Atrial Myopathy

Shen, Mark J.; Arora, Rishi; Jalife, José

doi:10.1016/j.jacbts.2019.05.005

Cited by 135 publications

(122 citation statements)

References 142 publications

(166 reference statements)

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“…Indeed, risk stratification as "risk of AF" by the AA was associated with coronary artery disease and congestive heart failure, both common clinical risk factors of atrial cardiopathy. 27,28 This suggests that the AA-based risk stratification used here could potentially aid in detecting electrical changes within the left atrium associated with atrial cardiopathy.…”

Section: Discussionmentioning

confidence: 96%

Software‐based analysis of 1‐hour Holter ECG to select for prolonged ECG monitoring after stroke

Gröschel

Lange

Wasser

et al. 2020

Ann Clin Transl Neurol

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Objective: Identification of ischemic stroke patients at high risk for paroxysmal atrial fibrillation (pAF) during 72 hours Holter ECG might be useful to individualize the allocation of prolonged ECG monitoring times, currently not routinely applied in clinical practice. Methods: In a prospective multicenter study, the first analysable hour of raw ECG data from prolonged 72 hours Holter ECG monitoring in 1031 patients with acute ischemic stroke/TIA presenting in sinus rhythm was classified by an automated software (AA) into "no risk of AF" or "risk of AF" and compared to clinical variables to predict AF during 72 hours Holter-ECG. Results: pAF was diagnosed in 54 patients (5.2%; mean age: 78 years; female 56%) and was more frequently detected after 72 hours in patients classified by AA as "risk of AF" (n = 21, 17.8%) compared to "no risk of AF" (n = 33, 3.6%). AA-based risk stratification as "risk of AF" remained in the prediction model for pAF detection during 72 hours Holter ECG (OR3.814, 95% CI 2.024-7.816, P < 0.001), in addition to age (OR1.052, 95% CI 1.021-1.084, P = 0.001), NIHSS (OR 1.087, 95% CI 1.023-1.154, P = 0.007) and prior treatment with thrombolysis (OR2.639, 95% CI 1.313-5.306, P = 0.006). Similarly, risk stratification by AA significantly increased the area under the receiver operating characteristic curve (AUC) for prediction of pAF detection compared to a purely clinical risk score (AS5F alone: AUC 0.751; 95% CI 0.724-0.778; AUC for the combination: 0.789, 95% CI 0.763-0.814; difference between the AUC P = 0.022). Interpretation: Automated software-based ECG risk stratification selects patients with high risk of AF during 72 hours Holter ECG and adds predictive value to common clinical risk factors for AF prediction.

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Section: Discussionmentioning

confidence: 96%

Software‐based analysis of 1‐hour Holter ECG to select for prolonged ECG monitoring after stroke

Gröschel

Lange

Wasser

et al. 2020

Ann Clin Transl Neurol

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“…The authors considered atrial remodelling as the initial cardiomyocyte response to various stressors (pressure and/or volume overload, arrhythmias), such as electrical and structural remodelling in response to repeated arrhythmic events (atrial fibrillation) with resulting changes in atrial geometry (size and sphericity), function and electrophysiology. Atrial cardiomyopathy translates into a diseased and fibrotic myocardium, with a subsequent risk of developing heart failure and atrial dysfunction [11][12][13]. The previously attempted classifications of atrial cardiomyopathies are, however, rarely used in clinical practice, since it is mostly histological-based and hard to implement in day-to-day clinical practice [5,11].…”

Section: Atrial Cardiomyopathy and Left Atrial Remodellingmentioning

confidence: 99%

Left Atrial Structural Remodelling in Non-Valvular Atrial Fibrillation: What Have We Learnt from CMR?

