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Journal articles on the topic 'Atrial fibrillation'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 September 2024

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1

S., Sinha,, Kumari, S., and Mishra, K. "Molecular Docking Study of Crocetin with Interleukin–18 for the Treatment of Atrial Fibrillation." CARDIOMETRY, no. 24 (November 30, 2022): 379–84. http://dx.doi.org/10.18137/cardiometry.2022.24.379384.

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The most frequent arrhythmias are atrial fibrillation. Although the mechanisms underlying are not fully understood, they encompass postoperative and intraoperative phenomena like cardiac ischemia sympathetic activation and inflammation that ends up causing atrial fibrillation. Atrial fibrillation is frequently associated with the presence of pre-existing factors, making the atria susceptible to atrial fibrillation. There are various treatments have been used to manage the condition. However, they are sometimes ineffective, costly, and have side effects stressing the need to explore alternative medicine. The alternative medicine which is now being explored for treating a variety of conditions is primarily involving botanical sources. However, the present research aims at exploring the potential targeting ability of crocetin, a phytochemical from saffron against Interleukin-18 which is an emerging target for atrial fibrillations using a computational approach with Autodock4. The results of the study revealed binding energy of -7.01 Kcal/mol for the most favorable docked confirmation which further suggests the potential of phytocompounds from saffron in treating and managing atrial fibrillation.

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2

Hulsmans, Maarten, Maximilian J. Schloss, I.-Hsiu Lee, Aneesh Bapat, Yoshiko Iwamoto, Claudio Vinegoni, Alexandre Paccalet, et al. "Recruited macrophages elicit atrial fibrillation." Science 381, no. 6654 (July 14, 2023): 231–39. http://dx.doi.org/10.1126/science.abq3061.

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Atrial fibrillation disrupts contraction of the atria, leading to stroke and heart failure. We deciphered how immune and stromal cells contribute to atrial fibrillation. Single-cell transcriptomes from human atria documented inflammatory monocyte and SPP1 + macrophage expansion in atrial fibrillation. Combining hypertension, obesity, and mitral valve regurgitation (HOMER) in mice elicited enlarged, fibrosed, and fibrillation-prone atria. Single-cell transcriptomes from HOMER mouse atria recapitulated cell composition and transcriptome changes observed in patients. Inhibiting monocyte migration reduced arrhythmia in Ccr2 −∕− HOMER mice. Cell-cell interaction analysis identified SPP1 as a pleiotropic signal that promotes atrial fibrillation through cross-talk with local immune and stromal cells. Deleting Spp1 reduced atrial fibrillation in HOMER mice. These results identify SPP1 + macrophages as targets for immunotherapy in atrial fibrillation.

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3

Wu, Shaohui, Guangchen Zou, Xu Liu, Weifeng Jiang, Mu Qin, and Daoliang Zhang. "Key Role of Left Atrial Appendage during Redo Ablation in a Case of Long-Standing Persistent Atrial Fibrillation." Case Reports in Cardiology 2020 (June 19, 2020): 1–4. http://dx.doi.org/10.1155/2020/9691584.

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Extrapulmonary vein focal sources have been recognized as the source of atrial fibrillation in some cases, and empiric electric isolation of the left atrial appendage has been proposed for long-standing persistent atrial fibrillation by some. Here, we present a case of redo ablation of long-standing persistent atrial fibrillation in which the left atrial appendage played a key role in maintaining AF during ablation, and atrial fibrillation was terminated by electrical isolation of the LAA. During the ablation, a rare phenomenon of half of the atria in atrial fibrillation while the other half of the atria in atrial flutter was seen.

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4

Lu, Zhibing, Benjamin J. Scherlag, Jiaxiong Lin, Guodong Niu, Kar-Ming Fung, Lichao Zhao, Muhammad Ghias, et al. "Atrial Fibrillation Begets Atrial Fibrillation." Circulation: Arrhythmia and Electrophysiology 1, no. 3 (August 2008): 184–92. http://dx.doi.org/10.1161/circep.108.784272.

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5

Wijffels, Maurits C. E. F., Charles J. H. J. Kirchhof, Rick Dorland, and Maurits A. Allessie. "Atrial Fibrillation Begets Atrial Fibrillation." Circulation 92, no. 7 (October 1995): 1954–68. http://dx.doi.org/10.1161/01.cir.92.7.1954.

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6

Medeiros de Vasconcelos, J. Tarcísio. "Obesidade e Fibrilação Atrial." Journal of Cardiac Arrhythmias 32, no. 3 (January 17, 2020): 153–54. http://dx.doi.org/10.24207/jca.v32i3.984_pt.

