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.

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.

Radiofrequency Lesion in the Atrial Wall: How Variable Is It? 9.4 Tesla MRI Analysis of Radiofrequency Lesion Volume in a Swine Model.

Background/Objectives: Most data on radiofrequency (RF) effects come from ex vivo or in vitro studies that quantify lesions using width and/or depth, while electrophysiologists use manufacturers' indirect indices. The objective of this study was to evaluate RF lesion volume by high-resolution MRI of excised lesions in an in vivo porcine model, comparing a low-energy long-duration (LE) (20 W, 50 s) RF application strategy with a high-energy short-duration (HE) (50 W, 20 s) one. Methods: Eighteen piglets were divided into LE (n = 9) and HE groups (n = 9). RF applications were performed at four locations in both atria. Animals were sacrificed after 5-7 days, and RF lesion specimens were excised, fixed, and analyzed by 9.4 Tesla MRI. RF lesion volume, variability (variance), depth, and any extracardiac lesions were compared between the groups. Results: Seventy RF applications were performed (36 LE, 34 HE). MRI analyzed 26 LE and 28 HE samples. The HE group showed 35% higher volume than the LE group (100.2 mm3 (±81.2) in LE vs. 178.3 mm3 (±163.7) in HE, p = 0.033). RF volume variance was 6.6 mm3 in LE and 40.3 mm3 in HE. The HE group had more complications (seven vs. zero, p = 0.02) and extracardiac lesions (18 vs. 14, p = 0.613). Conclusions: There was large and unpredictable variability in RF injury on the atrial wall, even under controlled conditions, which could explain arrhythmia recurrences. The greatest lesion variability was found during HE applications. The dose/effect relationship of RF needs careful study for treating cardiac arrhythmias.

A dynamic online nomogram predicting post-traumatic arrhythmias: A retrospective cohort study.

BACKGROUND: A nomogram is a visualized clinical prediction models, which offer a scientific basis for clinical decision-making. There is a lack of reports on its use in predicting the risk of arrhythmias in trauma patients. This study aims to develop and validate a straightforward nomogram for predicting the risk of arrhythmias in trauma patients. METHODS: We retrospectively collected clinical data from 1119 acute trauma patients who were admitted to the Advanced Trauma Center of the Affiliated Hospital of Zunyi Medical University between January 2016 and May 2022. Data recorded included intra-hospital arrhythmia, ICU stay, and total hospitalization duration. Patients were classified into arrhythmia and non-arrhythmia groups. Data was summarized according to the occurrence and prognosis of post-traumatic arrhythmias, and randomly allocated into a training and validation sets at a ratio of 7:3. The nomogram was developed according to independent risk factors identified in the training set. Finally, the predictive performance of the nomogram model was validated. RESULTS: Arrhythmias were observed in 326 (29.1%) of the 1119 patients. Compared to the non-arrhythmia group, patients with arrhythmias had longer ICU and hospital stays and higher in-hospital mortality rates. Significant factors associated with post-traumatic arrhythmias included cardiovascular disease, catecholamine use, glasgow coma scale (GCS) score, abdominal abbreviated injury scale (AIS) score, injury severity score (ISS), blood glucose (GLU) levels, and international normalized ratio (INR). The area under the receiver operating characteristic curve (AUC) values for both the training and validation sets exceeded 0.7, indicating strong discriminatory power. The calibration curve showed good alignment between the predicted and actual probabilities of arrhythmias. Decision curve analysis (DCA) indicated a high net benefit for the model in predicting arrhythmias. The Hosmer-Lemeshow goodness-of-fit test confirmed the model's good fit. CONCLUSION: The nomogram developed in this study is a valuable tool for accurately predicting the risk of post-traumatic arrhythmias, offering a novel approach for physicians to tailor risk assessments to individual patients.

Cardiovascular abnormalities in patients with SHANK3 pathogenic variants: Beyond neurodevelopmental disorders and epilepsy.