et al. 2020

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Left atrial structural, functional and electrical remodelling are linked to atrial fibrillation (AF) pathophysiology and mirror the phrase “AF begets AF”. A structurally remodelled left atrium (LA) is fibrotic, dysfunctional and enlarged. Fibrosis is the hallmark of LA structural remodelling and is associated with increased risk of stroke, heart failure development and/or progression and poorer catheter ablation outcomes with increased recurrence rates. Moreover, increased atrial fibrosis has been associated with higher rates of stroke even in sinus-rhythm individuals. As such, properly assessing the fibrotic atrial cardiomyopathy in AF patients becomes necessary. In this respect, late-gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging is the gold standard in imaging myocardial fibrosis. LA structural remodelling extension offers both diagnostic and prognostic information and influences therapeutic choices. LGE-CMR scans can be used before the procedure to better select candidates and to aid in choosing the ablation technique, during the procedure (full CMR-guided ablations) and after the ablation (to assess the ablation scar). This review focuses on imaging several LA structural remodelling CMR parameters, including size, shape and fibrosis (both extension and architecture) and their impact on procedure outcomes, recurrence risk, as well as their utility in relation to the index procedure timing.

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“…The most clinically important cardiac arrhythmias, atrial fibrillation and ventricular fibrillation, are invariably associated with significant underlying heart disease [1,2]. One of the major difficulties with managing these arrhythmias is that despite often decades of progressive heart disease these arrhythmias have an abrupt onset that cannot be predicted in advance [2,21].…”

Section: Impact Of Disease Progressionmentioning

confidence: 99%

“…Cardiac arrhythmias, which impair the heart's ability to pump blood effectively, are a major cause of morbidity [1] and mortality [2]. Arrhythmic activity is underpinned by re-entrant rotors of electrical activity in the myocardium [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

“…First, topological defects in the heart that form anatomical re-entry circuits, such as AV nodal accessory pathways [10]. Second, reduced intercellular connectivity, as for example occurs in stretched atria with diffuse interstitial fibrosis [1]. And third, heterogeneity in the refractoriness of cardiac cells, which is also thought to be key to the breakdown of orderly waves into multiple wavelets [5,9,11,12].…”

Section: Introductionmentioning

confidence: 99%

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Arrhythmogenesis as the failure of repolarization

Heitmann

Vandenberg

Hill

2020

Preprint

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AbstractContemporary theories of cardiac fibrillation typically rely on the emergence of rotors to explain the transition from regular sinus rhythm to disordered electrophysiological activity. How those rotors spontaneously arise in the absence of re-entrant anatomical circuits is not fully understood. Here we propose a novel mechanism where arrhythmias are initiated by cardiac cells that fail to repolarize following a normal heartbeat. Those cells subsequently act as a focal ectopic source that drive the ensuing fibrillation. We used a simple computational model to investigate the impact of such cells in both homogeneous and heterogeneous excitable media. We found that heterogeneous media can tolerate a surprisingly large number of abnormal cells and still support normal rhythmic activity. At a critical limit the medium becomes chronically arrhythmogenic. Numerical analysis revealed that the critical threshold for arrhythmogenesis depends on both the strength of the coupling between cells and the extent to which the abnormal cells resist repolarization. Arrhythmogenesis was also found to emerge first at tissue boundaries where cells naturally have fewer neighbors to influence their behavior. These findings may explain why atrial fibrillation typically originates from the cuff of the pulmonary vein.Author summaryCardiac fibrillation is a medical condition where normal heart function is compromised as electrical activity becomes disordered. How fibrillation arises spontaneously is not fully understood. It is generally thought to be triggered by premature depolarization of the cardiac action potential in one or more cells. Those premature beats, known as early-afterdepolarizations, subsequently initiate a self-sustaining rotor in the otherwise normal heart tissue. In this study, we propose an alternative mechanism whereby arrhythmias are initiated by cardiac cells that fail to repolarize of their own accord but still operate normally when embedded in functional heart tissue. We find that such cells can act as focal ectopic sources under appropriate conditions of inter-cellular coupling. Moreover, cells on natural tissue boundaries are more susceptible to arrhythmia because they are coupled to fewer cells. This may explain why the pulmonary vein is often implicated as a source of atrial fibrillation.

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Atrial Myopathy

Cited by 135 publications

References 142 publications

Software‐based analysis of 1‐hour Holter ECG to select for prolonged ECG monitoring after stroke

Software‐based analysis of 1‐hour Holter ECG to select for prolonged ECG monitoring after stroke

Left Atrial Structural Remodelling in Non-Valvular Atrial Fibrillation: What Have We Learnt from CMR?

Arrhythmogenesis as the failure of repolarization

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