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Journal articles on the topic 'Arrhythmic syndrome'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 July 2025

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1

van Bavel, Joanne J. A., Henriëtte D. M. Beekman, Agnieszka Smoczyńska, Marcel A. G. van der Heyden, and Marc A. Vos. "IKs Activator ML277 Mildly Affects Repolarization and Arrhythmic Outcome in the CAVB Dog Model." Biomedicines 11, no. 4 (2023): 1147. http://dx.doi.org/10.3390/biomedicines11041147.

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Long QT syndrome type 1 with affected IKs is associated with a high risk for developing Torsade de Pointes (TdP) arrhythmias and eventually sudden cardiac death. Therefore, it is of high interest to explore drugs that target IKs as antiarrhythmics. We examined the antiarrhythmic effect of IKs channel activator ML277 in the chronic atrioventricular block (CAVB) dog model. TdP arrhythmia sensitivity was tested in anesthetized mongrel dogs (n = 7) with CAVB in series: (1) induction experiment at 4 ± 2 weeks CAVB: TdP arrhythmias were induced with our standardized protocol using dofetilide (0.025

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Eremeev, A. "Atrial extrasystoles associated with hypervitaminosis D3 (clinical case)." Vrach 35, no. 4 (2024): 52–56. http://dx.doi.org/10.29296/25877305-2024-04-10.

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The article discusses a clinical case of a patient with hypervitaminosis D3. Cholecalciferol intoxication occurred against the background of long-term oral use of vitamin complexes and was manifested by the manifestation of arrhythmic syndrome – frequent atrial extrasystole of the “P on T” type. The probable pathogenetic cause of arrhythmia was a violation of ion homeostasis in the form of hypercalcemia. Calcium imbalance, affecting cardiac conduction and automatism, can provoke cardiac arrhythmias by increasing the dispersion of refractoriness. At the electrophysiological level, the cause of

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Agarwal, Nitin, Payodh Chaudhary, Malini Kulshrestha, and RR Chaudhary. "Brugada Syndrome: Killer Genetic Heart Disorder." International Journal of Advanced and Integrated Medical Sciences 1, no. 4 (2016): 186–87. http://dx.doi.org/10.5005/jp-journals-10050-10058.

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ABSTRACT Brugada syndrome is a rare inherited arrhythmic disorder, which predisposes to ventricular arrhythmia that is responsible for sudden and unexpected nocturnal death syndrome. How to cite this article Chaudhary P, Agarwal N, Kulshrestha M, Chaudhary RR. Brugada Syndrome: Killer Genetic Heart Disorder. Int J Adv Integ Med Sci 2016; 1(4):186-187.

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Balasundaram, Lakshmi, Bharatraj Kidambi, and Surya Singaravelu. "Thorough QT/QTc (TQT) study." International Journal of Basic & Clinical Pharmacology 10, no. 8 (2021): 1019. http://dx.doi.org/10.18203/2319-2003.ijbcp20212933.

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With a number of drugs entering the market, cardiac safety remains a cause of major concern for the regulatory authorities, before approval. The incidence of drug induced arrhythmia with non-cardiovascular drugs is low, however the result is fatal, hence much focus is being given to assess the pro-arrhythmic potential of a drug. The arrhythmogenic risk of the drug is higher if the patient is on polypharmacy or has other risk factors such as an electrolyte imbalance or an underlying structural heart disease. QT prolongation can be either due to congenital causes such as Long QT syndromes (LQTS)

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Asatryan, Babken, Marina Rieder, Alessandro Castiglione, and Katja E. Odening. "Arrhythmic risk during pregnancy and postpartum in patients with long QT syndrome." Herzschrittmachertherapie + Elektrophysiologie 32, no. 2 (2021): 180–85. http://dx.doi.org/10.1007/s00399-021-00757-4.

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AbstractCongenital long QT syndrome (LQTS) is a genetic disorder characterized by a prolonged QT interval in the surface electrocardiogram (ECG) that predisposes affected individuals to arrhythmic syncope, ventricular torsades-de-pointes, and sudden cardiac death at a young age. Investigations of large patient cohorts revealed sex-related differences in the LQTS phenotype. Adult women with LQTS are at higher risk for cardiac arrhythmias than are adult men with LQTS. Sex hormones are thought to play the primary role for these gender differences. Clinical experience and translational studies ind

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Probst, Vincent, Stéphanie Chatel, Jean-Baptiste Gourraud, and Hervé Le Marec. "Risk Stratification and Therapeutic Approach in Brugada Syndrome." Arrhythmia & Electrophysiology Review 1 (2012): 17. http://dx.doi.org/10.15420/aer.2012.1.17.

