Long-term effects of catheter ablation for lone atrial fibrillation: Progressive atrial electroanatomic substrate remodeling despite successful ablation

Teh, A.; Kistler, Peter M.; Lee, Geoffrey; Medi, Caroline; Heck, Patrick; Spence, S.; Morton, Joseph B.; Sanders, Prashanthan; Kalman, Jonathan M.

doi:10.1016/j.hrthm.2011.11.013

Cited by 130 publications

(96 citation statements)

References 24 publications

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“…They develop rapid progression of disease in the form of conversion of paroxysmal to persistent AF, and exhibit limited response to catheter ablation of AF. 43 Although patients with fibrotic atrial cardiomyopathy may be classified as lone AF because of the absence of any traditional risk factors for AF, the extent of structural remodeling evident on mapping is consistent with an underlying atrial myopathic process with global and regional conduction slowing, atrial fibrosis, and impaired SN function. 44 MRI imaging with late gadolinium enhancement demonstrates extensive biatrial fibrosis, 45 and atrial mechanical function is extensively impaired despite a low CHA 2 DS 2 VASc score, increasing the risk of stroke and necessitating prophylactic chronic oral anticoagulation.…”

Section: Fibrotic Atrial Cardiomyopathymentioning

confidence: 98%

“…76 In some patients, however, reversal of atrial remodeling may not occur and may in fact progress despite successful elimination of AF with catheter ablation. 43 This suggests that some patients may have an underlying independent myopathic process that progresses inexorably independent of efforts directed at reversal of the remodeling-inducing stimuli.…”

Section: Time Course Of Recovery Of Sn Function After Termination Of Afmentioning

confidence: 99%

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Sinus Node and Atrial Arrhythmias

2016

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Sinus node dysfunction (SND) and atrial arrhythmias frequently coexist and interact to initiate and perpetuate each other. Atrial arrhythmias are present in 40% to 70% of patients at the time of diagnosis of SND.1,2 However, the complex relationship between the 2 remains ill defined. The documented degenerative changes in atrial myocardial structure relating to SND are primarily right atrial. Yet, the majority of triggers and substrates for atrial fibrillation (AF) originate from the left atrium. Although progressive biatrial fibrosis is a feature in patients with structural heart disease and in senescence, paroxysmal AF that occurs in patients with no structural heart disease may have a different pathophysiology. SND associated with this latter condition is likely to be primarily a result of electric remodeling and potentially reversible. The time course of the progression of SND and AF 3 and their individual clinical manifestations also vary depending on the underlying pathology. The purpose of this review is to summarize the state of our knowledge of sinus node (SN) function in both health and disease, and to understand the complex relationship between SN disease and atrial arrhythmias. Structure and Functional Components of the Sinus NodeIn the adult human heart, the SN is a crescent-shaped structure 1 to 2 cm long and 0.5 cm wide that lies at the junction of the superior vena cava with the right atrium and lies along the sulcus terminalis. The node itself is composed of clusters of pacemaker myocytes arranged in parallel rows with short digitations that frequently anastomose with the surrounding atrial tissue. The specialized pacemaker cells are interspersed with nerves and capillaries and scaffolded by dense connective tissue to form the SN pacemaker complex. The caudal portion fragments to merge with the atrial myocardium. The lack of a distinct encapsulation and the radiating sinoatrial connections explains the lack of a single breakthrough of the sinus impulse. The position of the leading pacemaker site shifts within the node and varies with sympathetic and vagal stimulation. 3The SN pacemaker cells are interspersed with interstitial collagen that varies in extent as a function of older age. 4 Collagen content increases from 24% in the infant to 70% in the adult heart.5 The fibrous matrix with surrounding fatty insulation of the SN together with distinct electrophysiological properties (see below) provides insulation and prevents the depression of pacemaker automaticity from the hyperpolarizing electric load of the surrounding atrial myocardium. 6 Multiple currents are involved in the activation of the SN. The predominant inward current in the center of the node is I CaL . Action potentials with slow upstrokes initiated in the center spreads peripherally and into the musculature of the terminal crest. However, in the periphery of the node, I Na is operative and is necessary for providing sufficient inward current to depolarize the larger mass of atrial tissue. Delayed rectifier potassium currents facili...