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A fibrilação atrial ocupa uma discussão central hoje no universo das arritmias cardíacas. O aumento da expectativa de vida que trouxe um substancial aumento de sua prevalência na população geral1 implicou em um aprofundamento marcante na compreensão dos seus mecanismos eletrofisiológicos, na identificação de fatores determinantes ou de potencialização da sua ocorrência e obviamente no desenvolvimento de estratégias efetivas de tratamento e de prevenção das suas complicações. Desde o clássico estudo de Wijffels et al., publicado em 1995 (Atrial Fibrillation Begets Atrial Fibrillation)2 demonstrando experimentalmente que frequências atriais artificialmente impostas ao miocárdio atrial implicam em mudanças eletrofisiológicas marcantes determinantes da própria ocorrência da fibrilação atrial, ficou claro que a arritmia uma vez iniciada potencializa a sua própria ocorrência e um processo constante de retroalimentação, cujo desfecho final ao longo do tempo é a instalação da arritmia em uma forma permanente. Contudo para que a fibrilação atrial ocorra é necessária a presença de um ambiente eletrofisiológico adequado, consequente à presença de diversos elementos que agridem o miocárdio atrial sob o aspecto elétrico e estrutural.

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7

Adeyana, Sri, Haryadi Haryadi, and Chandra Wijaya. "Hubungan Kejadian Fibrilasi Atrium dengan Diameter Atrium Kiri pada Fibrilasi Atrium Valvular dan Fibrilasi Atrium Non-Valvular Di RSUD Arifin Achmad." Jurnal Ilmu Kedokteran 11, no. 1 (March 15, 2018): 31. http://dx.doi.org/10.26891/jik.v11i1.2017.31-38.

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Atrial Fibrillationis a kind of arrhythmia which has the most incidence. Based on its Etiology, atrial fibrillationcouldbe divided in to two, valvular and nonvalvular atrial fibrillation. This study was aimed toknow the correlation ofatrial fibrillation incidence between valvular and nonvalvular with its left atrium diameter in Arifin Achmad ProvinsiRiau’s General Hospital. This study was analytical and done by cross sectional approach with 185 patient. The datawere processing with computerize to univariate analysis and chi-square for bivarite analysis. From this study it can beconcluded that the most occurrence of atrial fibrillation was non valvular atrial fibrillation which was 76,8% with theetiology mostly of hypertension which was 41,5%. Valvular atrial fibrillation was mostly caused by mitral stenosiswhich was 37,2% and there were no correlation between the diameter of left atrium to the occurrence of valvular andnon valvular atrial fibrillation (p=0,273.)

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8

Yim, Jeffrey, and Andrew D. Krahn. "Postoperative Atrial Fibrillation Begets Atrial Fibrillation." JACC: Clinical Electrophysiology 10, no. 7 (July 2024): 1720–21. http://dx.doi.org/10.1016/j.jacep.2024.06.009.

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9

Algalarrondo, Vincent, and Fabrice Extramiana. "Autoimmune Atrial Fibrillation or Atrial Fibrillation–Induced Autoimmunity? A New Atrial Fibrillation Begets Atrial Fibrillation Pathway?" Circulation 148, no. 6 (August 8, 2023): 499–501. http://dx.doi.org/10.1161/circulationaha.123.063672.

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10

Opie, Lionel H. "Tedisamil in Coronary Disease: Additional Benefits in the Therapy of Atrial Fibrillation?" Journal of Cardiovascular Pharmacology and Therapeutics 8, no. 1_suppl (March 2003): S33—S37. http://dx.doi.org/10.1177/107424840300800105.

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Atrial fibrillation has recently come into clinical and research focus. In particular, ventricular rate control has been carefully compared with atrial rhythm control. Additionally, the recent discovery of atrial stunning has initiated clinical and research interest in atrial remodeling. Atrial fibrillation is more likely to occur when the atria are damaged by increased fibrosis. The ideal way to prevent atrial fibrillation and the risk of repetition is by tackling the root causes, such as ischemic heart disease, heart failure, and left ventricular hypertrophy. Tedisamil is an unusual antifibrillatory compound that has a novel mechanism of action by inhibiting the transient outward current (Ito) and the repolarizing potassium currents in the sinoatrial node. Tedisamil works acutely against atrial fibrillation. Importantly, atrial fibrillation is often caused by or related to cardiac ischemia, and conversely, ischemia is caused by the increased oxygen demand of atrial fibrillation. Hence, the double properties of tedisamil as a drug that both inhibits atrial fibrillation and acts in an anti-ischemic mode are an attractive basis for future clinical research.

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11

Jandrić-Kočič, Marijana. "The incidence of atrial fibrillation in type 2 diabetes mellitus patients." Sestrinska rec 23, no. 81 (2020): 20–24. http://dx.doi.org/10.5937/sestrec2081020j.

