Pathophysiologie von Vorhofflimmern - müssen wir umdenken?

Background: Although several classical studies seemed to provide clear ideas on the pathophysiology of atrial fibrillation, current concepts have to be modified on the basis of more recent findings. Aims of the study: The present review is an attempt to integrate current knowledge into the system of established hypotheses and concepts. Methods: The review is based on the available literature from the beginning of this century to the present. Results: Based on the findings of Garrey and of Moe and Abildskov, atrial fibrillation has been considered as the prototype of an arrhythmia being caused by multiple, random reentrant circuits, the number of which would determine the stability of the reentrant process. Local refractory and conduction properties would determine the size of individual circuits, a hypothesis quite convincing with respect to refractoriness, but so far hard to prove with respect to conduction. Atrial fibrillation as a random phenomenon is questioned not only by the dominat role of the left atrium for the maintenance of the arrhythmia, but also by most recent data demonstrating a spatio-temporal periodicity in activation patterns. Finally, ablation studies have provided convincing evidence that there is a subset of patients with focal or at least focally induced atrial fibrillation. Conclusions: More recent insights into the pathophysiology of atrial fibrillation do not imply a complete reappraisal of current ideas and concepts, but definitely a thorough revision. Hintergrund: Obwohl die Pathophysiologie von Vorhofflimmern durch eine Reihe grundlegender, fast schon historischer Arbeiten weitgehend aufgeklärt schien, zwingen neue Erkenntnisse zu einer Modifikation gängiger Konzepte. Studienziel: Durch die vorliegende Übersicht soll die aktuelle Datenlage in das System etablierter Hypothesen und Konzepte integriert werden. Methoden: Analysiert wurde die verfügbare Literatur seit Anfang des Jahrhunderts bis hin zu aktuellen, auch eigenen Befunden. Ergebnisse: Basierend auf den Befunden von Garrey sowie von Moe und Abildskov galt Vorhofflimmern bislang als der Prototyp einer durch multiple, zufällig sich etablierende Kreiserregungen bedingte Rhythmusstörung, deren Stabilität von der Anzahl simultan aktivierter Erregungskreise abhängt. Lokale Refraktär- und Leitungseigenschaften sollen die Größe individueller Erregungskreise festlegen, wobei sich diese Hypothese zwar schlüssig für die Refraktärzeit, aber bislang kaum für die Leitungsgeschwindigkeit belegen läßt. Die Zufälligkeit im Aktivierungsmuster multipler kreisender Erregungen wird durch die dominierende Rolle des linken Vorhofs für die Aufrechterhaltung von Vorhofflimmern in Frage gestellt, ebenso durch eine erst jüngst beschriebene, räumliche und zeitliche Periodizität der elektrischen Aktivierung. Schließlich belegen die Erfahrungen mit ablativen Verfahren, daß auch fokales oder zumindest fokal induziertes Vorhofflimmern klinisch eine Rolle spielt. Schlußfolgerungen: Aufgrund neuerer Erkenntnisse müssen die Vorstellungen zur Pathophysiologie von Vorhofflimmern zwar nicht gänzlich revidiert, aber doch erheblich modifiziert werden.     

Mechanisms of initiation in atrial fibrillation

Atrial fibrillation is the most relevant arrhythmia in daily clinical practice. The pathophysiology is determined by multiple independent reentrant wavelets in both atria. Repetitive triggers and an underlying substrate may favor the initiation and maintenance of atrial fibrillation. Mapping studies in patients with drug-refractory paroxysmal atrial fibrillation identified potentials from the ostia of pulmonary veins as a main source of triggers that initiate atrial fibrillation. In ongoing clinical trials, catheter ablation of pulmonary vein foci is used to eliminate atrial premature beats and thereby prevent the initiation of atrial fibrillation. The autonomic modulation of the heart rate and the occurrence of other supraventricular tachycardias that degenerate into atrial fibrillation are also considered as triggering mechanisms of atrial fibrillation. Since symptomatic bradycardia is associated with an increased incidence of atrial fibrillation, atrial pacing therapies for prevention of atrial fibrillation are another concept. Ongoing clinical trials evaluating the efficacy of pacing in patients with and without a primary pacemaker indication are currently under investigation. To date, data to which extent anatomical and electrophysiological characteristics of the atria influence the initiation and maintenance of atrial fibrillation are still missing. The myocardial adaptation to atrial fibrillation, the so-called "atrial remodeling", includes shortening of the atrial refractory period, slowing of atrial conduction, shortening of the atrial action potential, a progressive reduction of L-type calcium channel expression and microfibrosis of the myocardial tissue. New drug developments target atrial remodeling by modulating ion channel function and receptors of the angiotensin metabolism.     