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Brugada syndrome (BrS) is a clinical entity characterised by an incomplete right bundle branch block associated with an ST segment elevation in the right precordial leads and a risk of ventricular arrhythmia and sudden death in the absence of structural abnormalities. Patients with a personal history of sudden death have an annual arrhythmia risk of recurrence as high as 10 %. Similarly, the presence of syncope is consistently associated with an increased arrhythmic risk. This risk can be estimated at about 1.5 % per year. The risk is lower in asymptomatic patients. Regarding the relatively hi

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Koplan, B. A., and W. G. Stevenson. "Sudden arrhythmic death syndrome." Heart 93, no. 5 (2007): 547–48. http://dx.doi.org/10.1136/hrt.2006.108134.

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8

Alharbi, Mishari, Islam Ibrahim, Sultan Alzahrani, et al. "Lifestyle Modification and Medical Treatment of Long QT Syndrome." JOURNAL OF HEALTHCARE SCIENCES 04, no. 05 (2024): 195–200. http://dx.doi.org/10.52533/johs.2024.40501.

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Long QT Syndrome (LQTS) is a genetic or acquired cardiac disorder characterized by a prolonged QT interval on an electrocardiogram, predisposing individuals to life-threatening arrhythmias and sudden cardiac death. Management of LQTS involves both lifestyle modifications and pharmacological treatments to mitigate risks and enhance patient outcomes. Lifestyle interventions include avoiding strenuous physical activities, especially swimming, and managing emotional stress to prevent arrhythmic triggers. Dietary modifications, such as maintaining adequate levels of potassium and magnesium, are ess

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De Nigris, Angelica, Angela Pepe, Giangiacomo Di Nardo, et al. "Brugada Pattern in a Child with Severe SARS-CoV-2 Related Multisystem Inflammatory Syndrome." Pediatric Reports 13, no. 3 (2021): 504–10. http://dx.doi.org/10.3390/pediatric13030058.

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This report presents the first case of Brugada pattern complicated by a supraventricular arrhythmia in a child with SARS-CoV-2 related Multisystem Inflammatory Syndrome in Children (MIS-C). A 7-year-old boy came to our Emergency Department with 7 days of abdominal pain and fever. MIS-C was diagnosed on the basis of the clinical, laboratory and instrumental tests. On admission, ECG showed type 1 Brugada pattern in the right precordial leads. During hospitalization the onset of supraventricular arrhythmias complicated the clinical picture. This case underlines management complexity of supraventr

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Vásquez, Javier Pinos, Tiago Luiz Luz Leiria, Marcelo Lapa Kruse, and Gustavo Glotz de Lima. "Early Repolarization Pattern and Idiopatic Sustained Monomorphic Ventricular Tachycardia: an Infrequent Combination." Journal of Cardiac Arrhythmias, no. 2 (May 22, 2021): 57–62. http://dx.doi.org/10.24207/jca.v34i2.3443.

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Malignant early repolarization as cause of sudden death has taken on great importance in recent years. It has been described as an entity capable of producing ventricular arrhythmic events, causing from episodes of syncope to sudden cardiac death. Ventricular fibrillation is the typical arrhythmia in these patients, with no clear relationship to date with idiopathic monomorphic ventricular tachycardia. Electrocardiographic markers related to the development of arrhythmic events in early repolarization syndrome have been described. They seem not only related to the development of ventricular fi

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Drakopoulou, Maria, Heba Nashat, Aleksander Kempny, et al. "Arrhythmias in adult patients with congenital heart disease and pulmonary arterial hypertension." Heart 104, no. 23 (2018): 1963–69. http://dx.doi.org/10.1136/heartjnl-2017-312881.

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ObjectivesApproximately 5%–10% of adults with congenital heart disease (CHD) develop pulmonary arterial hypertension (PAH), which affects life expectancy and quality of life. Arrhythmias are common among these patients, but their incidence and impact on outcome remains uncertain.MethodsAll adult patients with PAH associated with CHD (PAH-CHD) seen in a tertiary centre between 2007 and 2015 were followed for new-onset atrial or ventricular arrhythmia. Clinical variables associated with arrhythmia and their relation to mortality were assessed using Cox analysis.ResultsA total of 310 patients (me

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Ataíde Silva, Rita, Ana R Sousa, Maria Salomé Leal de Carvalho, and Rui Anjos. "Congenital long QT syndrome presenting as unexplained bradycardia." BMJ Case Reports 15, no. 3 (2022): e242362. http://dx.doi.org/10.1136/bcr-2021-242362.

