and cAMP; restoring Cx43 coupling function; and upregulating SOD, Ca2+-ATPase, and Na+-K+-ATPase levels. PK-PD association showed that nobiletin, methylophiopogonanone A, trigonelline, cinnamic acid, liquiritin, dehydropolisic acid, berberine, and puerarin were the main pharmacodynamic substances responsible for inhibiting the inflammatory response in arrhythmia. Methylophiopogonanone A, dehydropalingic acid, nobiletin, trigonelline, berberine, and puerarin in LGNXT exerted antiarrhythmic effects by inhibiting oxidative stress. Dehydropalingic acid, berberine, cinnamic acid, liquiritin, puerarin, trigonelline, methylophiopogonanone A, nobiletin, and tetrahydropalmatine exerted antiarrhythmic effects by inhibiting the energy-metabolism process. Conclusions: LGNXT had a positive intervention effect on arrhythmias, especially ventricular tachyarrhythmias, which could inhibit inflammation, oxidative stress, and energy metabolism; positively stabilize the structure, and remodify the function of myocardial cell membranes. Additionally, the PD-PK association study revealed that methylophiopogonanone A, berberine, trigonelline, liquiritin, puerarin, tetrahydropalmatine, nobiletin, dehydropachymic acid, and cinnamic acid directly targeted inflammation, oxidative stress, and energy metabolism, which could be considered the pharmacodynamic substances of LGNXT. Thus, the antiarrhythmic mechanisms of LGNXT were further elucidated.

Brugada Syndrome: Anesthetic Implications in an Incidentally Diagnosed Patient.

Brugada syndrome (BS) is characterized by abnormal repolarization in cardiac cells, occurring in the absence of structural heart disease, which elevates the risk of ventricular arrhythmias and sudden cardiac death. While most BS patients are asymptomatic, a notable percentage experience syncope or sudden cardiac death. Diagnosis is primarily based on electrocardiographic (ECG) findings. A 40-year-old male with a history of syncope and a family history of sudden cardiac death was scheduled for urgent clavicle osteosynthesis. Preoperative ECG revealed type 1 BS. A multidisciplinary approach was taken, and anesthetic management involved combined general and regional anesthesia, utilizing ultrasound-guided clavipectoral and superficial cervical blocks. Postoperative pain was managed with paracetamol and ketorolac. The patient remained stable throughout the procedure, was monitored for 36 hours postoperatively, and was discharged without complications. BS poses significant perioperative risks, necessitating careful anesthetic management. This case report highlights the successful use of combined general and regional anesthesia in a BS patient, contributing to the limited evidence on safe anesthesia practices for this pathology.

Clinical Course and Treatment of Patients With Apical Aneurysms Due to Hypertrophic Cardiomyopathy.

Background: There is controversy about risk of malignant arrhythmias and stroke in patients with apical aneurysms in hypertrophic cardiomyopathy (HCM). Objectives: The aim of this study was to estimate the associations of aneurysm size and major HCM risk factors with the incidence of lethal and potentially lethal arrhythmias and to estimate incidence of unexplained stroke. Methods: In 108 patients (age 57.4 ± 13.5 years, 37% female) from 3 HCM centers, we assessed American Heart Association/American College of Cardiology guidelines risk factors and initial aneurysm size by echocardiography and cardiac magnetic resonance imaging and assessed outcomes after median 5.9 (IQR: 3.7-10.0) years. Results: Implantable cardioverter defibrillator discharges or sudden cardiac death (SCD) occurred in 21 (19.4%) patients. Of patients with a risk factor, 55% subsequently had ventricular tachycardia (VT), ventricular fibrillation (VF), or SCD at follow-up, compared with 10% in those who did not (P < 0.001). The upper tercile of size had a 5-year cumulative risk of 35%, while the lower tercile had 5-year risk of 6% (P = 0.0046). In those with the smallest aneurysms <2 cm2 and also without risk factors VT, VF, or SCD occurred in only 2.5%. Clinical atrial fibrillation (AF) was prevalent, occurring in 49 (45%). Stroke was commonly associated with AF. Stroke without conventional cause had an incidence of 0.5%/year. Surgery in 19% was effective in reducing symptoms. VT ablation and surgery were moderately effective in preventing recurrent VT. Conclusions: Risk factors and aneurysm size were associated with subsequent VT, VF, or SCD. Patients with aneurysms in the lowest tercile of size have a low cumulative 5-year risk. Clinical AF occurred frequently. Stroke prevalence in absence of known stroke etiologies is uncommon and comparable to risk of severe bleeding.

