scholarly journals Recent Clinical and Experimental Advances in Atrial Fibrillation

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Shigeru Miyagawa ◽  
Taichi Sakaguchi ◽  
Hiroyuki Nishi ◽  
Yasushi Yoshikawa ◽  
Satsuki Fukushima ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Extracellular Matrix ◽  
Structural Changes ◽  
Heart Diseases ◽  
Atrial Remodeling ◽  
Clinical Settings ◽  
Atrial Myocytes ◽  
General Classification ◽  
Surgical Treatments

Atrial fibrillation (AF) is the most common arrhythmia in clinical settings (Fuster et al., 2001), and it is often associated with congestive heart diseases (Issac et al., 2007). Many studies in both laboratory and clinical settings have sought to analyze the mechanisms of AF, develop treatments based on these mechanisms, and examine atrial remodeling in chronic AF. The aim of this paper is to analyze recent findings regarding the atrial remodeling that occurs in AF. In particular, we will describe the electrical and structural changes that involve atrial myocytes and the extracellular matrix. We will also describe the general classification and basic pathophysiology of AF and its surgical treatments.

Abstract 3863: Deletion Of Integrin Alpha7 Leads To Altered Cardiac Conduction And Sudden Death Associated With Connexin43 Downregulation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Raja Nadif ◽  
Michael Emerson ◽  
Ulrike Mayer ◽  
Ludwig Neyses ◽  
Elizabeth Cartwright
Keyword(s):  
Atrial Fibrillation ◽  
Extracellular Matrix ◽  
Ventricular Hypertrophy ◽  
Structural Changes ◽  
Cellular Adhesion ◽  
Left Ventricular ◽  
Cardiac Conduction ◽  
Cardiac Phenotype ◽  
One Year ◽  
Deficient Mice

Effective propagation of the electrical impulse throughout the myocardium is highly dependent on cell-to-cell and cell-to-extracellular matrix interactions. Increasing evidence indicates that dysregulation of cellular adhesion is a critical determinant in the genesis of arrhythmia. Null mutations in the integrin α7 gene, an essential mediator of cellular adhesion in cardiac and skeletal muscles, have been linked to myopathy in humans, however, the in vivo role of the integrin α7 subunit in the heart is undefined. The mouse model of integrin α7 deletion dies prematurely at one year of age. We therefore analysed the cardiac phenotype in integrin α7 deficient mice (α7 −/− ) to determine whether their premature death was associated with altered cardiac conduction. One year old integrin α7 −/− mice exhibited altered cardiac conduction characterised by spontaneous atrial fibrillation and prolonged QTc duration (α7 −/− : 25.7±0.74ms, α7 +/+ : 19.5±0.61ms; n=6; p<0.001, QTc=QT/(RR/100) 1/2 ). The abnormal cardiac conduction was associated with downregulation of connexin43. However, no significant changes were observed in the expression of ion chanels that have been linked to long QT syndrome or atrial fibrillation (kv1.1, kv1.5, kcne1, kcnq1, erg1, Cav1.2 and Cav1.3). In addition, α7 −/− mice displayed increased susceptibility to drug-induced arrhythmias: treatment with ouabain (2mg/kg BW) in combination with isoprenaline (2.5mg/kg BW) induced atrial fibrillation and ventricular tachycardia and eventually death in 6 month-old integrin α7 −/− mice, but not in α7 +/+ mice. Interestingly, α7 −/− also displayed concentric ventricular hypertrophy with increased septal wall thickness and reduced left ventricular end-diastolic diameter starting from 6 months of age. These structural changes were accompanied by an increase in myocyte size and increased ERK1/2 phosphorylation. In conclusion, deletion of the integrin α7 gene in mice leads to ventricular hypertrophy and to abnormal cardiac conduction. The integrin α7 deficient mice have a marked propensity to lethal arrhythmias through alterations in gap junctions but not ion channels. The integrin α7 knockout model provides new insight into the link between the extracellular matrix and cardiac conduction.

Abstract 18601: Impact of Right and Left Atrial Remodeling on Outcomes From Atrial Fibrillation Rotor Ablation

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Amir Schricker ◽  
Tina Baykaner ◽  
Junaid Zaman ◽  
Gautam Lalani ◽  
Kenneth Hopper ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Structural Changes ◽  
Unknown Etiology ◽  
Atrial Remodeling ◽  
Left Atrial Remodeling ◽  
Single Procedure ◽  
Clinical Indices ◽  
The Right