Neurodevelopmental disorders have been linked to numerous genes, particularly pathogenic variants in genes encoding postsynaptic scaffolding proteins, like SHANK3. This study aims to provide insights into the cardiovascular profile of patients with pathogenic SHANK3 variants, expanding beyond the well-established associations with neurodevelopmental disorders and epilepsy. We conducted a prospective study involving patients affected by neurodevelopmental disorders with pathogenic SHANK3 variants. Comprehensive cardiovascular assessments were performed and molecular genetic testing included chromosomal microarray followed by clinical exome sequencing. We identified five patients with de novo SHANK3 variants, all of whom exhibited cardiac involvement, including myocardial dysfunction, congenital heart disease (patent ductus arteriosus), and a case of postictal atrial fibrillation. Our findings emphasize an elevated risk of cardiovascular abnormalities in patients with SHANK3 pathogenic variants compared to prior reports. Despite their young age, these patients displayed significant cardiac abnormalities. The study highlights the necessity of integrating cardiac evaluation and ongoing cardiovascular monitoring into multidisciplinary care, facilitating early detection of heart failure and assessment of the risk of sudden unexpected death in epilepsy (SUDEP). Further research is needed to elucidate the underlying mechanisms of cardiac manifestations in SHANK3 mutation carriers.

Mesenchymal Stem Cells Increase Resistance Against Ventricular Arrhythmias Provoked in Rats with Myocardial Infarction.

This study evaluated the role of the mesenchymal stem cells derived from adipose tissue (MSCs) in provoked ventricular arrhythmias (VAs) in animals with myocardial infarction (MI). The experimental groups were: sham, subjected to sham surgery and intramyocardial saline injection; MIV, infarcted rats subjected to intramyocardial saline injection; MI + MSCs, infarcted rats subjected to intramyocardial MSCs injection. Injections were performed two days after infarction and the arrhythmogenic inducibility experiment was performed the next day. Only 35% of the MI + MSCs group developed VAs, while the one in the MIV group was 65%. The proportion of nonsustained ventricular tachycardia, sustained tachycardia, and ventricular fibrillation was similar between the infarcted groups, but MSCs animals had shorter duration of nonsustained ventricular tachycardia. However, MSCs increased connexin 43 content in the remote area, even above the levels found in the sham group. MSCs prevented the increase of IL-1ß in the different areas of the myocardium. There was higher carbonylation and content of 4-hydroxynonenal (4-HNE, a marker of lipoperoxidation) in the myocardium of infarcted rats, but MSCs attenuated the increase of 4-HNE in the infarcted area. In conclusion, MSCs have a protective effect against the development of arrhythmias, but do not imply a significant benefit for animals that have developed VAs. It is possible to think that the cardioprotection of MSCs involves anti-inflammatory/oxidative actions and improvement in the formation of communicating junctions.Graphical abstract.

Pathophysiological correlations between SARS-CoV-2 and arrhythmogenesis: a literature review.

Introduction: SARS-CoV-2 represents one of the most extensively researched pathogens in the last decade due to its major impact on humanity. Not only does this viral infection cause respiratory disturbances, but it also generates cardiovascular injury. Cardiac arrhythmias represent one of the main consequences of SARS-CoV-2 infection, but they can also occur in the context of antiviral treatment. Furthermore, arrhythmias do not always seem to be correlated with the severity of the lung injury. However, they represent a poor prognostic factor in terms of mortality, increasing the need for intensive care and the length of hospitalization. Methods: In accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 Statement, from September 2022 to October 2023, we conducted this study by examining the literature through the PubMed database using the following keywords: COVID-19, cardiac arrhythmias, and, in terms of study design, observational studies. Results: We initially identified 266 studies across PubMed. After applying the inclusion/exclusion criteria, we managed to include 22 studies in our review. Conclusions: Deducing the pathophysiological mechanisms behind SARS-CoV-2's ability to disrupt the electrical activity of the heart, as well as identifying associated risk factors in patients with SARS-CoV-2 infection, could allow targeted therapeutic interventions to decrease the risk of mortality in hospitalized patients.

