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 Table of Contents  
REVIEW ARTICLE
Year : 2019  |  Volume : 4  |  Issue : 2  |  Page : 43-47

Atrial fibrillation, what exactly do we know? (English version)


Department of Cardiology, Renmin Hospital of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, Hubei Province, China

Date of Submission25-Mar-2020
Date of Acceptance25-Apr-2020
Date of Web Publication15-Jun-2020

Correspondence Address:
Dr. Congxin Huang
Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan 430060, Hubei Province; Cardiovascular Research Institute, Wuhan University, Jiefang Road 238, Wuhan 430060, Hubei Province; Hubei Key Laboratory of Cardiology, Jiefang Road 238, Wuhan 430060, Hubei Province
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJHR.IJHR_4_20

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  Abstract 

Trigger and reentry are the main mechanisms of atrial fibrillation (AF), but underlying diseases and causes may provide necessary conditions for trigger and reentry, which suggests the importance of primary prevention. For the treatment of AF itself, we should pay more attention to the methods of ablation to improve the long-term success rate. In addition, we should pay close attention to the stroke prevention by anticoagulation and left atrial appendage occlusion, to reduce the incidence of embolism events. This article reviews basic and clinical studies of AF over the past century.

Keywords: Anticoagulation, atrial arrhythmia, atrial fibrillation, radiofrequency ablation


How to cite this article:
Huang C. Atrial fibrillation, what exactly do we know? (English version). Int J Heart Rhythm 2019;4:43-7

How to cite this URL:
Huang C. Atrial fibrillation, what exactly do we know? (English version). Int J Heart Rhythm [serial online] 2019 [cited 2020 Sep 27];4:43-7. Available from: http://www.ijhronline.org/text.asp?2019/4/2/43/286766

This manuscript is an English version based on Huang C. Atrial fibrillation, what exactly do we know? Chin J Cardiac Arrhyth 2020;24(1):5-9. DOI: 10.3760/cma. j. issn.1007-6638.2020.01.002. The second publication of this manuscript has obtained the permission from Chinese Journal of Cardiac Arrhythmias.


  Introduction Top


Atrial fibrillation (AF) is a rapid atrial arrhythmia, with an age -adjusted prevalence of 0.65%. The prevalence rate increases by age, and up to 7.5% in patients older than 80 years.[1] AF may decrease the quality of life, even cause disability and death.[2],[3],[4],[5] The study of the pathogenesis of AF and the exploration of treatment has gone through a difficult process in the past century.[6],[7],[8],[9],[10],[11] We retrieved 78,634 relevant English literature in the PubMed database using the keywords “AF” [Table 1], and 36,947 and 25,524 Chinese literature in WanFang and CNKI databases, respectively, with the keyword “AF” [Table 2]. It is not difficult to find that the relevant studies on AF has become prevalent since the 1990s, which brings endless results and provides researches basis understanding the cause of AF and the selection of prevention and treatment strategy. This article reviews the advances in studies of AF over the past century.
Table 1: Number of articles included using keywords “atrial/auricularfibrillation”in the PubMed database

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Table 2: Number of articles included using the keyword “ atrial/auricularfibrillation”in WanFang and CNKI databases

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  Mechanisms Top


The description of AF may date back to the 3rd century BCE. Shuhe Wang, a Chinese physician, who wrote the Maijing (The Pulse Classics), in which he described the similar pulse as AF “on the left wrist, the pulse surges at high-low unbalance… on the right wrist, the pulse weakens at low-high irregularity.”

Professor Willian Stokes also described the irregular pulse condition in 1854.[12] In 1907, Mackenzie recorded simultaneous tracings of jugular and radial pulses in a patient that had a continuing irregular pulse, and one can see that there are absent a-waves.[13] It was not until Einthoven invented the electrocardiograph in 1903, the true AF wave was recorded in 1906.[14]

The earliest research on the mechanism of AF was reported by Garrey.[15] He applied faradic current to the tip of the auricle appendix until there were sustained fibrillatory contractions. He then separated the appendix from the fibrillating auricles. The auricle fibrillation stopped, while the AF continued to fibrillate. Based on the result, Garrey speculated that there needed to be a critical tissue mass to AF to continue.

Lewis[16],[17] attempted to explain the mechanism of AF after making a number of important observations in patients with AF. He described AF as “different form and sustained vibrations from the atrium,” and then he further stated that AF affects the whole atrium surface with the excitation wave or its offshoots, and it has a varying path of excitation. So, he thought reentry might be the potential mechanism.

However, Scherf et al.[18] did not agree with the speculation. He injected aconitine into the canine atria, and this led to rapid excitation with the appearance of AF. When the temperature of this area was decreased, AF stopped and restarted after the temperature increased. He then concluded that AF was caused by a rapid stimulus rather than reentry. He stated that “as the impulses move into the larger mass of auricular muscle, islands of refractory tissue appear, which cause a weaving and interweaving of the contraction process that is characteristic of fibrillation.” Thus, the subsequent possible reentry waves of excitation are not the cause of the arrhythmia but were a concomitant feature of AF, which was called “heterotopic pacing point trigger theory.”