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Section: Fibrotic Atrial Cardiomyopathymentioning

confidence: 98%

Section: Time Course Of Recovery Of Sn Function After Termination Of Afmentioning

confidence: 99%

Sinus Node and Atrial Arrhythmias

2016

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“…218 In contrast, atrial remodelling did not reverse in patients with lone AF undergoing successful AF ablation; indeed, substrate abnormalities progressed (decreased voltage and increased regional refractoriness) over the subsequent 6 -14 months. 219 Atrial enlargement and fibrosis are important determinants for the development and maintenance of AF. Increases in collagen I and collagen III (the latter which increase in cultured fibroblasts exposed to mechanical stretch) 220 were seen in patients with AF and MVD, but only type I was seen in patients with lone AF.…”

Section: Atrial Cardiomyopathy Due To Valvular Heart Diseasementioning

confidence: 99%

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

et al. 2016

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“…(11) Successful surgical ablation of AF does not eradicate progression of fibrosis, suggesting that the process occurs irrespective of the presence of arrhythmia. (12) Impairment in diastolic function leads to increased left atrial (LA) volume which, in turn, has been independently associated with an increased risk of myocardial infarction, congestive heart failure, coronary revascularisation and stroke. (13,14) Yet many of these variables which contribute to LA fibrosis are also associated with an increased risk of cardiovascular disease in general and AF may simply be a surrogate marker of vascular disease burden.…”

Section: Atrial Fibrillation As a Vascular Diseasementioning

confidence: 99%

Approach to device-detected subclinical atrial fibrillation

Zyl

McLeod²,

Gersh³

2017

SAHJ

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INTRODUCTIONCardiac implantable electronic devices (CIEDs) are becoming more and more common due to an aging global population and expanded criteria for implantation. During 2009, over 1.3 million new or replaced implantable cardiac devices were implanted worldwide, with around a quarter of these occurring in the United States (US) alone.(1,2) South Africa has experienced substantial growth with an almost 25% rise in CIEDs implanted between 2005 and 2009, as opposed to only 8% in the US.(1) In addition, there is a greater availability of external surface monitoring and implantable loop recorders (ILR). Out of this vast increase in continuous arrhythmia monitoring arises the challenge of how to approach the abundance of data that identifies subclinical arrhythmia, and germane to this discussion, atrial fibrillation (AF).As the most pervasive sustained arrhythmia encountered in clinical practice, AF has risen in age-adjusted incidence over the last half century -a trend which may be plateauing over the last decade.(3,4) After age 40 the lifetime risk of developing AF is almost 1 in 4.(2) As many as 40% of patients are entirely asymptomatic -also termed subclinical AF -and the arrhythmia may only come to the attention of the patient and provider as an incidental finding.(5) Population screening of those over 65 years of age would detect subclinical AF in an estimated 1.4% of patients -of whom, more than two thirds would be at high risk for stroke based on clinical risk prediction models.(6) AF shares many risk factors -including age, male gender, heart failure and coronary disease -with indications for a permanent pacemaker or implantable cardioverter defibrillator (ICD) and, as such, the detection of clinically silent paroxysms of AF by device interrogation is not uncommon. In patients with CIEDs placed for unrelated indications, without a prior history of permanent AF, 43% had 5 minutes or more of AF detected over 2 years of follow-up in a pooled analysis of 5 large prospective trials (n=10 016).(7) Therefore, adoption of a strategy for dealing with device-detected subclinical AF is vital for clinicians.In the midst of several studies which demonstrate the con-

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Long-term effects of catheter ablation for lone atrial fibrillation: Progressive atrial electroanatomic substrate remodeling despite successful ablation

Cited by 130 publications

References 24 publications

Sinus Node and Atrial Arrhythmias

Sinus Node and Atrial Arrhythmias

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

Approach to device-detected subclinical atrial fibrillation

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