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Congenital long QT syndrome (LQTS) is a genetically autosomal heterogeneous disorder of the ion channels and causes about 10% of sudden death infant syndrome in newborns. Its estimated prevalence is approximately 1 in 2500, probably underestimated because of its clinical heterogenicity. Few cases of neonatal LQTS have been reported. In 4% of them, life-threatening arrhythmic events can be the first manifestation of LQTS. The authors report two cases of neonatal LQTS with heterogeneous genetic mutations. Both manifested by bradycardia, one since fetal life. One case had serious arrhythmias duri

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Padeletti, Luigi, Lisa Innocenti, Alessandro Paoletti Perini, and Edoardo Gronda. "Arrhythmic complication in cardiorenal syndrome." Heart Failure Reviews 16, no. 6 (2010): 569–73. http://dx.doi.org/10.1007/s10741-010-9210-6.

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14

Scacchi, Simone, Luca F. Pavarino, Andrea Mazzanti, Alessandro Trancuccio, Silvia G. Priori, and Piero Colli Franzone. "Transmural APD heterogeneity determines ventricular arrhythmogenesis in LQT8 syndrome: Insights from Bidomain computational modeling." PLOS ONE 19, no. 7 (2024): e0305248. http://dx.doi.org/10.1371/journal.pone.0305248.

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Long QT Syndrome type 8 (LQT8) is a cardiac arrhythmic disorder associated with Timothy Syndrome, stemming from mutations in the CACNA1C gene, particularly the G406R mutation. While prior studies hint at CACNA1C mutations’ role in ventricular arrhythmia genesis, the mechanisms, especially in G406R presence, are not fully understood. This computational study explores how the G406R mutation, causing increased transmural dispersion of repolarization, induces and sustains reentrant ventricular arrhythmias. Using three-dimensional numerical simulations on an idealized left-ventricular model, integr

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15

Forleo, C., M. Carella, P. Basile, et al. "C70 WEARABLE CARDIOVERTER DEFIBRILLATOR IN LONG QT SYNDROME DURING PREGNANCY: TIME TO USE THE SHIELD." European Heart Journal Supplements 25, Supplement_D (2023): D29—D30. http://dx.doi.org/10.1093/eurheartjsupp/suad111.069.

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Abstract Introduction Long QT Syndrome (LQTS) is a rare cardiac channelopathy characterized by a high risk of lethal arrhythmias. Pregnancy and post–partum period may induce an increased vulnerability, so an appropriate prevention is needed. Case presentation A 31–year–old primigravid woman at 36 weeks of pregnancy was referred to our Cardiomyopathy Unit located in a tertiary centre for LQTS screening. The patient had a family history of LQTS (mother and brother) and Brugada syndrome (cousin). The 12–lead ECG (Figure 1) showed a long QT interval (QT corrected: 508 msec), while the transthoraci

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Obeyesekere, Manoj N., and Andrew D. Krahn. "Early Repolarisation – What Should the Clinician Do?" Arrhythmia & Electrophysiology Review 04, no. 2 (2015): 96. http://dx.doi.org/10.15420/aer.2015.04.02.96.

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The early repolarisation (ER) pattern is a common ECG finding. Most individuals with the ER pattern are at minimal risk for arrhythmic events. In others, ER increases the arrhythmic risk of underlying cardiac pathology. Rarely ER syndrome will manifest as a primary arrhythmogenic disorder causing ventricular fibrillation (VF). ER syndrome is defined as syncope attributed to ventricular arrhythmias or cardiac arrest attributed to ER following systematic exclusion of other etiologies. Some ECG features associated with ER portend a higher risk. However, clinically useful risk-stratifying tools to

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Chen, Xinguang, Hongyan Zhao, Ling Sun, Wenwu Zhu, and Fengxiang Zhang. "Electrocardiogram Characteristics and Arrhythmic Events during Fever in Patients with Fever-Induced Brugada Syndrome." Cardiology 145, no. 3 (2020): 130–35. http://dx.doi.org/10.1159/000505642.

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Introduction: Changes in electrocardiogram (ECG) parameters and the incidence of arrhythmic events in patients with fever-induced Brugada syndrome (BrS) remain unknown. Objective: We aimed to investigate the effect of hyperthermia on the ECG pattern and the occurrence of fever-triggered arrhythmic events (FTAEs) in patients with fever-induced BrS. Methods: We retrospectively analyzed a series of fever-induced BrS cases from January 1966 to November 2018. Clinical characteristics and ECG parameters were evaluated in the presence or absence of fever. Results: Syncope and implantable cardioverter

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Giuranna, M., M. Freschini, F. Notaristefano, et al. "STELLATE GANGLION BLOCK: CLINICAL MONITORING AFTER INJECTION." European Heart Journal Supplements 26, Supplement_2 (2024): ii54. http://dx.doi.org/10.1093/eurheartjsupp/suae036.120.