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Goal: Diabetes mellitus type 2 is a metabolic syndrome with systemic disorders of carbohydrate metabolism, fat and protein due to the absolute or relative lack of biologically active insulin. Atrial fibrillation is characterized by high frequency excitation of atria, consequent asynchronous atrial contraction, and irregular ventricular excitation. Diabetes predisposes fibrillation through metabolic abnormalities, structural, electrical, electromechanical, and autonomic remodeling of atrias. The study had to examine the incidence of atrial fibrillation in type 2 diabetes mellitus patients and to investigate the effect of continuous anti-diabetic therapy on the frequency of atrial fibrillation. Materials and methods: The test was conducted from 01. 10. 2017 to 01.01.2019. 106 patients with type 2 diabetes mellitus were evaluated. The data were collected on the basis of history, available medical documentation, laboratory analyzes and electrocardiograms. Data processing is done using standard statistical methods. Results: The survey covered 10 (9%) men and 96 (91%) women. The age of the respondents was 30-44 years (5 subjects, 4.7%), 44-59 years (38 subjects, 35.8%), 60 years and more (63 respondents, 59.5%). The therapeutic modalities included metformin (24 subjects, 22.6%), metformin and insulin (35 subjects, 33%), insulin (8 subjects, 7.5%), metformin and sulfonylurea derivatives (39 subjects, 36.9%). Diabetes in subjects was up to 5 years (8 subjects, 7.5%), 5-10 years (26 subjects, 24.5%), 10-15 years (32 subjects, 30.2%), over 15 years (40 respondents, 37.8% ). A healthy electrocardiogram had 83 (78.3%) subjects, atrial fibrillation 21 (19.8%) subjects, other rhythm disorders 2 (1.9%) subjects. The frequency of fibrillation within the therapeutic modality was: metformin therapy, 1 (4.2%) subjects, metformin and insulin therapy, 9 (25.7%) subjects, insulin therapy, 3 (37.5%) subjects, metformin therapy and sulfonillureas 9 (20.5%) respondents. Conclusion: Type 2 diabetes mellitus patients have high incidence of atrial fibrillation (19.8%). Continuous metformin therapy results in statistically significantly lower incidence of atrial fibrillation compared to other therapeutic modalities (p <0.001). Early detection, metformin administration, and diet regimen can significantly reduce the incidence of atrial fibrillation in patients.

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12

Schotten, Ulrich, Sunniva de Haan, Hans-Ruprecht Neuberger, Sabine Eijsbouts, Yuri Blaauw, Robert Tieleman, and Maurits Allessie. "Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 5 (November 2004): H2324—H2331. http://dx.doi.org/10.1152/ajpheart.00581.2004.

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Atrial fibrillation (AF) induces a progressive dilatation of the atria which in turn might promote the arrhythmia. The mechanism of atrial dilatation during AF is not known. To test the hypothesis that loss of atrial contractile function is a primary cause of atrial dilatation during the first days of AF, eight goats were chronically instrumented with epicardial electrodes, a pressure transducer in the right atrium, and piezoelectric crystals to measure right atrial diameter. AF was induced with the use of repetitive burst pacing. Atrial contractility was assessed during sinus rhythm, atrial pacing (160-, 300-, and 400-ms cycle length), and electrically induced AF. The compliance of the fibrillating right atrium was measured during unloading the atria with diuretics and loading with 1 liter of saline. All measurements were repeated after 6, 12, and 24 h of AF and then once a day during the first 5 days of AF. Recovery of the observed changes after spontaneous cardioversion was also studied. After 5 days of AF, atrial contractility during sinus rhythm or slow atrial pacing was greatly reduced. During rapid pacing (160 ms) or AF, the amplitude of the atrial pressure waves had declined to 20% of control. The compliance of the fibrillating atria increased twofold, whereas the right atrial pressure was unchanged. As a result, the mean right atrial diameter increased by ∼12%. All changes were reversible within 3 days of sinus rhythm. We conclude that atrial dilatation during the first days of AF is due to an increase in atrial compliance caused by loss of atrial contractility during AF. Atrial compliance and size are restored when atrial contractility recovers after cardioversion of AF.

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13

Mazur, Evgeniy S., Vera V. Mazur, Nikolay D. Bazhenov, Sergey V. Kolbasnicov, and Oksana V. Nilova. "Epicardial obesity and atrial fibrillation: emphasis on atrial fat depot." Obesity and metabolism 17, no. 3 (December 6, 2020): 316–25. http://dx.doi.org/10.14341/omet12614.