Mechanisms of induction of atrial fibrillation: what do we really know?

Background: Insights into the mechanisms of induction or paroxysmal atrial fibrillation hold the potential to develop preventive or even curative therapies for the arrhythmia. Aim of study: To review basic principles of induction of reentrant activation with respect to their applicability to clinical observations. Methods: Literature search regarding relevant clinical and experimental studies. Analysis of the epicardial activation pattern during induction of atrial flutter in dogs with sterile pericarditis using a custom-designed electrode array (128 bipolar electrodes, interelectrode distance 3-8 mm) and a computerized multiplexer-mapping system. Results: Limited clinical data reveal a marked intra- and interindividual variability in the onset mechanisms of atrial fibrillation. Episodes of atrial fibrillation initiated by rapid focal discharges from the pulmonary veins or by increased sympathetic or parasympathetic tone appear to represent rare entities. Induction of reentrant activation generally depends on the occurrence of functional conduction block and regional conduction delay. Conduction block in the atria seems to be primarily based on local dispersion of refractoriness. Refractory periods are modified by various factors, potentially resulting in temporary, nonhomogenous changes. Conclusions: Regional conduction and refractory properties are of major relevance for the initiation or reentry. With a plethora of modifying factors thereof, marked intra- and interindividual variability in the onset mechanisms of atrial fibrillation is more than conceivable.     

Methodology for patient-specific modeling of atrial fibrosis as a substrate for atrial fibrillation

Personalized computational cardiac models are emerging as an important tool for studying cardiac arrhythmia mechanisms, and have the potential to become powerful instruments for guiding clinical anti-arrhythmia therapy. In this article, we present the methodology for constructing a patient-specific model of atrial fibrosis as a substrate for atrial fibrillation. The model is constructed from high-resolution late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) images acquired in vivo from a patient suffering from persistent atrial fibrillation, accurately capturing both the patient's atrial geometry and the distribution of the fibrotic regions in the atria. Atrial fiber orientation is estimated using a novel image-based method, and fibrosis is represented in the patient-specific fibrotic regions as incorporating collagenous septa, gap junction remodeling, and myofibroblast proliferation. A proof-of-concept simulation result of reentrant circuits underlying atrial fibrillation in the model of the patient's fibrotic atrium is presented to demonstrate the completion of methodology development.     

Efficacy of propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up

The efficacy and safety of intravenous propafenone was studied in 10 patients with Wolff-Parkinson-White syndrome and in 2 patients with a concealed accessory pathway. During electrophysiologic study, the effect of propafenone on the effective refractory period of the accessory pathway was determined, as well as its effect during orthodromic atrioventricular (AV) reentrant tachycardia and atrial fibrillation. Propafenone caused significant increases in the accessory pathway refractory period, both in the anterograde direction (290 +/- 19 versus 474 +/- 50 ms, p less than 0.05) and in the retrograde direction (238 +/- 15 versus 408 +/- 44 ms, p less than 0.05). Complete anterograde accessory pathway conduction block occurred in four patients. Sustained AV reentrant tachycardia was inducible in 11 patients before administration of propafenone. Drug infusion during AV reentrant tachycardia promptly terminated arrhythmia in 10 of these 11 patients and caused slowing of AV reentrant tachycardia in the remaining patient. Before propafenone, sustained atrial fibrillation was inducible in six patients and nonsustained atrial fibrillation in four patients. After propafenone, no patient had inducible sustained atrial fibrillation. Furthermore, propafenone caused a marked decrease in peak ventricular rate during atrial fibrillation. Eight patients have been treated with oral propafenone and followed up for 12 +/- 2 months. All have remained virtually free of recurrent arrhythmia and none has developed significant side effects. Propafenone is a very promising agent for emergency intravenous therapy as well as long-term oral therapy in patients with Wolff-Parkinson-White syndrome.     