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Abstract 70–year–old man with chronic coronaric syndrome (CABG x 6 in 2006) and HFrEF. ICD implant in primary prevention in 2011. He was admitted for arrhythmic storms refractory to IV lidocaine therapy. Following sedation with midazolam, a left stellate ganglion block was performed using the ultrasound–guided lateral approach, injecting 200 mg of Lidocaine and 200 mg of Mepivacaine. After a few minutes, there was the appearance of anisocoria, different thermotouch in the upper limbs, ptosis, dysphonia, as an effect of local anesthetics on the sympathetic nervous system fibers and on the recur

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Nechaeva, G. I., A. N. Dakuko, E. N. Loginova, and I. V. Bogatyrev. "Structural features of the heart in children with arrhythmic syndrome due to nonspecific connective tissue disorder." Meditsinskiy sovet = Medical Council, no. 17 (November 1, 2023): 204–13. http://dx.doi.org/10.21518/ms2023-359.

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Introduction. Connective tissue is highly organized system, its disorders are characterized by a pronounced polymorphism of morphological and clinical manifestations. The cardiovascular pathology in patients with nonspecific connective tissue disorder attracts attention due to the high risk of complications: rhythm and conduction disorders, infective endocarditis, vascular thromboembolism and sudden cardiac death. Therefore, it’s very important to use up-to-date equipment and methods of early diagnosis of a high risk of fatal events in young.Aim. To investigate the structural features of the h

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Mahmoodi, Ehsan, and Haris M. Haqqani. "Arrhythmic Mitral Valve Prolapse Syndrome and Ventricular Arrhythmias: A Comprehensive Review and the Role of Catheter Ablation." Journal of Cardiovascular Development and Disease 11, no. 7 (2024): 218. http://dx.doi.org/10.3390/jcdd11070218.

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Mitral valve prolapse (MVP) affects 2–3% of the general population, and despite its benign prognosis overall, it is associated with sudden death in a small subset of patients. The term “arrhythmic MVP syndrome” (AMVPS) refers to the presence of frequent or complex ventricular arrhythmias, commonly reported in female patients with a stereotypical phenotype including bileaflet myxomatous disease, ECG repolarisation abnormalities in inferior leads, mitral annular disjunction, and significant fibrosis in the inferolateral LV and papillary muscles. Modern imaging technologies have led to the identi

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Camkiran, Volkan, Ozge Ozden, and Ilyas Atar. "Long-term follow-up of patients with Brugada syndrome: Foremost risk factors associated with overall arrhythmic events." Medicine 103, no. 18 (2024): e37990. http://dx.doi.org/10.1097/md.0000000000037990.

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Brugada syndrome (BS) is characterized by ST segment elevation in right precordial leads (V1–V3), ventricular tachycardia (VT), ventricular fibrillation (VF), and sudden cardiac death (SCD) in individuals without structural heart disease. The aim of this study is to contribute to the controversial issue of finding the most valuable marker that can predict poor prognosis during follow-up in patients with a diagnosis of BS. A total of 68 patients diagnosed with BS or had Brugada-type ECG change between January 1997 and July 2012 at the Department of Cardiology of Başkent University Faculty of Me

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Duzhyi, I. D., V. Ya Pak, A. D. Klochko, L. A. Bondarenko, and R. Z. Elastal. "Peculiarities of the Development of Frederick’s Syndrome as a Marker of the Severe Course of Coronavirus Disease." Tuberculosis, Lung Diseases, HIV Infection, no. 2 (May 29, 2025): 64–69. https://doi.org/10.30978/tb2025-2-64.

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Frederick’s syndrome is a rare arrhythmic disease of the cardiac conduction system that affects the development or progression of ischemic changes in the myocardium (tissue hypoxemia of cardiomyocytes) caused by hypoxia. Coronavirus infection, affecting the lung parenchyma, leads to respiratory failure, which creates ideal conditions for the clinical manifestations of this complication, the most serious of which is Morgagni—Adams—Stokes syndrome. The latter syndrome is considered an indication for urgent implantation of a pacemaker, which may be impossible in severe oxygen-dependent patients.

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Jennings, K. "Sudden cardiac death." Journal of the Royal College of Physicians of Edinburgh 36, no. 2 (2006): 117–19. https://doi.org/10.1177/1478271520063602007.

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The majority of the approximately 100,000 sudden cardiac deaths each year in the UK are associated with coronary heart disease, but most sudden deaths in those under 30 years of age are caused by inherited cardiomyopathies and arrhythmias. In those aged 16–64 years, a coroner's post mortem examination is unable to identify a structural cardiac abnormality in 4·0%. The cause of death is therefore uncertain. These deaths are termed ‘sudden arrhythmic death syndrome’ or ‘sudden unexpected death syndrome’.