Introduction: Targets for the ablation of atrial fibrillation (AF) are debated. In particular, recent studies questioning fractionated electrograms and lines has increased focus on AF substrates of rotors and focal impulses. These AF sources are seen in both atria, but have unknown etiology. We hypothesized that differential remodeling between the right atrium (RA), whose structural changes are largely undefined, and left atrium (LA) influence the distribution of AF sources and the outcomes from AF source ablation. Methods: In 60 patients at AF ablation (62±10 years, 60% persistent, 5% long-standing persistent), we compared size differences between RA and LA to the number of sources in each chamber and outcomes from AF source-guide ablation. We studied if a 64-pole basket differentially fit the LA or RA, judged by deformation of its splines by the atria (fig. A, B) over multiple cardiac cycles on fluoroscopy. Ablation targeted sources in both atria and was followed by PVI, with follow-up per guidelines. Results: Using baskets in both atria, 205 sources (LA 138; RA 67) were identified and ablated. Notably, the same basket in each patient was dynamically deformed by RA in 51 (85%) of cases but in the LA in only 39 (65%), indicating greater LA remodeling. The number of AF sources was higher in the presence of basket deformation of RA (n=174) than LA (n=130). LA deformation correlated with LVEF (p=0.05). Freedom from AF at 1 year was reduced in patients with no basket deformation (i.e. dilation) in LA (p=0.07) or RA (p=0.06). Notably, single procedure AF freedom was substantially lower in patients with differential remodeling (deformation in only 1 chamber) of 84% vs. 60% (fig C). Conclusions: Structural atrial remodeling influences the number of electrical rotors and focal sources in each chamber. A mismatch between right and left atrial remodeling predicts lower success from rotor ablation. These data also provide novel clinical indices of effective basket positioning.

scholarly journals Echocardiography in Patients with Atrial Fibrillation - What Should the Internist Doctor Know?

2020 ◽  
Vol 17 (4) ◽  
pp. 49-60
Author(s):  
Maria-Luiza Toplicianu-Dimitriu ◽  
Ioan Tiberiu Nanea
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Structural Changes ◽  
Excess Mortality ◽  
Ventricular Dysfunction ◽  
Imaging Technique ◽  
Left Ventricular ◽  
Clinical Impact ◽  
Atrial Remodeling ◽  
Routine Imaging

AbstractAtrial fibrillation (AF) is the most common cardiac arrhythmia, with an increasing prevalence and an enormous clinical impact due to the high stroke rate, left ventricular dysfunction and excess mortality. The occurrence and maintenance of AF is favored by both the degree of left atrial (LA) dilation and the association of fibrotic lesions of the myocardium. The LA is a marker of adverse cardiovascular events in patients with AF. Atrial remodeling can be electrical (shortening atrial refractory), structural (altering geometry and altering collagen content) and contractile (loss of contractility). Cardiac imaging plays a central role in the clinical management of this arrhythmia. Echocardiography represents the routine imaging technique used in patients with AF, with a role in detecting LA dysfunction and cardiac structural changes that predispose to this arrhythmia, also having the ability to predict the maintenance of sinus rhythm after cardioversion and after ablation.

scholarly journals Fibroblast Growth Factor 21 Protects Against Atrial Remodeling via Reducing Oxidative Stress

2021 ◽  
Vol 8 ◽  
Author(s):  
Miao Chen ◽  
Jiawei Zhong ◽  
Zhen Wang ◽  
Hongfei Xu ◽  
Heng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Atrial Remodeling ◽  
Protective Effects ◽  
Fibroblast Growth ◽  
Atrial Myocytes ◽  
Antioxidant Genes

Aim: The structural and electrical changes in the atrium, also known as atrial remodeling, are the main characteristics of atrial fibrillation (AF). Fibroblast growth factor 21 (Fgf21) is an important endocrine factor, which has been shown to play an important role in cardiovascular diseases. However, the effects of Fgf21 on atrial remodeling have not been addressed yet. The purpose of the present study is to evaluate the effects of Fgf21 on atrial remodeling.Methods and Results: Adult mice were treated with Ang II, and randomly administrated with or without Fgf21 for 2 weeks. The susceptibility to AF was assessed by electrical stimulation and optical mapping techniques. Here, we found that Fgf21 administration attenuated the inducibility of atrial fibrillation/atrial tachycardia (AF/AT), improved epicardial conduction velocity in the mice atria. Mechanistically, Fgf21 protected against atrial fibrosis and reduced oxidative stress of the atria. Consistently, in vitro study also demonstrated that Fgf21 blocked the upregulation of collagen by Tgf-β in fibroblasts and attenuated tachypacing-induced oxidative stress including reactive oxygen species (ROS), Tgf-β, and ox-CaMKII in atrial myocytes. We further found that Fgf21 attenuated oxidative stress by inducing antioxidant genes, such as SOD2 and UCP3. Fgf21 also improved tachypacing-induced myofibril degradation, downregulation of L-type calcium channel, and upregulation of p-RyR2, which implicated protective effects of Fgf21 on structural and electrical remodeling in the atria. Moreover, Nrf2 was identified as a downstream of Fgf21 and partly mediated Fgf21-induced antioxidant gene expression in atrial myocytes.Conclusion: Fgf21 administration effectively suppressed atrial remodeling by reducing oxidative stress, which provides a novel therapeutic insight for AF.