Moe and Abildskov[19] used rapid atrial pacing and vagal stimulation to induce sustained AF in dogs. He found that when AF occurs, the auricle is clamped and AF stops, while the atrium continues to fibrillate. He stated that “the grossly irregular wavefront becomes randomly wandering wavelets and coexist.” He believed that multiple wavelet hypothesis for AF and reentry constituted the major pathogenesis.

In 1998, Haïssaguerre et al.[20] reported that the pulmonary vein foci as a trigger for AF. It is a milestone in the history of AF mechanism study and has an extremely important theoretical contribution and practical guidance value. Haïssaguerre and his team open a new door for AF treatment. The result also enlightened some domestic scholars to conduct relevant studies on the relationship between the cardiac vein (including pulmonary vein, vena cava, cardiac vein, and marshall ligament) and the occurrence of AF.[21] The results indicate that there are muscle sleeves in the cardiac vein and pacemaker cells in the sleeve. Under certain conditions, these pacemaker cells can spontaneously drive AF.

In 1998, Skanes et al.[22] reported that there were relatively stable rotation sites around the anatomical or functional block area. They are the source of fibrillatory wavefronts. Such wavefronts can collide/fuse and exhibit rotational activation within a variable and often small spatial domain. If multiple rotors are present simultaneously, distal wavefronts collide at varying locations, also contributing to the appearance of global disorganization. It was known as the “rotor” theory. After that Narayan et al.[23] found that rotor ablation based on circumferential pulmonary vein ablation (CPVA) could improve the success rate of operation. According to the results, Narayan believed that “rotor” was the main mechanism of AF. Single or small numbers of localized rotors might underlie AF has important therapeutic implications, particularly for AF ablation.

Undoubtedly, AF is probably the most complex arrhythmia. Trigger and reentry are the key mechanisms. However, certain conditions are required for trigger and reentry to cause AF, such as atrial remodeling, neural remodeling, electrical remodeling, and any other underlying diseases. At present, the consensus is that paroxysmal AF is mainly caused by pulmonary vein trigger, whereas other types of AF involve multiple factors other than pulmonary vein trigger. In addition to pulmonary vein triggering, other types of AF involve multiple factors. However, there is no one theory that can fully explain the causes of all types of AF, which is the difficulty in the clinical prevention and treatment of AF.


  Clinical Prevention and Therapy Top


The key to the prevention and treatment of AF is to convert AF to sinus rhythm and reduce the risk of complications to the largest extent.[24],[25],[26]

In 1962, Lown et al.[27] reported the first successful conversion to sinus rhythm in patients by synchronous direct current defibrillation. This routine is considered for patients with AF and a life-saving effect for them. However, AF may occur again for different reasons after conversion. Therefore, this method is often used to terminate life-threatening or unstable tachycardic arrhythmia (unstable ventricular and supraventricular rhythms) in patients with unstable hemodynamics.

The cardioversion has another advantage since the subsequent heart failure also could find in patients with AF. Phillips and Levine[28] noted that quinidine can restore AF to sinus, and then improve the state of the heart function. After then, Selzer and Wray[29] observed that quinidine can induce torsade de pointes and cause quinidine syncope syndrome. Therefore, neither domestic nor foreign guidelines recommend the usage of quinidine for cardioversion now. The current guideline has recommended several drugs for cardioversion,[30] such as flecainide, amiodarone, propafenone, ibutilide, nifekalant, and dofetilide. Unfortunately, neither the success rate of conversion nor the duration of sinus rhythm is satisfactory.

For some researchers, patients would have better outcomes in sinus rhythm compared with AF. However, the AFFIRM study shows that there appeared to be no difference in mortality or stroke risk regardless of whether one chose a rhythm or rate control strategy.[31] Although the result seems puzzling, it reminds the clinician could choose rate control for symptom relief in appropriate patients first if it is not achieved with cardioversion to sinus rhythm easily. Moreover, according to the results from the RACE II study,[32] the guideline usually recommends a lenient rate-control strategy (resting heart rate <110 beats/min).[30]

The initial nonpharmacologic treatment for AF was catheter ablation. In 1998, Haïssaguerre et al.[20] reported that radiofrequency catheter ablation could be a treatment for paroxysmal AF originating from the pulmonary vein. After 8-month follow-up, 62% of patients had no recurrence of AF. It was a preeminence result that marked the prospect of transcatheter ablation in AF. In 2000, Haïssaguerre et al.[33] reported pulmonary vein isolation used in paroxysmal AF. After 4 months of follow-up, 73% of patients remained sinus rhythm. This showed that pulmonary vein isolation had an advantage when compared with the pulmonary vein trigger. After that Oral et al.[34] successfully applied CPVA to chronic AF. As a cornerstone, CPVA is widely recognized as surgery to ablate any type of AF.