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Yuan, David, and Hariharan Raju. "Spotlight on sudden arrhythmic death syndrome." Research Reports in Clinical Cardiology Volume 10 (September 2019): 57–66. http://dx.doi.org/10.2147/rrcc.s187480.

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Dejgaard, Lars A., Eystein T. Skjølsvik, Øyvind H. Lie, et al. "The Mitral Annulus Disjunction Arrhythmic Syndrome." Journal of the American College of Cardiology 72, no. 14 (2018): 1600–1609. http://dx.doi.org/10.1016/j.jacc.2018.07.070.

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Wenzelburger, Frauke Wilma Gisela, Axel Poesch, Alexander Bleckmann, and Burghard Schumacher. "Fokus: Mitral Annulus Disjunction Arrhythmic Syndrome." Aktuelle Kardiologie 9, no. 06 (2020): 556–61. http://dx.doi.org/10.1055/a-1293-6775.

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ZusammenfassungAls „Mitral annular Disjunction“ (MAD) bezeichnet man eine pathologische, umschriebene, bindegewebige Dehiszenz zwischen dem kompakten Myokard des linken Ventrikels und dem Mitralklappenanulus. Das Bindegewebe ersetzt anulusnah das Myokard und strahlt in unregelmäßiger Form in die benachbarte Muskulatur des linken Ventrikels ein. Die MAD tritt oft in Verbindung mit einem Mitralklappenprolaps (MVP) auf. Die inhomogene Fibrosierung des klappennahen Myokards sowie eingelagerte und versprengte Purkinje-Fasern bilden ein arrhythmogenes Substrat. Die MAD wird deshalb gehäuft bei Patie

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Wu, Katherine C., and Ilan S. Wittstein. "Ventricular Arrhythmic Risk in Takotsubo Syndrome." JACC: Clinical Electrophysiology 8, no. 12 (2022): 1511–14. http://dx.doi.org/10.1016/j.jacep.2022.10.009.

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Golukhova, E. Z., O. I. Gromova, R. A. Shomahov, N. I. Bulaeva, and L. A. Bockeria. "Monogenec Arrhythmic Syndromes: From Molecular and Genetic Aspects to Bedside." Acta Naturae 8, no. 2 (2016): 62–74. http://dx.doi.org/10.32607/20758251-2016-8-2-62-74.

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The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called sudden cardiac death (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to

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Ker, J., L. Du Toit-Prinsloo, W. F. P. Van Heerden, and G. Saayman. "Sudden Infant Death Syndrome and Left Ventricular Hypertrabeculation-Hidden Arrhythmogenic Entity?" Clinical Medicine Insights: Cardiology 4 (January 2010): CMC.S5933. http://dx.doi.org/10.4137/cmc.s5933.

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Left ventricular noncompaction/hypertrabeculation is a condition which is characterized by a highly trabeculated, “spongy” myocardium. It can present at any age with heart failure, arrhythmia and/or thromboembolic events. A wide variety of mutations have been found to be a cause of hypertrabeculation and it is possible that there is a continuum of hypertrophic cardiomyopathy, dilated cardiomyopathy and hypertrabeculation/noncompaction. We present a case of left ventricular hypertrabeculation which presented as sudden infant death syndrome and we propose that this entity may be a hidden cause o

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Porta-Sánchez, Andreu, Andrea Mazzanti, Carmen Tarifa, et al. "Unexpected impairment of INa current underpins reentrant arrhythmias in a knock-in swine model of Timothy syndrome." Nature Cardiovascular Research 2, no. 12 (2023): 1291–309. http://dx.doi.org/10.1038/s44161-023-00393-w.

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AbstractTimothy syndrome 1 (TS1) is a multi-organ form of long QT syndrome associated with life-threatening cardiac arrhythmias, the organ-level dynamics of which remain unclear. In this study, we developed and characterized a novel porcine model of TS1 carrying the causative p.Gly406Arg mutation in CACNA1C, known to impair CaV1.2 channel inactivation. Our model fully recapitulated the human disease with prolonged QT interval and arrhythmic mortality. Electroanatomical mapping revealed the presence of a functional substrate vulnerable to reentry, stemming from an unforeseen constitutional slow

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Batchvarov, Velislav N. "The Brugada Syndrome – Diagnosis, Clinical Implications and Risk Stratification." European Cardiology Review 9, no. 2 (2014): 82. http://dx.doi.org/10.15420/ecr.2014.9.2.82.