scholarly journals Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models

2021 ◽  
Author(s):  
Fumin Fu ◽  
Michael Pietropaolo ◽  
Lei Cui ◽  
Shilpa Pandit ◽  
Weiyan Li ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Structural Changes ◽  
Optical Mapping ◽  
Histological Evaluation ◽  
Atrial Remodeling ◽  
Atrial Tachyarrhythmia ◽  
P Waves ◽  
Disease Etiology ◽  
Preclinical Species ◽  
Liver Kinase B1

AbstractThe 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 better characterize atrial fibrillation (AF), 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-LKB 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 are poor representations of human AF, and raise a cautionary note about the use of any murine model to study AF.

scholarly journals Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0256512
Author(s):  
Fumin Fu ◽  
Michael Pietropaolo ◽  
Lei Cui ◽  
Shilpa Pandit ◽  
Weiyan Li ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Structural Changes ◽  
Optical Mapping ◽  
Histological Evaluation ◽  
Atrial Remodeling ◽  
Murine Models ◽  
Atrial Tachyarrhythmia ◽  
P Waves ◽  
Disease Etiology ◽  
Preclinical Species

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.

scholarly journals Echocardiography-derived total atrial conduction time (PA-TDI duration): risk stratification and guidance in atrial fibrillation management

2021 ◽  
Author(s):  
Patrick Müller ◽  
Bob Weijs ◽  
Nadine M. A. A. Bemelmans ◽  
Andreas Mügge ◽  
Lars Eckardt ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cardiac Imaging ◽  
Structural Changes ◽  
Clinical Care ◽  
Imaging Modalities ◽  
Atrial Remodeling ◽  
Conduction Time ◽  
Cardiovascular Morbidity And Mortality ◽  
Atrial Conduction Time ◽  
Patients At Risk

AbstractAtrial fibrillation (AF) is a major cause of cardiovascular morbidity and mortality. To early detect and to avoid AF-related complications, several cardiac imaging modalities and approaches aim to quantify the severity of the underlying atrial cardiomyopathy (i.e., the extent of atrial remodeling). However, most established cardiac imaging modalities just incorporate single components of atrial remodeling and do not reflect the complete multifactorial process, which may contribute to their limited predictive value. Echocardiography-derived PA-TDI duration is a sophisticated echocardiographic parameter to assess total atrial conduction time and directly reflects both electrical and structural changes to the atria. Therefore, PA-TDI duration provides a more comprehensive quantification of the extent of atrial remodeling than other imaging modalities. In this article we review the role of PA-TDI duration as a marker of atrial remodeling and summarize the available data on PA-TDI duration to identify patients at risk for AF, as well as to guide AF management. Moreover, we discuss how to assess PA-TDI duration and provide recommendations on the implementation of PA-TDI duration into routine clinical care. Graphic abstract

HEART COMPLICATIONS IN HYPERTHYROIDISM

2011 ◽  
pp. 7-17
Author(s):  
Hai Thuy Nguyen ◽  
Anh Vu Nguyen
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Diseases ◽  
Systolic Dysfunction ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Cardiac Complications ◽  
Cardiac Symptoms

Thyroid hormone increases the force of the contraction and the amount of the heart muscle oxygen demand. It also increases the heart rate. Due to these reasons, the work of the heart is greatly increased in hyperthyroidism. Hyperthyroidism increases the amount of nitric oxide in the intima, lead them to be dilated and become less stiff. Cardiac symptoms can be seen in anybody with hyperthyroidism, but can be particularly dangerous in whom have underlying heart diseases. Common symptoms include: tachycardia and palpitations. Occult hyperthyroidism is a common cause of an increased heart rate at rest and with mild exertion. Hyperthyroidism can also produce a host of other arrhythmias such as PVCs, ventricular tachycardia and especially atrial fibrillation. Left ventricular diastolic dysfunction and systolic dysfunction, Mitral regurgitation and mitral valve prolapsed are heart complications of hyperthyroism could be detected by echocardiography. The forceful cardiac contraction increases the systolic blood pressure despite the increased relaxation in the blood vessels reduces the diastolic blood pressure. Atrial fibrillation, atrial enlargement and congestive heart failure are important cardiac complications of hyperthyroidism. An increased risks of stroke is common in patients with atrial fibrillation. Graves disease is linked to autoimmune complications, such as cardiac valve involvement, pulmonary arterial hypertension and specific cardiomyopathy. Worsening angina: Patients with coronary artery disease often experience a marked worsening in symptoms with hyperthyroidism. These can include an increase in chest pain (angina) or even a heart attack.

Sign in / Sign up

Export Citation Format

Share Document