Novel Sleep Phenotypic Profiles Associated With Incident Atrial Fibrillation in a Large Clinical Cohort.

BACKGROUND: While sleep disorders are implicated in atrial fibrillation (AF), the interplay of physiologic alterations and symptoms remains unclear. Sleep-based phenotypes can account for this complexity and translate to actionable approaches to identify at-risk patients and therapeutic interventions. OBJECTIVES: This study hypothesized discrete phenotypes of symptoms and polysomnography (PSG)-based data differ in relation to incident AF. METHODS: Data from the STARLIT (sleep Signals, Testing, And Reports LInked to patient Traits) registry on Cleveland Clinic patients (≥18 years of age) who underwent PSG from November 27, 2004, to December 30,2015, were retrospectively examined. Phenotypes were identified using latent class analysis of symptoms and PSG-based measures of sleep-disordered breathing and sleep architecture. Phenotypes were included as the primary predictor in a multivariable-adjusted Cox proportional hazard models for incident AF. RESULTS: In our cohort (N = 43,433, age 51.8 ± 14.5 years, 51.9% male, 74.9% White), 7.3% (n = 3,166) had baseline AF. Over a 7.6- ± 3.4-year follow-up period, 8.9% (n = 3,595) developed incident AF. Five phenotypes were identified. The hypoxia subtype (n = 3,245) had 48% increased incident AF (HR: 1.48; 95% CI: 1.34-1.64), the apneas + arousals subtype (n = 4,592) had 22% increased incident AF (HR: 1.22; 95% CI: 1.10-1.35), and the short sleep + nonrapid eye movement subtype (n = 6,126) had 11% increased incident AF (HR: 1.11; 95% CI: 1.01-1.22) compared with long sleep + rapid eye movement (n = 26,809), the reference group. The hypopneas subtype (n = 2,661) did not differ from reference (HR: 0.89; 95% CI: 0.77-1.03). CONCLUSIONS: Consistent with prior evidence supporting hypoxia as an AF driver and cardiac risk of the sleepy phenotype, this constellation of symptoms and physiologic alterations illustrates vulnerability for AF development, providing potential value in enhancing our understanding of integrated sleep-specific symptoms and physiologic risk of atrial arrhythmogenesis.

CaMKIIδ-dependent dysregulation of atrial Na+ homeostasis promotes pro-arrhythmic activity in an obstructive sleep apnea mouse model.

Background: Obstructive sleep apnea (OSA) has been linked to various pathologies, including arrhythmias such as atrial fibrillation. Specific treatment options for OSA are mainly limited to symptomatic approaches. We previously showed that increased production of reactive oxygen species (ROS) stimulates late sodium current through the voltage-dependent Na+ channels via Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ), thereby increasing the propensity for arrhythmias. However, the impact on atrial intracellular Na+ homeostasis has never been demonstrated. Moreover, the patients often exhibit a broad range of comorbidities, making it difficult to ascertain the effects of OSA alone. Objective: We analyzed the effects of OSA on ROS production, cytosolic Na+ level, and rate of spontaneous arrhythmia in atrial cardiomyocytes isolated from an OSA mouse model free from comorbidities. Methods: OSA was induced in C57BL/6 wild-type and CaMKIIδ-knockout mice by polytetrafluorethylene (PTFE) injection into the tongue. After 8 weeks, their atrial cardiomyocytes were analyzed for cytosolic and mitochondrial ROS production via laser-scanning confocal microscopy. Quantifications of the cytosolic Na+ concentration and arrhythmia were performed by epifluorescence microscopy. Results: PTFE treatment resulted in increased cytosolic and mitochondrial ROS production. Importantly, the cytosolic Na+ concentration was dramatically increased at various stimulation frequencies in the PTFE-treated mice, while the CaMKIIδ-knockout mice were protected. Accordingly, the rate of spontaneous Ca2+ release events increased in the wild-type PTFE mice while being impeded in the CaMKIIδ-knockout mice. Conclusion: Atrial Na+ concentration and propensity for spontaneous Ca2+ release events were higher in an OSA mouse model in a CaMKIIδ-dependent manner, which could have therapeutic implications.