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The Brugada syndrome (BrS) is a hereditary arrhythmic syndrome manifesting as syncope or sudden cardiac death (SCD) in individuals without overt structural heart disease. Currently, its diagnosis is mainly based on the presence of a spontaneous or Na+-channel blocker induced so-called “type 1” Brugada electrocardiographic (ECG) pattern typically seen in leads V1 and V2 recorded from the 4th to 2nd intercostal spaces. Presently the main unresolved clinical problem in the BrS is the identification of patients at high risk of SCD who need implantable cardioverter-defibrillator (ICD). Current guid

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Muscogiuri, Giuseppe, Andrea Igoren Guaricci, Nicola Soldato, et al. "Multimodality Imaging of Sudden Cardiac Death and Acute Complications in Acute Coronary Syndrome." Journal of Clinical Medicine 11, no. 19 (2022): 5663. http://dx.doi.org/10.3390/jcm11195663.

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Sudden cardiac death (SCD) is a potentially fatal event usually caused by a cardiac arrhythmia, which is often the result of coronary artery disease (CAD). Up to 80% of patients suffering from SCD have concomitant CAD. Arrhythmic complications may occur in patients with acute coronary syndrome (ACS) before admission, during revascularization procedures, and in hospital intensive care monitoring. In addition, about 20% of patients who survive cardiac arrest develop a transmural myocardial infarction (MI). Prevention of ACS can be evaluated in selected patients using cardiac computed tomography

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T. V. Naluzhna. "Drug correction of cardiac arrhythmias in patients with сoronary heart disease combined with mitral valve prolapse syndrome". Bukovinian Medical Herald 17, № 2 (66) (2013): 94–96. http://dx.doi.org/10.24061/2413-0737.xvii.2.66.2013.74.

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The paper presents data of cardiac arrhythmias in patients with coronary heart disease combined with the mitral valve prolapse syndrome. In these patients were dominated Sinus tachycardia, atrioventricular extrasystole, atrial fibrillation, paroxysmal tachycardia predominated in such patients. It has been proposed to include to the basic therapy these patients such preparations of magnesium, in particular, a domestic preparation – Rythmocor, taking into account the principal mechanisms of the development of arrhythmias. The antiarrhythmic, antiischemic, membranostabilizing action of the drug h

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HINCH, ROBERT. "MODELING OF WOLFF–PARKINSON–WHITE SYNDROME." International Journal of Bifurcation and Chaos 13, no. 12 (2003): 3827–34. http://dx.doi.org/10.1142/s0218127403008922.

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Wolff–Parkinson–White syndrome is a disease where an arrhythmia is caused by the ventricles being electrically excited by an additional accessory pathway that links the atria to the ventricles. The spread of the activation wave from this pathway to the ventricles is modeled using a simplified model of Hodgkin–Huxley sodium channel kinetics, in a two ion-channel model. The model is investigated both analytically (using an asymptotic analysis) and numerically, and both methods are shown to give the same result. It is found that for a given width of the accessory pathway, there is a critical sodi

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Baghel, Anita, Manoj Kumar, J. P. Soni, Mudit Agarwal, and Ravi Kumar. "Experience with Holter monitoring for evaluation of infant arrhythmia." International Journal of Contemporary Pediatrics 6, no. 3 (2019): 1362. http://dx.doi.org/10.18203/2349-3291.ijcp20192044.

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Background: Arrhythmia is defined as abnormal heart rates. Sometimes they are intermittent and difficult to diagnose on routine ECG. Neonatologist and Pediatrician needs to rapidly establish accurate diagnosis and management for infants suspected to have arrhythmia. Hence Holter monitoring of the infants presenting with symptoms suggestive of arrhythmia is necessary as it provides a continuous record of heart’s electrical activity. The aim of this paper is to find out the role of continuous ambulatory electrocardiographic monitoring in daily clinical practice of Pediatrics.Methods: All infants

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Borile, Giulia, Tania Zaglia, Stephan E. Lehnart, and Marco Mongillo. "Multiphoton Imaging of Ca2+ Instability in Acute Myocardial Slices from a RyR2R2474S Murine Model of Catecholaminergic Polymorphic Ventricular Tachycardia." Journal of Clinical Medicine 10, no. 13 (2021): 2821. http://dx.doi.org/10.3390/jcm10132821.

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Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a familial stress-induced arrhythmia syndrome, mostly caused by mutations in Ryanodine receptor 2 (RyR2), the sarcoplasmic reticulum (SR) Ca2+ release channel in cardiomyocytes. Pathogenetic mutations lead to gain of function in the channel, causing arrhythmias by promoting diastolic spontaneous Ca2+ release (SCR) from the SR and delayed afterdepolarizations. While the study of Ca2+ dynamics in single cells from murine CPVT models has increased our understanding of the disease pathogenesis, questions remain on the mechanisms trigg

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Calvelli, Pierangelo, Natascia Cerrato, Carla Giustetto, Andrea Saglietto, Matteo Anselmino, and Antonio Curcio. "Which Brugada patient deserves continuous ECG monitoring through implantable loop recorder? An evidence update." Journal of Cardiovascular Medicine 26, no. 2 (2024): 64–71. https://doi.org/10.2459/jcm.0000000000001696.