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The studies, performed with MRI and CT, showed that the increase of fat, immediately adjacent to the myocardium (epicardial fat) is correlated more strongly with the risk of atrial fibrillation than the general or abdominal obesity. According to some studies, epicardial fat around the left atrium is a strong predictor of the development at atrial fibrillation. Also, the amount of the fat is associated with the effectiveness of cardioversion and the risk of developing thromboembolic stroke in patients with atrial fibrillation. The number of such works is small, since tomographic examinations are not needed if intra-atrial thrombosis is suspected, and transthoracic echocardiograthy does not allow visualization of atrial fat. However, transesophageal echocardiography is widely used in patients with atrial fibrillation and allows to measure the structures that serve as depots of epicardial fat, namely the interatrial septum and left lateral ridge. Accumulation of epicardial fat leads to thickening of these structures. This can be used to study the relationship between epicardial obesity and the risk of thromboembolic complications in patients with atrial fibrillations.

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14

Yashin, Sergei, and Yuri Shubik. "Atriopathy and atrial fibrillation. Part I." Vestnik of Saint Petersburg University. Medicine 17, no. 4 (2022): 254–71. http://dx.doi.org/10.21638/spbu11.2022.402.

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Atrial fibrillation is the most common supraventricular tachycardia, the incidence of which increases with age. This arrhythmia is the consequenсe of multiple cardiac and noncardiac pathology. The most significant side effects of atrial fibrillation are thromboembolic complications. It is generally accepted that the source of these embolisms is a thrombus in the left atrial appendage. However, the risk of thromboembolism also occurs after the onset of atrial rhythm, which can lead to a more complex hemostasis mechanism in this disease. There is no unambiguous definition of the relationship between structural and functional changes in the atria and atrial fibrillation, which manifests itself in the appearance of treatment. Essential methods of catheter operations in patients with atrial fibrillation do not take into account the peculiarities of the rhythm mechanism, which has an influence on the treatment’s results. The first part of the review reflects the anatomy, histology, and physiology of atria, their main cellular elements, and electrophysiological features. The main experimental and clinical models of arrhythmia are described; as factors provoking atrial fibrillation and mechanisms of its stabilization. The analysis of electrophysiological and structural remodeling. The concepts of atriopathy and atrial cardiomyopathy are discussed, and classification is given. The mechanisms of hemostasis disorders and possible directions of correction are presented.

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15

Psychari, Stavroula N., Dionysios Tsoukalas, Dimitrios Varvarousis, Anastasios Papaspyropoulos, Eleni Gkika, Athanasios Kotsakis, Ioannis A. Paraskevaidis, and Efstathios K. Iliodromitis. "Opposite relations of epicardial adipose tissue to left atrial size in paroxysmal and permanent atrial fibrillation." SAGE Open Medicine 6 (January 2018): 205031211879990. http://dx.doi.org/10.1177/2050312118799908.

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Objectives: Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation. Methods: This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects. Results: Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness ( b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume ( R = 0.3, p = 0.03), but in the permanent one the relation was inverse ( R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size. Conclusion: Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.

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Carrero, Juan Jesus, Marco Trevisan, Manish M. Sood, Peter Bárány, Hong Xu, Marie Evans, Leif Friberg, and Karolina Szummer. "Incident Atrial Fibrillation and the Risk of Stroke in Adults with Chronic Kidney Disease." Clinical Journal of the American Society of Nephrology 13, no. 9 (July 20, 2018): 1314–20. http://dx.doi.org/10.2215/cjn.04060318.