In vitro to in vivo extrapolation from 3D hiPSC-derived cardiac microtissues and physiologically based pharmacokinetic modeling to inform next-generation arrhythmia risk assessment.

Proarrhythmic cardiotoxicity remains a substantial barrier to drug development as well as a major global health challenge. In vitro human pluripotent stem cell-based new approach methodologies have been increasingly proposed and employed as alternatives to existing in vitro and in vivo models that do not accurately recapitulate human cardiac electrophysiology or cardiotoxicity risk. In this study, we expanded the capacity of our previously established 3D human cardiac microtissue model to perform quantitative risk assessment by combining it with a physiologically based pharmacokinetic model, allowing a direct comparison of potentially harmful concentrations predicted in vitro to in vivo therapeutic levels. This approach enabled the measurement of concentration responses and margins of exposure for 2 physiologically relevant metrics of proarrhythmic risk (i.e. action potential duration and triangulation assessed by optical mapping) across concentrations spanning 3 orders of magnitude. The combination of both metrics enabled accurate proarrhythmic risk assessment of 4 compounds with a range of known proarrhythmic risk profiles (i.e. quinidine, cisapride, ranolazine, and verapamil) and demonstrated close agreement with their known clinical effects. Action potential triangulation was found to be a more sensitive metric for predicting proarrhythmic risk associated with the primary mechanism of concern for pharmaceutical-induced fatal ventricular arrhythmias, delayed cardiac repolarization due to inhibition of the rapid delayed rectifier potassium channel, or hERG channel. This study advances human-induced pluripotent stem cell-based 3D cardiac tissue models as new approach methodologies that enable in vitro proarrhythmic risk assessment with high precision of quantitative metrics for understanding clinically relevant cardiotoxicity.

Atrial fibrillation and flutter and ocular diseases. The Ural eye and medical study and the Ural very old study.

PURPOSE: To assess associations between atrial fibrillation/atrial flutter (AF) and ocular parameters and diseases. METHODS: The population-based Ural Eye and Medical Study (UEMS) and the Ural Very Old Study (UVOS) included 4894 individuals (age: 40+ years) and 835 individuals (age: 85+ years), respectively. RESULTS: In the UEMS, AF prevalence (80/4894; 1.6%; 95% CI: 1.3, 2.0) increased from 1/1029 (0.1%) in the age group of 40 to <50 years to 29/619 (4.7%) and 12/159 (7.5%) in the age groups of 70 to <80 years and 80+ years, respectively. Higher AF prevalence correlated with older age (OR: 1.08; 95% CI: 1.04, 1.12; p < 0.001), urban region of habitation (OR: 1.08; 95% CI: 1.04, 1.12; p < 0.001), higher prevalence of cardiovascular disease/stroke (OR: 2.50; 95% CI: 1.32, 4.72; p < 0.001) and lower prevalence of neck pain (OR: 0.35; 95% CI: 0.14, 0.85; p = 0.02), higher serum concentration of bilirubin (OR: 1.03; 95% CI: 1.02, 1.05; p < 0.001) and lower prothrombin index (OR: 0.96; 95% CI: 0.93, 0.99; p = 0.003), higher stage of arterial hypertension (OR: 1.52; 95% CI: 1.01, 2.28; p = 0.04) and higher ankle-brachial index (OR: 22.1; 95% CI: 4.45, 1.10; p < 0.001). In that model, AF prevalence was not associated with ocular parameters such as intraocular pressure (p = 0.52), retinal nerve fibre layer thickness (p = 0.70), refractive error (p = 0.13), axial length (p = 0.14), nuclear cataract degree (p = 0.50) and prevalence (p = 0.40), cortical cataract degree (p = 0.43) and presence (p = 0.17), lens pseudoexfoliation (p = 0.58), status after cataract surgery (p = 0.38), age-related macular degeneration prevalence (p = 0.63), open-angle glaucoma presence (p = 0.90) and stage (p = 0.55), angle-closure glaucoma prevalence (p = 0.99) and stage (p = 0.99), diabetic retinopathy prevalence presence (p = 0.37) and stage (p = 0.32), and myopic macular degeneration (p = 0.98). In the UVOS, similar results were obtained. CONCLUSIONS: In these multi-ethnic populations from Russia, AF prevalence was not associated with any major ocular disease and may not play a major role in the pathogenesis of these disorders.