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Brugada syndrome (BrS) is a genetic condition that increases the risk of life-threatening arrhythmias, which can result in sudden cardiac death (SCD). Implantable loop recorders (ILRs) have become a key tool in managing patients with unexplained syncope, and guidelines advise their use in individuals with recurrent, unexplained syncope or palpitations. However, the role of ILRs in inherited arrhythmic conditions like BrS remains a topic of debate. Most patients newly diagnosed with BrS show no symptoms, but around 30% may experience symptoms such as syncope or palpitations, which can arise fro

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ROBERTS, JASON D., and MICHAEL H. GOLLOB. "Early Repolarization: A Rare Primary Arrhythmic Syndrome and Common Modifier of Arrhythmic Risk." Journal of Cardiovascular Electrophysiology 24, no. 7 (2013): 837–43. http://dx.doi.org/10.1111/jce.12156.

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Kaufman, Elizabeth S. "Arrhythmic risk in congenital long QT syndrome." Journal of Electrocardiology 44, no. 6 (2011): 645–49. http://dx.doi.org/10.1016/j.jelectrocard.2011.07.023.

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Loginova, Loginova E. N., Nechaeva G. I. Nechaeva, Dakuko A. N. Dakuko, Bogatyrev I V. Bogatyrev I, Potapov V. V. Potapov, and Kirichenko N. A. Kirichenko. "Arrhythmic syndrome of undifferentiated connective tissue dysplasia." Therapy 9_2023 (December 25, 2023): 150–56. http://dx.doi.org/10.18565/therapy.2023.9.150-156.

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Massara, M., M. Casella, and A. Dello Russo. "BRUGADA SYNDROME: NEWEST DATA ON RISK STRATIFICATION." European Heart Journal Supplements 26, Supplement_2 (2024): ii71—ii72. http://dx.doi.org/10.1093/eurheartjsupp/suae036.165.

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Abstract Background Brugada Syndrome (BrS) is a rare genetically based channelopathy responsible for malignant arrhythmias and sudden cardiac death (SCD) in young adults. Objectives The aims was to evaluate prognostic indicators useful for accurate arrhythmic risk stratification in BrS by studying genetic, clinical, anamnestic, instrumental parameters, and those derived from electrophysiological study (EPS) and intracavitary mapping. Materials and Methods 209 patients with Brugada type 1 were recruited between 01/01/2018 and 01/10/2023. Results In the first study, predictive factors related to

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Sicouri, Serge, and Charles Antzelevitch. "Mechanisms Underlying the Actions of Antidepressant and Antipsychotic Drugs That Cause Sudden Cardiac Arrest." Arrhythmia & Electrophysiology Review 7, no. 3 (2018): 199. http://dx.doi.org/10.15420/aer.2018.29.2.

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A number of antipsychotic and antidepressant drugs are known to increase the risk of ventricular arrhythmias and sudden cardiac death. Based largely on a concern over the development of life-threatening arrhythmias, a number of antipsychotic drugs have been temporarily or permanently withdrawn from the market or their use restricted. While many antidepressants and antipsychotics have been linked to QT prolongation and the development of torsade de pointes arrhythmias, some have been associated with a Brugada syndrome phenotype and the development of polymorphic ventricular arrhythmias. This ar

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Tian, Chao, Na An, Mengchen Yuan, et al. "A Pooled Analysis of the Prognostic Significance of Brugada Syndrome with Atrial Fibrillation." Current Pharmaceutical Design 26, no. 1 (2020): 129–37. http://dx.doi.org/10.2174/1381612826666200114112029.

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Background: Guidelines have previously suggested that atrial fibrillation (AF) is associated with an increased risk of arrhythmic death in Brugada syndrome (BrS) patients. However, only two articles consisting of 17 AF patients with BrS supported these views. The risk stratification of BrS patients with AF remains controversial. Thus, a meta-analysis is used to estimate the risk stratification of BrS patients with AF. Methods: We searched for relevant studies published from 2000 to December 30, 2018. A total of 1712 patients with BrS from five studies were included: 200 patients (12%) were rep

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Badiuk, N. V. "Influence of arrhythmogenic activity on postinfarction heart remodeling at comorbid hypertension and diabetes mellitus." Clinical Endocrinology and Endocrine Surgery, no. 1 (April 6, 2022): 42–48. http://dx.doi.org/10.30978/cees-2022-1-42.