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Background and objectivesPatients with CKD have a high risk of atrial fibrillation. Both CKD and atrial fibrillation are associated with higher risk of stroke and death. However, the effect of incident atrial fibrillation on stroke risk among patients with CKD is unknown.Design, setting, participants, & measurementsOur study included adults with CKD (eGFR<60 ml/min per 1.73 m2) without previously documented atrial fibrillation who had been in contact with health care in Stockholm, Sweden during 2006–2011. Incident atrial fibrillation was identified by administrative diagnostic codes in outpatient or inpatient care and treated as a time-updated exposure in the analysis of stroke and death risk. Stroke events and deaths were ascertained from regional and national registers with complete coverage. Covariates included demographics, comorbidities, therapeutic procedures, and medications. Multivariable Cox regression analysis and competing risk analysis (accounting for death) were used to estimate the association between incident atrial fibrillation and stroke.ResultsAmong 116,184 adults with CKD, 13,412 (12%) developed clinically recognized atrial fibrillation during a mean follow-up of 3.9 years (interquartile range, 2.3–5.7 years). Incidence of atrial fibrillation increased across lower eGFR strata: from 29.4 to 46.3 atrial fibrillations per 1000 person-years in subjects with eGFR=45–60 and <30 ml/min per 1.73 m2, respectively; 1388 (53.8 per 1000 person-years) cases of stroke and 5592 (205.1 per 1000 person-years) deaths occurred after incident atrial fibrillation compared with 6850 (16.6 per 1000 person-years) cases of stroke and 28,613 (67.5 per 1000 person-years) deaths during periods without atrial fibrillation. After adjustment, incident atrial fibrillation was associated with higher risk of stroke (hazard ratio, 2.00; 95% confidence interval, 1.88 to 2.14) and death (hazard ratio, 1.76; 95% confidence interval, 1.71 to 1.82). This was attributed to both ischemic stroke (hazard ratio, 2.11; 95% confidence interval, 1.96 to 2.28) and intracranial bleeds (hazard ratio, 1.64; 95% confidence interval, 1.42 to 1.90). Stroke risk was similar across all eGFR strata. In competing risk analyses accounting for death, the association between incident atrial fibrillation and stroke was attenuated but remained higher (subhazard ratio, 1.49; 95% confidence interval, 1.39 to 1.60).ConclusionsPatients with CKD who develop atrial fibrillation are at higher risk of stroke and death.

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17

Leistad, E., G. Christensen, and A. Ilebekk. "Effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (April 1, 1993): H1093—H1097. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1093.

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The effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances were examined in two groups of seven barbiturate-anesthetized open-chest pigs. Atrial diameters and pressures were recorded during atrioventricular (AV) pace and thereafter during atrial fibrillation. Both rhythms were studied with constant ventricular rate after complete AV block. Left atrial maximal diameter, which appeared at the end of the atrial filling phase, decreased from 32.4 (28.9-36.7; median and 95% confidence interval) to 31.3 (28.4-35.7) mm after induction of atrial fibrillation. The right atrial maximal diameter also decreased, although not significantly. Atrial pressure at the peak of the v wave rose from 7.0 (5.5-8.5) to 9.6 (8.3-11.2) mmHg in the left atrium and from 5.0 (4.3-5.6) to 7.3 (6.2-8.7) mmHg in the right atrium. Left and right atrial chamber stiffness constants increased from 0.25 (0.19-0.48) to 0.41 (0.28-0.66) mm-1 and from 0.21 (0.11-0.31) to 0.33 (0.30-0.39) mm-1, respectively. Instantaneous diastolic atrial compliance decreased in both atria after induction of atrial fibrillation. Thus, during atrial fibrillation with regular ventricular rate, changes in atrial diameter, pressure, and compliance take place.

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18

Ioannou, Adam. "Atrial Fibrillation with Ventricular Pre-Excitation: A Diagnosis That Must Not Be Missed." Archives of Medical Case Reports and Case Study 5, no. 4 (April 25, 2022): 01–03. http://dx.doi.org/10.31579/2692-9392/106.

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Wolff-Parkinson-White (WPW) syndrome is caused by an accessory pathway that communicates between the atria and ventricles known as the Bundle of Kent. The development of atrial fibrillation, can result in the atrial impulses all being conducted via the accessory pathway and result in a sinister, board complex, irregular tachycardia, with varying QRS morphology (known as pre-excited atrial fibrillation) Adenosine is a potent atrioventricular node blocker, which can be used in the treatment of supraventricular tachycardias, but also has diagnostic utility, particularly in differentiating between supraventricular tachycardia with aberrant conduction (which would often terminate) and a ventricular tachycardia (which would not respond to adenosine). However, the administration of adenosine in pre-excited atrial fibrillation can precipitate 1:1 atrial to ventricular conduction, which can degenerate into life-threatening ventricular arrythmias. This case describes a patient who presented with pre-excited atrial fibrillation and received intravenous adenosine that resulted in development of broad complex tachycardia with haemodynamic compromise. In patients with pre-exited atrial fibrillation, AV nodal blocking agents should be avoided and direct current cardioversion should be utilised.

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19

Aidietis, Audrius, Jūratė Barysienė, Germanas Marinskis, Sigita Aidietienė, Diana Kairevičiūtė, Paulius Jurkuvėnas, Jūratė Aganauskienė, Kęstutis Bagdonas, Vladimiras Ježovas, and Aleksandras Laucevičius. "Factors influencing development of atrial fibrillation after implantation of cardiac pacemaker for sinus node dysfunction." Medicina 45, no. 3 (February 10, 2009): 169. http://dx.doi.org/10.3390/medicina45030022.