Predictors of Premature Ventricular Contractions Development in Patients With SARS-CoV-2 Infection.

Background: Epidemiological studies have demonstrated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive patients often develop atrial fibrillation, premature ventricular contractions (PVCs), and conduction disorders. The manifestation of ventricular cardiac arrhythmias accentuates the risk of sudden cardiac death. Methods: A retrospective study was conducted on the cohort of 1,614 patients admitted for coronavirus disease 2019 (COVID-19). Patients were categorized into two groups based on the occurrence of PVCs. Group I comprised 172 patients diagnosed with PVCs of Lown-Wolf class II - IV upon hospital admission; group II (control group) consisted of 1,442 patients without this arrhythmia. Each patient underwent comprehensive clinical, laboratory, and instrumental evaluations. Results: The emergence of PVCs in individuals afflicted with COVID-19 was associated with a 5.879-fold heightened risk of lethal outcome, a 2.904-fold elevated risk of acute myocardial infarction, and a 2.437-fold increased risk of pulmonary embolism. Upon application of diagnostic criteria to evaluate the "cytokine storm", it was discovered that the occurrence of the "cytokine storm" was notably more frequent in the group with PVCs, manifesting in six patients (3.5%), compared to 16 patients (1.1%) in the control group (P < 0.05). The mean extent of lung tissue damage in group I was significantly greater than that of patients in group II (P < 0.05). Notably, the average oxygen saturation level, as measured by pulse oximetry upon hospital admission was 92.63±3.84% in group I and 94.20±3.50% in group II (P < 0.05). Conclusions: The presence of PVCs in COVID-19 patients was found to elevate the risk of cardiovascular complications. Significant independent predictors for the development of PVCs in patients with SARS-CoV-2 infection include: age over 60 years (risk ratio (RR): 4.6; confidence interval (CI): 3.2 - 6.5), a history of myocardial infarction (RR: 3.5; CI: 2.6 - 4.6), congestive heart failure (CHF) with reduced left ventricular ejection fraction (RR: 5.5; CI: 3.9 - 7.6), respiratory failure (RR: 2.3; CI: 1.7 - 3.1), and the presence of a "cytokine storm" (RR: 4.5; CI: 2.9 - 6.0).

Simultaneous epicardial ablation based on intraoperative electroanatomic mapping during left ventricular assist device implantation.

Intraoperative ventricular tachycardia (VT) ablation targeting the epicardial substrate using three-dimensional electroanatomic mapping (EAM) was performed during left ventricular assist device (LVAD) implantation. We proved that EAM can be safely performed during LVAD implantation and that an ablation strategy based on electrophysiological information may reduce VT recurrence after LVAD implantation.

Impaired Intracellular Calcium Buffering Contributes to the Arrhythmogenic Substrate in Atrial Myocytes From Patients With Atrial Fibrillation.