To improve the success rate (especially persistent AF), Zimmerman et al.[35] proposed adjunctive complete vagal denervation during CPVA; Nademanee et al.[36] added fragmentation potential ablation; Willems et al.[37] and Verma et al.[38] added matrix ablation; and Narayan et al.[23] added rotor ablation, ablation diameter, and nonpulmonary vein trigger ablation. Undoubtedly, these combined operations improve the success rate to some extent. On this basis, new ablation energy, the new catheter, and the new mapping system provide support for increasing the success rate. The data from China AF center indicate that the immediate success rate of catheter ablation of AF is 95%. After 1-year follow-up, 79.5% maintain sinus rhythm, heart remodeling, and function improve. Obviously, the outcomes of catheter ablation are much better than drug treatment. Therefore, the guideline recommends catheter ablation as the primary treatment of paroxysmal AF. Because the method of ablation of AF is various, “standardization” seems to be an important issue.

Thromboembolic disease is a serious complication of AF.[39],[40],[41] Although not aimed at AF itself, the strategy and treatment of this complication are of great significance. It has been suggested that standardized anticoagulation can effectively prevent thromboembolism. The guideline suggests that CHA2 DS2-VASc should be applied to evaluate the risk of thromboembolism of patients with AF. For example, a male with a score ≥2 or a female with a score ≥3 should receive a long-term anticoagulation therapy. Warfarin and novel oral anticoagulants can be selected as anticoagulants. The international standardized ratio should be monitored and controlled between 2.0 and 3.0 when using warfarin, while the later should monitor the function of the liver and kidney.[30] The positive effect of novel oral anticoagulants is noninferior to warfarin, while the negative effect is lower than warfarin. At present, medical staffs and patients have formed a standardized “anticoagulation concept.” The data analysis of China AF center indicates that the anticoagulation rate in AF patients with anticoagulation indications has reached 56.4%.

Another strategy to prevent thromboembolism in patients with nonvalvular AF is percutaneous left atrial appendage closure (LAAC), which is based on the results of the study of Al-Saady et al.[42] For nonvalvular AF, 90% of thrombus originate from the left atrial appendage, while only 60% in valvular AF. This means LAAC can avoid 90% embolism risk in nonvalvular AF patients. After a 5-year follow-up, the results found that the clinical effect of LAAC is not inferior to warfarin.[43] Huang et al.[44] found LAmbre device could reduce the incidence of stroke by 80%. The data analysis from China AF center indicated that the success rate of LAAC operation is 96.7%, 1.3% of residual shunt and low complication. After 1-year follow-up, LAAC induces only 0.2% of ischemic stroke and no hemorrhagic stroke; it may also improve heart remodeling and function.

The treatment of AF itself and the treatment of its complications are developing rapidly and improving in good quality. However, it should be noted that there are many shortcomings in drug treatments. It is urgent to study new drugs with strong positive effect and low negative effect. Although there are many highlights in interventional therapy, however, with the extension of follow-up time, the maintenance rate of sinus rhythm abates gradually. Due to the complex nature of this disease, many aspects of AF therapy remain unsolved, and the real answers are still lacking.


  Prospects Top


The prevalence and incidence of AF is on the rapid rise. To slow down the AF epidemic, effective primary prevention strategies are needed to be instituted. Unfortunately, this is an area that has not been well explored. Data analysis of 300,000 cases from the China AF center indicates that the top four underlying diseases are hypertension, coronary heart disease, heart failure, and diabetes. Therefore, the first-line pharmacologic therapies may have potential roles in the primary prevention of AF. However, the lack of large high-quality randomized clinical trials on these drugs evaluates the efficacy and safety of AF primary preventive purpose. Moreover, the performance of antiarrhythmic drugs is unsatisfactory. There is, therefore, a major need for innovative treatment strategies, which will minimize heart remodeling, electrical remodeling, neural remodeling, and eliminate or weaken the fundamentals of AF.

AF is a complex disease. Although trigger or reentry constitutes the main mechanism of AF, there are widespread, ongoing disagreements about the interpretation of various studies, and the principal mechanisms underlying AF. The precise mechanisms maintaining AF will be clarified eventually, but when this will happen is uncertain. In my point of view, the range of potential pathophysiological contributors to atrial cardiomyopathy is vast. Moreover, AF itself induces regulatory deviations that alter atrial properties to promote pathological alterations in atrial electrophysiological properties, structure, and function. Everyone may have “susceptibility genes” for AF, but not everyone may be diagnosed with AF. We need further to understand the mechanism of AF.To strengthen the basic and interventional therapy for AF. The interventional diagnosis and treatment for AF is a milestone progress, but the current method of operation is diversified. In addition to CPVA, all the other techniques are in the exploration stage. The short-term and long-term success rates of catheter ablation of persistent AF are not ideal. Why the follow-up results of Cox maze III and IV (48% for paroxysmal AF, 52% for persistent AF and long-term AF)[45] show that the sinus rhythm maintenance rate is still 89%? Does this indicate that transcatheter endocardial ablation of AF does not have a clear “roadmap”? I certainly do not agree with the blind “crazy bombing” in the atrium. So, whether the scientific “circuit diagram” needs to be seriously studied?

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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