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Objective. The aim of this study was to evaluate factors influencing the success of atrial fibrillation treatment associated with the sick sinus syndrome after pacemaker implantation. Methods and results. In 163 patients with sick sinus syndrome followed up after pacemaker implantation, statistical analysis showed that the recurrence of atrial fibrillation increased 2.8 times and 2.5 times when the left atrium or the right atrium, respectively, were increased by 1 cm (P=0.001). In addition, the recurrence of atrial fibrillation increased 2.5 times when the interventricular septum was thickened (P=0.007). Probability of atrial fibrillation recurrence was 2.73 times higher in the presence of grade II mitral regurgitation as compared to absent or grade I mitral regurgitation (P=0.029). The results of atrial fibrillation treatment did not significantly depend on age, gender, duration of atrial fibrillation symptoms, other cardiac structural changes, and concomitant noncardiac diseases. Conclusions. In patients with sick sinus syndrome, the effectiveness of atrial fibrillation treatment after pacemaker implantation is influenced by enlargement of the left and the right atria, increased interventricular septum thickness, and grade II mitral regurgitation. Evaluation of echocardiographic data before pacemaker implantation has prognostic value for determining the probability of maintenance of sinus rhythm.

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20

Cohen, Mitchell I., Jordan A. Cohen, Connor Shope, Lauren Stollar, and Lucas Collazo. "Ivabradine as a stabilising anti-arrhythmic agent for multifocal atrial tachycardia." Cardiology in the Young 30, no. 6 (June 2020): 899–902. http://dx.doi.org/10.1017/s1047951120001195.

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AbstractMultifocal atrial tachycardia has certain electrocardiographic similarities to atrial fibrillation. The mechanism of atrial fibrillation is heterogenous but in some cases may arise from a single ectopic driver with fibrillatory conduction to the rest of the atria. This has led to the speculation that multifocal atrial tachycardia may have a similar mechanistic unifocal site that disperses through the atrium in a fibrillatory pattern. Ivabradine has been reported to be efficacious in an adult with paroxysmal atrial fibrillation as well as in children with junctional or ectopic atrial tachycardias. This is the first report of successfully using ivabradine, a novel anti-arrhythmic If blocking agent, to convert multifocal atrial tachycardia in a 5-month-old critically ill infant to a pattern indicating a single ectopic atrial focus. This allowed the patient’s single atrial focus to be ablated with return to sinus rhythm and decannulation from ventriculoarterial extracorporeal membrane oxygenation. This case suggests that multifocal atrial tachycardia may arise from a single automatic focus with downstream fibrillatory conduction to the atria.

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Sharikov, Nikita L., S. M. Chibisov, O. N. Ragozin, and S. Sh Gasimova. "Variants of the anatomical structure of the coronary arteries and the left atrium remodeling in patients with different forms of atrial fibrillation." Clinical Medicine (Russian Journal) 96, no. 9 (December 30, 2018): 809–13. http://dx.doi.org/10.18821/0023-2149-2018-96-9-809-813.

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One of the reasons leading to dilatation of the left atrium is atrial fibrillation. A retrospective analysis of 136 case histories of patients with various forms of “non-valvular” atrial fibrillation was performed, depending on the shape of atrial fibrillation, the patients were divided into 3 groups. In patients with atrial fibrillation in 62.5%, the source of the atrial branches was the envelope branch of the left coronary artery. Atrial branches originating from the right coronary artery system were identified in 35.8%. In men, atrial arteries occur significantly more often. The results differ from publications, according to which the blood supply of the atria and sinoatrial node from 60 to 75% is carried out by branches departing from the basin of the right coronary artery. The degree of dilatation of the left atrium does not depend on the source of blood supply, but a correlation between the size of the left atrium and the diameter of the branches of the artery of the sinatrial node in the group of patients with paroxysmal atrial fibrillation is traced.

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Fu, Fumin, Michael Pietropaolo, Lei Cui, Shilpa Pandit, Weiyan Li, Oleg Tarnavski, Suraj S. Shetty, et al. "Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models." PLOS ONE 17, no. 1 (January 7, 2022): e0256512. http://dx.doi.org/10.1371/journal.pone.0256512.