BACKGROUND: Alterations in the buffering of intracellular Ca2+, for which myofilament proteins play a key role, have been shown to promote cardiac arrhythmia. It is interesting that although studies report atrial myofibrillar degradation in patients with persistent atrial fibrillation (persAF), the intracellular Ca2+ buffering profile in persAF remains obscure. Therefore, we aimed to investigate the intracellular buffering of Ca2+ and its potential arrhythmogenic role in persAF. METHODS: Transmembrane Ca2+ fluxes (patch-clamp) and intracellular Ca2+ signaling (fluo-3-acetoxymethyl ester) were recorded simultaneously in myocytes from right atrial biopsies of sinus rhythm (Ctrl) and patients with persAF, alongside human atrial subtype induced pluripotent stem cell-derived cardiac myocytes (iPSC-CMs). Protein levels were quantified by immunoblotting of human atrial tissue and induced pluripotent stem cell-derived cardiac myocytes. Mouse whole heart and atrial electrophysiology were measured on a Langendorff system. RESULTS: Cytosolic Ca2+ buffering was decreased in atrial myocytes of patients with persAF because of a depleted amount of Ca2+ buffers. In agreement, protein levels of selected Ca2+ binding myofilament proteins, including cTnC (cardiac troponin C), a major cytosolic Ca2+ buffer, were significantly lower in patients with persAF. Small interfering RNA (siRNA)-mediated knockdown of cTnC (si-cTNC) in atrial iPSC-CM phenocopied the reduced cytosolic Ca2+ buffering observed in persAF. Si-cTnC treated atrial iPSC-CM exhibited a higher predisposition to spontaneous Ca2+ release events and developed action potential alternans at low stimulation frequencies. Last, indirect reduction of cytosolic Ca2+ buffering using blebbistatin in an ex vivo mouse whole heart model increased vulnerability to tachypacing-induced atrial arrhythmia, validating the direct mechanistic link between impaired cytosolic Ca2+ buffering and atrial arrhythmogenesis. CONCLUSIONS: Our findings suggest that loss of myofilament proteins, particularly reduced cTnC protein levels, causes diminished cytosolic Ca2+ buffering in persAF, thereby potentiating the occurrence of spontaneous Ca2+ release events and atrial fibrillation susceptibility. Strategies targeting intracellular buffering may represent a promising therapeutic lead in persAF management.

A Comprehensive Analysis of Conventional Acupuncture and Pharmacological Approaches for Cardiac Arrhythmias: An Umbrella Review.

With a global incidence of approximately 3.4% and an annual mortality rate of 3.7 million, cardiac arrhythmias (CAs) are a pressing global health issue. Their increasing prevalence, especially among older people, is intensifying the challenge for health care systems worldwide. This study aims to compare the safety and effectiveness of acupuncture and pharmacological treatments for CAs, addressing critical gaps in understanding optimal therapeutic approaches. A search of PubMed, EMBASE, and the Cochrane database of systematic reviews was performed to identify data compiled through September 2023 for this umbrella review. Randomized controlled trials (RCTs) as the foundation for meta-analyses and peer-reviewed systematic reviews were the primary focus of the literature search. The Grading of Recommendations Assessment, Development, and Evaluation method was used to assess the overall certainty of the evidence, whereas AMSTAR 2 and the Cochrane Collaboration tool were used to evaluate the quality of the included reviews. Following a comprehensive review, three systematic analyses of 27 RCTs were integrated. Acupuncture led to a slightly greater reduction in the recurrence rate of paroxysmal supraventricular tachycardia (SVT) compared to standard pharmaceutical therapy (risk ratio [RR], 1.06; 95% confidence interval [CI], 0.88-1.27; I2 = 56%; P = .55), although the difference was not statistically significant. In contrast, acupuncture significantly outperformed pharmacological treatment in the context of ventricular premature beats (VPBs) (RR, 1.16; 95 CI, 1.08-1.25; I2 = 0%; P < .0001). The reduction in paroxysmal atrial fibrillation (AF)/atrial flutter was increased with acupuncture, albeit without statistical significance (RR, 1.12; 95% CI, 0.88-1.42; I2 = 0%; P = .36). Acupuncture also led to a greater reduction in heart rate (HR) compared to pharmaceutical treatment despite notable heterogeneity and a lack of statistical significance (mean difference, -1.55; 95% CI, -41.37 to 38.28; I2 = 99%; P = .94). Adverse events were effectively managed, affirming the favorable safety profile of acupuncture. Our study suggests that acupuncture leads to a greater reduction in the recurrence rates of VPBs, AF, and atrial flutter but not significantly so in paroxysmal SVT or post-treatment HR. While promising for specific arrhythmias, the varying effectiveness of acupuncture underscores the need for further research and clinical assessment to determine its precise role and suitability in managing particular cardiac conditions.