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Objective — to evaluate the morpho-functional features of heart remodeling in the acute period of myocardial infarction complicated by arrhythmias against the background of arterial hypertension and diabetes mellitus. Materials and methods. The study included 149 patients with acute myocardial infarction. Depending on the comorbid pathology, patients are divided into 3 groups. Myocardial arrhythmic activity was assessed by clinical examinations, ECG and Holter ECG monitoring. Results. The effects of hypertension duration (15.31 ± 0.94 years at average) on the formation of hypertrop

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Gass, Matthias, Christian Apitz, Schahriar Salehi-Gilani, Gerhard Ziemer, and Michael Hofbeck. "Use of the implantable loop recorder in children and adolescents." Cardiology in the Young 16, no. 6 (2006): 572–78. http://dx.doi.org/10.1017/s1047951106001156.

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Introduction: Recurrent but infrequent syncopes represent a diagnostic challenge, since they frequently remain unexplained despite extensive investigations. This applies specifically for patients who carry an increased risk of potentially lifethreatening arrhythmias, either due to congenital cardiac disease or primary electrical disorders. Implantable loop recorders permit long-term electrocardiographic monitoring. Experience with these devices is still limited in children. Patients and methods: Between January 1999 and August 2005, 12 patients underwent implantation of a loop recorder in our

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Chuprova, Svetlana N., and Irina Yu Melnikova. "Long <i>QT</i> Syndrome in Young Athletes." Cardiac Arrhythmias 3, no. 1 (2023): 41–48. http://dx.doi.org/10.17816/cardar321415.

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Long QT syndrome is a disease associated with a high risk of sudden cardiac (arrhythmic) death. The frequency of sudden cardiac death is approximately 1: 100,000 young athletes, while autopsies often do not detect changes, which indicates a primary arrhythmogenic death. The article describes two clinical cases of young athletes with prolongation of the QT interval. The possible causes of the long QT syndrome and the difficulties of diagnosing this syndrome in children and adolescents involved in sports are discussed. Regardless of the reasons leading to the prolongation of the QT interval, the

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Boidin, Maxime, Mathieu Gayda, Christine Henri, et al. "Effects of interval training on risk markers for arrhythmic death: a randomized controlled trial." Clinical Rehabilitation 33, no. 8 (2019): 1320–30. http://dx.doi.org/10.1177/0269215519840388.

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Objective: To compare the effects of high-intensity interval training versus moderate-intensity continuous training on risk markers of arrhythmic death in patients who recently suffered from an acute coronary syndrome. Design: Double-blind (patient and evaluator) randomized controlled trial. Setting: Cardiovascular Prevention and Rehabilitation Centre (EPIC Centre) of the Montreal Heart Institute, Montreal, Canada. Subjects: A total of 43 patients were randomized following an acute coronary syndrome. Interventions: Patients were assigned to either high-intensity interval training (n = 18) or i

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Jakovac, Hrvoje, Antun Ferenčić, Christophe Stemberger, Bojana Mohar Vitezić, and Dražen Cuculić. "Detection of SARS-CoV-2 Antigens in the AV-Node of a Cardiac Conduction System—A Case Report." Tropical Medicine and Infectious Disease 7, no. 3 (2022): 43. http://dx.doi.org/10.3390/tropicalmed7030043.

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Mounting evidence indicates that new arrhythmic events frequently occur during and after coronavirus disease (COVID-19), posing additional mortality risk in older-aged and critically ill patients. However, the underlying mechanisms and cardio pathological substrates of COVID-related arrhythmias have not been clarified yet. Here, we report findings of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigens and genes in the atrioventricular node (AV-node) of a cardiac conduction system, pointing to its direct infection as a possible arrhythmogenic factor.

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Harkness, Weston, Paula Watts, Michael Kopstein, Oliwier Dziadkowiec, Gregory Hicks, and Dmitriy Scherbak. "Correcting Hypokalemia in Hospitalized Patients Does Not Decrease Risk of Cardiac Arrhythmias." Advances in Medicine 2019 (September 24, 2019): 1–4. http://dx.doi.org/10.1155/2019/4919707.

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Background. It is currently standard practice to correct hypokalemia for the purpose of preventing cardiac arrhythmias in all hospitalized patients. However, the efficacy of this intervention has never been previously studied. Objective. The objective of our study was to evaluate whether patients without acute coronary syndrome or history of arrhythmias were at increased risk of clinically significant cardiac arrhythmias if their potassium level was not corrected to ≥3.5 mEq/L. Design. A retrospective case control study. Setting. A community hospital. Participants. We enrolled selected patient

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Michowitz, Yoav, Anat Milman, Georgia Sarquella-Brugada, et al. "Fever-related arrhythmic events in the multicenter Survey on Arrhythmic Events in Brugada Syndrome." Heart Rhythm 15, no. 9 (2018): 1394–401. http://dx.doi.org/10.1016/j.hrthm.2018.04.007.

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