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The mouse is a useful preclinical species for evaluating disease etiology due to the availability of a wide variety of genetically modified strains and the ability to perform disease-modifying manipulations. In order to establish an atrial filtration (AF) model in our laboratory, we profiled several commonly used murine AF models. We initially evaluated a pharmacological model of acute carbachol (CCh) treatment plus atrial burst pacing in C57BL/6 mice. In an effort to observe micro-reentrant circuits indicative of authentic AF, we employed optical mapping imaging in isolated mouse hearts. While CCh reduced atrial refractoriness and increased atrial tachyarrhythmia vulnerability, the left atrial (LA) excitation patterns were rather regular without reentrant circuits or wavelets. Therefore, the atrial tachyarrhythmia resembled high frequency atrial flutter, not typical AF per se. We next examined both a chronic angiotensin II (Ang II) infusion model and the surgical model of transverse aortic constriction (TAC), which have both been reported to induce atrial and ventricular structural changes that serve as a substrates for micro-reentrant AF. Although we observed some extent of atrial remodeling such as fibrosis or enlarged LA diameter, burst pacing-induced atrial tachyarrhythmia vulnerability did not differ from control mice in either model. This again suggested that an AF-like pathophysiology is difficult to demonstrate in the mouse. To continue searching for a valid murine AF model, we studied mice with a cardiac-specific deficiency (KO) in liver kinase B1 (Cardiac-LKB1), which has been reported to exhibit spontaneous AF. Indeed, the electrocardiograms (ECG) of conscious Cardiac-LKB1 KO mice exhibited no P waves and had irregular RR intervals, which are characteristics of AF. Histological evaluation of Cardiac-LKB1 KO mice revealed dilated and fibrotic atria, again consistent with AF. However, atrial electrograms and optical mapping revealed that electrical activity was limited to the sino-atrial node area with no electrical conduction into the atrial myocardium beyond. Thus, Cardiac-LKB1 KO mice have severe atrial myopathy or atrial standstill, but not AF. In summary, the atrial tachyarrhythmias we observed in the four murine models were distinct from typical human AF, which often exhibits micro- or macro-reentrant atrial circuits. Our results suggest that the four murine AF models we examined may not reflect human AF well, and raise a cautionary note for use of those murine models to study AF.

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23

Michaud, Gregory F., and William G. Stevenson. "Atrial Fibrillation." New England Journal of Medicine 384, no. 4 (January 28, 2021): 353–61. http://dx.doi.org/10.1056/nejmcp2023658.

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24

Jacek, Grace A. "Atrial Fibrillation." Home Healthcare Now 39, no. 1 (January 2021): 6–12. http://dx.doi.org/10.1097/nhh.0000000000000946.

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25

Elizabeth, Hunt. "Atrial fibrillation." Nursing Standard 27, no. 1 (September 5, 2012): 59–60. http://dx.doi.org/10.7748/ns.27.1.59.s54.

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Stevenson, Rebecca. "Atrial fibrillation." Nursing Standard 27, no. 14 (December 5, 2012): 59–60. http://dx.doi.org/10.7748/ns.27.14.59.s53.

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Lewis, Richard V. "Atrial Fibrillation." Drugs 40, no. 6 (December 1990): 841–53. http://dx.doi.org/10.2165/00003495-199040060-00006.

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Hunt, Elizabeth. "Atrial fibrillation." Nursing Standard 27, no. 1 (September 5, 2012): 59. http://dx.doi.org/10.7748/ns2012.09.27.1.59.c9272.

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Stevenson, Rebecca. "Atrial fibrillation." Nursing Standard 27, no. 14 (December 5, 2012): 59. http://dx.doi.org/10.7748/ns2012.12.27.14.59.c9477.

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Witham, Dawn. "Atrial fibrillation." Nursing Standard 27, no. 32 (April 10, 2013): 59. http://dx.doi.org/10.7748/ns2013.04.27.32.59.s54.

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James, Natalie. "Atrial fibrillation." Nursing Standard 27, no. 46 (July 17, 2013): 59. http://dx.doi.org/10.7748/ns2013.07.27.46.59.s48.

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32

Jolobe, OMP. "Atrial Fibrillation." Journal of the Royal College of Physicians of Edinburgh 30, no. 2 (June 2000): 180. http://dx.doi.org/10.1177/147827150003000221.

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Georgilis, Shenaz, and Carlene Byfield. "Atrial fibrillation." Nursing Made Incredibly Easy! 20, no. 5 (September 2022): 24–31. http://dx.doi.org/10.1097/01.nme.0000853772.24358.53.

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34

Spector, Peter. "Atrial Fibrillation." JACC: Clinical Electrophysiology 8, no. 5 (May 2022): 578–81. http://dx.doi.org/10.1016/j.jacep.2022.04.003.

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35

Callans, David J. "Atrial Fibrillation." Annals of Internal Medicine 149, no. 9 (November 4, 2008): ITC5–1. http://dx.doi.org/10.7326/0003-4819-149-9-200811040-01005.

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Zimetbaum, Peter. "Atrial Fibrillation." Annals of Internal Medicine 153, no. 11 (December 7, 2010): ITC6–1. http://dx.doi.org/10.7326/0003-4819-153-11-201012070-01006.