Cardiac implications in myasthenia gravis.

This editorial aimed to consolidate the current evidence in literature on the association between myasthenia gravis (MG) and cardiac involvement, focusing on the impact of thymoma, antistriational antibodies, and late-onset MG. Additionally, the study aimed to explore the influence of genetic differences among populations on the association with cardiac disease. We conducted a review of existing literature in PubMed and Google Scholar to find relevant studies on cardiac involvement in MG. We created search criteria using a combination of free text words, including MG, antistriational antibodies, thymectomy, cardiomyopathy, myocarditis, arrhythmias, autonomic dysfunction. Relevant articles published in English language were analyzed and incorporated. The findings indicate a strong association between thymoma, myasthenic crisis, antistriational antibodies, and late-onset MG with cardiac involvement. The study also revealed that genetic differences among populations influence the risk of cardiac disease and electrocardiography (ECG) abnormalities in MG patients. Autonomic dysfunctions altered cardiac autonomic response and increased susceptibility to arrhythmias and sudden cardiac death in MG patients. The study supports the significance of thymoma, antistriational antibodies, and late-onset MG as key factors associated with cardiac involvement in MG patients. It emphasizes the importance of ECG as the initial test in managing MG patients, particularly in the perioperative period, to identify and genetic testing if needed to address their cardiac risk effectively.

Traumatic Brain Injury is Associated with the Subsequent Risk of Atrial Fibrillation or Atrial Flutter.

BACKGROUND: Traumatic brain injury (TBI) is associated with a variety of adverse long-term outcomes and increases sympathetic nervous system activation which could increase the risk of arrhythmias including atrial fibrillation or atrial flutter (AF/AFL). OBJECTIVE: To examine episodes of TBI and subsequent AF/AFL in a large cohort of post-9/11 Servicemembers and Veterans. METHODS: The variable of interest was TBI, stratified by severity (mild, moderate/severe, and penetrating). The outcome was a subsequent diagnosis of AF/AFL. We used Fine-Gray competing risks models to evaluate the potential risk imparted by TBI on subsequent AF/AL. RESULTS: Among the 1,924,900 subjects included in the analysis, 369,891 (19.2%) experienced an episode of documented TBI. Most were young (63% less than 35 years), male (81.7%) and non-Hispanic White (62.7%). AF/AFL was diagnosed in 22,087 subjects. On univariate analysis, only penetrating TBI (hazard ratio [HR] 2.02, 95% confidence interval [CI] 1.84-2.23; p<0.001) was associated with AF/AFL compared to Veterans without TBI. After adjustment in the full multivariable model (adjusted for age, sex, race and ethnicity, service branch, rank, component, and comorbidities), mild (HR 1.27, 95% CI 1.22-1.32; p<0.001), moderate/severe (HR 1.34, 95% CI 1.24-1.44; p<0.001), and penetrating TBI (HR 1.82, 95% CI 1.65-2.02; p<0.001) were significantly associated with AF/AFL compared to no TBI. Post-hoc analyses demonstrated that the risk of AF/AFL was concentrated in female and younger patients. CONCLUSION: We found that an episode of TBI, particularly penetrating TBI, significantly increased the risk for AF/AFL. Further work is needed to delineate the long-term risk of arrhythmias after TBI.