Mechanisms of atrial remodeling and clinical relevance

PURPOSE OF REVIEW: Atrial fibrillation usually occurs in the context of an atrial substrate produced by alterations in atrial tissue properties referred to as remodeling. Remodeling can result from cardiac disease, cardiac arrhythmias, or biologic processes such as senescence. Recent advances in understanding remodeling have allowed for insights into mechanisms underlying atrial fibrillation that have been transferred from experimental models to humans. This paper reviews recent progress in understanding atrial remodeling, as well as the consequent clinical insights into atrial fibrillation pathophysiology and treatment. RECENT FINDINGS: Two principal forms of remodeling have been described in animal models of atrial fibrillation: ionic remodeling, which affects cellular electrical properties, and structural remodeling, which alters atrial tissue architecture. Atrial tachycardias (particularly rapid tachyarrhythmias such as atrial flutter and atrial fibrillation) cause ionic remodeling, which decreases the atrial refractory period and promotes atrial reentry. Congestive heart failure produces atrial interstitial fibrosis, which promotes arrhythmogenesis by interfering with atrial conduction properties. Recent animal studies have provided insights into the pathways involved in remodeling, and have indicated the pathophysiological role of remodeling in specific contexts. In addition, work in animal models has provided information about pharmacological interventions that can prevent the development of remodeling. Clinical studies have shown that novel approaches to remodeling prevention identified in animal work have potential therapeutic value in man. SUMMARY: Understanding atrial remodeling has the potential to improve our appreciation of the pathophysiology of clinical atrial fibrillation and to allow for the development of useful new therapeutic approaches.     

Prevention of atrial fibrillation

PURPOSE OF REVIEW: This review summarizes current concepts on the pathophysiology of atrial fibrillation, identifying predisposing factors to guide primary and secondary preventive approaches. RECENT FINDINGS: Many factors contribute to the development and progression of atrial fibrillation, including cardiovascular diseases, age, neurohormones, genetics, diet, autonomic influences, and inflammation. Therapeutic efforts have been directed to modify this altered milieu and prevent the development of atrial electrical and structural remodeling. This nonconventional antiarrhythmic management appears to have an important role also in secondary prevention of atrial fibrillation; the indications for conventional antiarrhythmic agents are decreasing because of side effects and limited efficacy. Interventional electrophysiology techniques have been developed to target the arrhythmia substrate responsible for the initiation or maintenance of atrial fibrillation, achieving high success rates. SUMMARY: Atrial fibrillation is the most commonly treated arrhythmia and its incidence is predicted to increase. It is associated with significant morbidity and mortality. Preventive efforts should be initiated early and include diversified interventions to correct predisposing factors and modify the altered atrial substrate.     

Paroxysmal atrial fibrillation in the wolff-parkinson-white syndrome

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p < 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p < 0.0005).Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p < 0.025).In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.     

MicroRNA与心房颤动关系的研究进展

心房颤动是最常见的持续性心律失常,并有较高的发病率和死亡率。其流行率预计在未来几年会进一步增加。尽管在过去十年中出现了心房颤动病理生理学的新分子概念,但目前可用的治疗方法仍存在主要局限性,包括效果差和严重的副作用,如心室恶性心律失常等。心房电重构、结构重构和自主神经重构是心房颤动的发病基础,但驱动这种重构的确切机制仍不完全清楚。MicroRNA代表大量小非编码RNA的亚组,降解或抑制其靶m RNA的翻译,从而调节基因表达并在广泛的生物学过程中起重要作用。临床上,越来越多的证据表明micro RNA在心血管疾病的发生发展中发挥关键作用。     

Atrial fibrillation: A progressive atrial myopathy or a distinct disease?

Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance. However, the exact pathophysiological mechanisms of atrial fibrillation are not completely understood and whether atrial fibrillation is an unclassified cardiomyopathy or a distinct disease still remains to be answered. This review highlights proarrhythmic and pathophysiological mechanisms of atrial fibrillation and approaches the molecular basis underlying atrial fibrillation susceptibility.     

Atrial flutter: an update

Invasive electrophysiologic studies have changed the clinical outlook for patients with atrial flutter. Recognition of the reentrant circuit responsible for typical atrial flutter has led to the development of catheter ablation techniques that can prevent recurrence in >90% of cases. In addition, general understanding of atrial tachycardias has changed radically, such that ECG-based classifications are now obsolete. Atypical reentrant circuits associated with surgical scars or fibrotic areas in either atrium, which are indistinguishable from focal tachycardias on ECG, have been identified. These circuits also seem amenable to treatment by ablation. Recently, a new type of reentrant tachycardia that could be problematic in the future has emerged in patients who have undergone extensive left atrial ablation for the treatment of atrial fibrillation. These atypical circuits can be characterized using the mapping and entrainment techniques initially developed for typical flutter. In these cases, electroanatomical mapping, involving the construction of a virtual anatomical model of the atria, is extremely helpful. Despite the success of ablation, long-term prognosis is frequently overshadowed by the appearance of atrial fibrillation, which suggests that flutter and fibrillation share a common arrhythmogenic origin that is not modified by cavotricuspid isthmus ablation. In contrast with our clear electrophysiologic understanding of atrial flutter, little is known about the natural history of the condition because the literature has traditionally grouped patients with flutter and fibrillation together. Consequently, the complex relationship between the two arrhythmias has still to be clearly delineated. Primary prevention and preventing the development of atrial fibrillation after ablation remain outstanding clinical challenges.     

Morphological remodeling in atrial fibrillation

In the recent years, a tremendous amount has been learned about the pathophysiology of atrial fibrillation (AF). AF induces electrophysiological changes in the atria causing a perpetuation of the arrhythmia ("electrical remodeling"). Besides such AF-induced electrophysiological changes, which involve the downregulation of L-type calcium channels and thereby the calcium inward current, AF induces structural and ultrastructural changes in atrial tissue ("structural remodeling"). Calcium-dependent tissue alterations are induced by proteases and phosphatases like calpain and calcineurin. Furthermore, cardiac diseases like hypertension, heart failure, etc. activate the atrial angiotensin II system, and thereby, a progressive pro-arrhythmogenic atrial fibrosis is induced. Besides first clinical trials assessing the antiarrhythmic effects of angiotensin II receptor blockers in patients with AF, experimental data suggest that viral gene transfer can be used to transform fibroblasts to electrically conducting cardiomyocytes. This highly interesting methodology may be helpful to restore electrical conduction in fibrotic cardiac tissue.     

Curative treatment of atrial fibrillation 2000: percutaneous catheter ablation techniques and intraoperative ablation with minimally invasive techniques

Summary Experimental and clinical mapping studies have indicated that the initiation of atrial fibrillation has to be differentiated from the perpetuation. Curative treatment of atrial fibrillation is one of the main challenges of today's electrophysiology, and the trigger as well as the substrate have recently been targeted. The arrhythmogenic foci which have been identified as being critical for the initiation of paroxysmal atrial fibrillation have been found in the vast majority of patients in the area of the proximal pulmonary veins. In a subset of patients with paroxysmal atrial fibrillation, these firing foci may be the only electrophysiologic abnormality. In other patients, different atrial arrhythmia types may be driven by pulmonary vein foci. Haissaguerre et al. have introduced mapping strategies to identify active foci within the pulmonary veins. The success rate of percutaneous pulmonary vein focus ablation strongly depends on the number of active foci. In contrast to elimination of the initiating triggers in patients with paroxysmal atrial fibrillation, modification of the maintaining substrate of atrial fibrillation is the alternative target for ablation in patients with chronic atrial fibrillation or in patients with prolonged episodes of paroxysmal atrial fibrillation. Different linear lesion line concepts within the right and/or left atrium have been followed within the last few years with moderate success rates. The lesion geometries that have been applied percutaneously so far seem to be empirical, and no successful lesion geometry concept for percutaneous application has been validated. A surgical curative treatment concept for patients with chronic atrial fibrillation is the maze procedure introduced by Cox et.al. which, however, is an extensive and time consuming surgical technique. Within the last few years, several attempts have been made to develop alternative surgical treatment strategies that should be safe, effective, and easy to apply. One of the promising new concepts is the intraoperative radiofrequency ablation of atrial fibrillation by elemination of anatomically determined so-called anchor reentrant circuits involving the pulmonary vein orifices and the mitral annulus. In this review, data on percutaneous ablation of pulmonary vein foci, percutaneous placement of linear right and/or left atrial lesion lines and, finally, intraoperative radiofrequency (RF) ablation using minimally invasive techniques are summarized.     