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37

Medi, Caroline, Graeme J. Hankey, and Saul B. Freedman. "Atrial fibrillation." Medical Journal of Australia 186, no. 4 (February 2007): 197–202. http://dx.doi.org/10.5694/j.1326-5377.2007.tb00862.x.

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38

Erol, Cetin. "Atrial Fibrillation." Anatolian Journal of Cardiology 26, no. 9 (August 31, 2022): 672. http://dx.doi.org/10.5152/anatoljcardiol.2022.9.

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Zimetbaum, Peter. "Atrial Fibrillation." Annals of Internal Medicine 166, no. 5 (March 7, 2017): ITC33. http://dx.doi.org/10.7326/aitc201703070.

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40

Baman, Jayson R., and Rod S. Passman. "Atrial Fibrillation." JAMA 325, no. 21 (June 1, 2021): 2218. http://dx.doi.org/10.1001/jama.2020.23700.

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Riaz, Rehan, Nabeel Ahmad, and Shahid Abbas. "ATRIAL FIBRILLATION;." Professional Medical Journal 24, no. 12 (November 29, 2017): 1852–59. http://dx.doi.org/10.29309/tpmj/2017.24.12.617.

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Introduction: Atrial Fibrillation (AF) is one of the most common arrhythmiaafter coronary artery bypass grafting (CABG). Many risk factors have been identified for thedevelopment of postoperative AF with varied level of evidence. AF is associated with increasedrisk of morbidity and mortality causing prolong hospital stay and utilizing more resources.Our study was aimed to identify high risk population for developing post-operative AF andto draw recommendations for its prevention. Objectives: Our objective was to determine thefrequency of Atrial Fibrillation (AF) and its predisposing factors in patients after Coronary ArteryBypass Grafting (CABG). Setting: The study was conducted at Cardiac Surgery Department /Faisalabad Institute of Cardiology, Faisalabad. Duration of Study: 15-12-2014 to 14-07-2015.Study Design: Cross sectional study. Results: The result showed that out of 130 patientsundergoing CABG surgery, 104 (80.3%) male and 26 (19.7%) females, 9(7%) patients sufferedAF in post-operative phase. A significant association was found between postoperative AF andadvanced age (p = 0.011), obesity (p = 0.028), low EF (p = 0.000), and post-operative useof β-blocker (p = 0.007). Significant difference was found between postoperative AF and daysstayed in hospital (p = 0.000) and magnesium level at first day (p = 0.038). On the other handthere was no significant relationship found between AF and prolongs cross clamp and bypasstime. Conclusion: Advance age, obesity, congestive heart failure, low ejection fraction andwithdrawal from beta blockers in post-operative period have been identified as a significant riskfactors for the development of post-operative atrial fibrillation.

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&NA;. "Atrial fibrillation." Drugs & Therapy Perspectives 6, no. 4 (August 1995): 9–12. http://dx.doi.org/10.2165/00042310-199506040-00004.

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Richardson, Rachael. "Atrial fibrillation." Nursing Standard 26, no. 26 (February 29, 2012): 59. http://dx.doi.org/10.7748/ns2012.02.26.26.59.c8970.

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McCartney, David E., Oliver Lomas, and Thomas J. Cahill. "Atrial fibrillation." InnovAiT: Education and inspiration for general practice 8, no. 8 (July 7, 2014): 485–92. http://dx.doi.org/10.1177/1755738014541425.

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Guha, Kaushik. "Atrial fibrillation." Clinical Medicine 19, no. 1 (January 2019): 90.1–90. http://dx.doi.org/10.7861/clinmedicine.19-1-90.

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Pradip Verma, Kunal, and Michael Wong. "Atrial fibrillation." Australian Journal of General Practice 48, no. 10 (October 1, 2019): 694–99. http://dx.doi.org/10.31128/ajgp-12-18-4787.

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Futterman, Laurie G., and Louis Lemberg. "Atrial Fibrillation." American Journal of Critical Care 14, no. 5 (September 1, 2005): 438–40. http://dx.doi.org/10.4037/ajcc2005.14.5.438.

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Ezekowitz, M. D., and J. A. Levine. "Atrial Fibrillation." Nurse Practitioner 24, no. 11 (November 1999): 108. http://dx.doi.org/10.1097/00006205-199911000-00016.

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LEMERY, ROBERT. "Atrial Fibrillation:." Journal of Cardiovascular Electrophysiology 14, no. 11 (November 2003): 1248–51. http://dx.doi.org/10.1046/j.1540-8167.2003.03283.x.

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Moss, Arthur J. "Atrial Fibrillation." Annals of Noninvasive Electrocardiology 8, no. 1 (January 2003): 1–2. http://dx.doi.org/10.1046/j.1542-474x.2003.08117.x.

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