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

Goette, Andreas; Kalman, Jonathan M.; Aguinaga, Luis; Akar, Joseph G.; Cabrera, José Ángel; Chen, Shih Ann; Chugh, Sumeet S.; Corradi, Domenico; d’Ávila, André; Dobrev, Dobromir; Fenelon, Guilherme; González, Mario D.; Hatem, Stéphane; Helm, Robert H.; Hindricks, Gerhard; Ho, Siew Yen; Hoit, Brian D.; Jalife, José; Kim, Young Hoon; Lip, Gregory Y.H.; Ma, Changsheng; Marcus, Gregory M.; Murray, Katherine T.; Nogami, Akihiko; Sanders, Prashanthan; Uribe, William; Wagoner, David R. Van; Nattel, Stanley

doi:10.1093/europace/euw161

Cited by 542 publications

(501 citation statements)

References 532 publications

(355 reference statements)

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“…This impressive derangement of the atrial walls fits with the recent concepts of ‘atrial cardiomyopathy’[29], corresponding to any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations [30]. The extent and the progression of atrial structure derangement in cardiolaminopathies are the basis for the progression of clinical arrhythmias, with atrial fibrillation and flutter (which require some amount of excitable atrial tissue) typically followed over time by atrial standstill, as an expression of an extensive loss of viable atrial tissue [4].…”

Section: Bradyarrhythmias Atrial Fibrillation and Atrial Fluttersupporting

confidence: 69%

Cardiolaminopathies from bench to bedside: challenges in clinical decision-making with focus on arrhythmia-related outcomes

Boriani

Biagini

Ziacchi

et al. 2018

Nucleus

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Lamin A/C gene mutations can be associated with cardiac diseases, usually referred to as ‘cardiolaminopathies’ characterized by arrhythmic disorders and/or left ventricular or biventricular dysfunction up to an overt picture of heart failure. The phenotypic cardiac manifestations of laminopathies are frequently mixed in complex clinical patterns and specifically may include bradyarrhythmias (sinus node disease or atrioventricular blocks), atrial arrhythmias (atrial fibrillation, atrial flutter, atrial standstill), ventricular tachyarrhythmias and heart failure of variable degrees of severity. Family history, physical examination, laboratory findings (specifically serum creatine phosphokinase values) and ECG findings are often important ‘red flags’ in diagnosing a ‘cardiolaminopathy’. Sudden arrhythmic death, thromboembolic events or stroke and severe heart failure requiring heart transplantation are the most dramatic complications of the evolution of cardiolaminopathies and appropriate risk stratification is clinically needed combined with clinical follow-up. Treatment with cardiac electrical implantable devices is indicated in case of bradyarrhythmias (implant of a device with pacemaker functions), risk of life-threatening ventricular tachyarrhythmias (implant of an ICD) or in case of heart failure with wide QRS interval (implant of a device for cardiac resynchronization). New technologies introduced in the last 5 years can help physicians to reduce device-related complications, thanks to the extension of device longevity and availability of leadless pacemakers or defibrillators, to be implanted in appropriately selected patients. An improved knowledge of the complex pathophysiological pathways involved in cardiolaminopathies and in the determinants of their progression to more severe forms will help to improve clinical management and to better target pharmacological and non-pharmacological treatments.

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Section: Bradyarrhythmias Atrial Fibrillation and Atrial Fluttersupporting

confidence: 69%

Cardiolaminopathies from bench to bedside: challenges in clinical decision-making with focus on arrhythmia-related outcomes

Boriani

Biagini

Ziacchi

et al. 2018

Nucleus

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“…AF affects more than 33 million people worldwide, with an incidence that is expected to increase further as the population ages [4]. A large number of cardiovascular and non-cardiovascular diseases, as well as AF itself, increase the risk of AF by promoting proarrhythmic atrial remodeling, giving rise to a progressive atrial cardiomyopathy [1,5,6]. Clinically, this progression of AF is reflected by its classification into paroxysmal AF (pAF), persistent AF or long-standing persistent (chronic) AF (cAF), depending on the duration of the arrhythmia [3].…”

Section: Introductionmentioning

confidence: 99%

Serine/Threonine Phosphatases in Atrial Fibrillation

Heijman

Ghezelbash

Wehrens

et al. 2017

Journal of Molecular and Cellular Cardiology

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Serine/threonine protein phosphatases control dephosphorylation of numerous cardiac proteins, including a variety of ion channels and calcium-handling proteins, thereby providing precise post-translational regulation of cardiac electrophysiology and function. Accordingly, dysfunction of this regulation can contribute to the initiation, maintenance and progression of cardiac arrhythmias. Atrial fibrillation (AF) is the most common heart rhythm disorder and is characterized by electrical, autonomic, calcium-handling, contractile, and structural remodeling, which include, among other things, changes in the phosphorylation status of a wide range of proteins. Here, we review AF-associated alterations in the phosphorylation of atrial ion channels, calcium-handling and contractile proteins, and their role in AF-pathophysiology. We highlight the mechanisms controlling the phosphorylation of these proteins and focus on the role of altered dephosphorylation via local type-1, type-2A and type-2B phosphatases (PP1, PP2A, and PP2B, also known as calcineurin, respectively). Finally, we discuss the challenges for phosphatase research, potential therapeutic significance of altered phosphatase-mediated protein dephosphorylation in AF, as well as future directions.

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“…Based on findings in animal models of AF and in patients, they provide evidence-based recommendations for first-line antithrombotic treatment in AF patients. Importantly, the concept of "atrial cardiomyopathy" is introduced and explained with regard to thrombogenesis [20].…”

Section: Novel Clinical and Experimental Aspects Of Atrial Fibrillationmentioning

confidence: 99%

Advances in cardiac cellular electrophysiology – Relevance for clinical translation

Ravens

Goette

2018

Herzschr Elektrophys

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

Cited by 542 publications

References 532 publications

Cardiolaminopathies from bench to bedside: challenges in clinical decision-making with focus on arrhythmia-related outcomes

Cardiolaminopathies from bench to bedside: challenges in clinical decision-making with focus on arrhythmia-related outcomes

Serine/Threonine Phosphatases in Atrial Fibrillation

Advances in cardiac cellular electrophysiology – Relevance for clinical translation

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