Atrial Fibrillation: Defining Potential Curative Ablation Targets

The concept that atrial fibrillation (or at least certain forms of the arrhythmia) may be amenable to reversal or amelioration by transcatheter ablation techniques has become increasingly accepted in recent years. As yet, however, the techniques being studied for ablation of atrial fibrillation address neither known critical anatomic elements nor well defined electrophysiologic markers. The approaches, although essentially empirical, are conceptually based on the ‘multiple wavelet’ or ‘focal origin’ hypotheses. To date, addressing ‘focal origin’ atrial fibrillation by transcatheter ablation has been the more encouraging. However, as technology evolves, both in terms of catheter design and possibly endocardial mapping techniques, approaches to wavelet or rotor mechanisms may become similarly effective. This communication examines concepts regarding the manner in which atrial fibrillation is initiated and maintained. The goals are to better understand the encouraging success of empirical ablation methods, and possibly derive insights which may help refine ablation targeting in the future.     

Remodeling in atrial fibrillation

BACKGROUND: Atrial fibrillation is associated with alterations in atrial electrophysiology that facilitate the initiation and persistence of the arrhythmia. This process was termed electrical remodeling in atrial fibrillation. The underlying cellular and molecular mechanisms have intensively been investigated over the past few years in patients with atrial fibrillation and in different experimental models. The results, that have substantially improved the understanding of the pathophysiology of atrial fibrillation, are reviewed. CELLULAR AND MOLECULAR MECHANISMS: On the cellular level, atrial fibrillation leads to a strong shortening and an impaired rate adaptation of the action potential as well as to changes in action potential morphology. Atrial fibrillation is associated with an altered gene expression of the L-type calcium channel (ICa,L) and of potassium channels (Ito, IK1, IKACh). The molecular mechanisms of intraatrial conduction slowing are less well understood, changes in the expression or distribution of gap junction proteins or a decrease of the fast sodium inward channel (INa) have been reported in some studies. A trigger of initiation for electrical remodeling is an overload of the cytoplasm with Ca2+ and a consecutive decrease of the systolic calcium gradient, furthermore changes in calcium-handling proteins are detectable in atrial fibrillation. CONCLUSION: These changes in the cellular and molecular milieu importantly determine the clinical course and the efficacy of therapeutical interventions in atrial fibrillation. The clinical relevance and potential new therapeutic approaches are discussed in the last part.     

转化生长因子-β1对心房结构重构及细胞骨架蛋白的影响

心房颤动是临床上最常见的持续性心律失常。大量研究发现,心房颤动的发生发展与心房结构重构密切相关,而心房纤维化是最主要的结构重构改变。转化生长因子-β1是心房颤动纤维化重构中重要的致纤维化因子,不仅能引起细胞间质重构,还能影响心肌细胞骨架重塑及相关骨架蛋白表达异常。特别是使心脏特异性肌动蛋白交联蛋白α-actinin-2表达增加。细胞骨架蛋白参与了结构重构改变。现对转化生长因子-β1对心房结构重构及心房肌细胞骨架蛋白的影响进行综述。     

Electrophysiologic predictors of the recurrence of persistent atrial fibrillation within 30 days of cardioversion

Patients with recurrence of persistent atrial fibrillation within 30 days of cardioversion had slower atrial conduction, a slower sinus rate, no difference in the absolute value of the effective refractory period, greater early reverse remodeling of the effective refractory period, and more premature atrial contractions than those who did not. These findings highlight the role of slow conduction and premature atrial contractions in the pathophysiology of atrial fibrillation and suggest a possible proarrhythmic effect of reverse remodeling.     

房性心动过速导管消融进展

Atrial tachycardias (ATs) may be divided into focal and reentrant forms. In recent years, great prngress achieved in catheter ablation of ATs and the success rate of catheter ablatiou has improved dramatically in both focal ATs and reentrant ATs.Focal ATs tend to originate in characteristic locations associated with anatomic structures, such as the erista terminalis,the interatrial septum,the atrioventricular annulus,the coronary sinus,the atrial appendages,the ostial portion of the pulmonary veins. In recent years, successful catheter ablation of focal AT from the nou-coronary aortic sinus, from the mitral annulus-aorta junction, or from the atrial ap-pendages has been reported. Catheter mapping and ablation in the non-coronary aortic sinus should be attempted in patients with narrow P waves on surface ECG and the earliest atrial activation located at the His bundle region. For the cases who had a failed ablation or recur-rence after ablation in the non-coronary aortic sinus,mapping and ablation in the mitral annulus-aorta junction should be considered.Catheter ablation of typical atrial flutter (AFL) has a very high success rate,approximately 100% in some centers. For few difficult cases,several measures can be employed to increase the likelihood of success. Firstly and most importantly,the mechanism of typical AFL other than other ATs should be revaluated and reconfirmed. Other measures include using three-dimensional cardiac electroanatomical mapping system to map the cavotricuspid isthmus (CTI) carefully, using large-curve catheters and/or long guiding sheaths to ensure cath-eter contact across the entire CTI,and employing a large-tip or cooled-tip catheter instead of standard 4 mm-tip ablation catheter.Reentrant ATs usually occur in patients with dilated, severely scarred right or left atria, including previous right or left atriotomy, any form of structural heart disease, or following catheter or surgical ablation of atrial fibrillation. Some reentrant ATs patients present with a large scarred right or left atrium without any other form of structural heart disease, were classified it as "idiopathic arrhythmogen-ic atrial myopathy" by some experts. The earlier experience in mapping and ablation of reentrant ATs came mainly from mapping and ablation of ATs in patients with sugical treatment of congenital heart disease,so the ATs were called "incisional reentrant ATs". In the past decade, the success rate for catheter ablation of reentrant ATs after surgery has improved significantly by combination of electroana-tomical scarred substrate mapping and entrainment mapping. It is noted that the "incisional reentrant ATs" often have multiple reentrant circuits and multiple ATs or coexist with typical AFL, and more than one linear lesions from scar to scar, or scar to anatomical obstacle, or between reentrant isthmuses are needed in most cases.The reentrant ATs after catheter ablation of atrial fibrillation have increased dramatically in recent years, which belong to "iatro-genic reentrant ATs". Different atrial fibrillation ablation approaches have different incidence of reentrant ATs, a few in patients with segmental isolation of the pulmonary vein ostia, more often in patients with circumferential pulmonary vein ablation and most often in pa-tients with stepped ablation of chronic atrial fibrillation (combination of pulmonary vein isolation, linear ablation and ablation of the complex fractionated atrial electrograms). In some cases, mapping and ablation of these reentrant ATs are very difficult.     

Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. The work discussed may open potentially exciting new diagnostic and therapeutic possibilities.     

老年性心房颤动心房结构重构与基质金属蛋白酶研究进展

心房颤动是常见的心律失常,随年龄的增长发病率逐渐的增加。在心房颤动的发生机制中,心房结构重构起着重要的作用,现就基质金属蛋白酶及抑制因子在心房结构重构中的作用以及老龄对心房结构重构影响的现阶段研究进展予以综述。