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Cardiomyocyte Remodeling in Atrial Fibrillation and Hibernating Myocardium: Shared Pathophysiologic Traits Identify Novel Treatment Strategies?

Weil BR, Ozcan C - Biomed Res Int (2015)

Bottom Line: Development of novel therapies for primary and secondary prevention of AF is critical and requires improved understanding of the cellular and molecular mechanisms underlying the AF disease process.These shared features, which include an array of structural, metabolic, and electrophysiologic changes, appear to represent a conserved adaptive myocyte response to chronic stress that involves dedifferentiation towards a fetal phenotype to promote survival.In this review, we discuss the pathophysiology of AF, summarize studies supporting a common remodeling program in AF and hibernating myocardium, and propose future therapeutic implications of this emerging paradigm.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiovascular Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY, USA.

ABSTRACT
Atrial fibrillation (AF) is the most common arrhythmia and is associated with a high risk of morbidity and mortality. However, there are limited treatment strategies for prevention of disease onset and progression. Development of novel therapies for primary and secondary prevention of AF is critical and requires improved understanding of the cellular and molecular mechanisms underlying the AF disease process. Translational and clinical studies conducted over the past twenty years have revealed that atrial remodeling in AF shares several important pathophysiologic traits with the remodeling processes exhibited by hibernating myocardium that develop in response to chronic ischemia. These shared features, which include an array of structural, metabolic, and electrophysiologic changes, appear to represent a conserved adaptive myocyte response to chronic stress that involves dedifferentiation towards a fetal phenotype to promote survival. In this review, we discuss the pathophysiology of AF, summarize studies supporting a common remodeling program in AF and hibernating myocardium, and propose future therapeutic implications of this emerging paradigm. Ultimately, better understanding of the molecular mechanisms of atrial myocyte remodeling during the onset of AF and the transition from paroxysmal to persistent stages of the disease may facilitate discovery of new therapeutic targets.

No MeSH data available.


Related in: MedlinePlus

Surface electrocardiogram shows sinus rhythm (a) with organized atrial electrical activity and contraction following impulse formation from the sinus node. There is a one-to-one relationship between atrial (p wave) and ventricular depolarization (QRS) with normal electrical conduction. However, atrial fibrillation (b) is associated with rapid, chaotic atrial electrical activity with variable ventricular conduction. Intracardiac recording of atria (c) shows disorganized electrical activity.
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fig1: Surface electrocardiogram shows sinus rhythm (a) with organized atrial electrical activity and contraction following impulse formation from the sinus node. There is a one-to-one relationship between atrial (p wave) and ventricular depolarization (QRS) with normal electrical conduction. However, atrial fibrillation (b) is associated with rapid, chaotic atrial electrical activity with variable ventricular conduction. Intracardiac recording of atria (c) shows disorganized electrical activity.

Mentions: Atrial fibrillation (AF) is the most common sustained arrhythmia, affecting about 1% of the general US population [1]. It is an abnormal heart rhythm characterized by rapid, irregular, and heterogeneous atrial electrical activity that is associated with ineffective atrial contraction (Figure 1) [1]. There is variable and irregular conduction of atrial electrical activity to the distal electrical system and ventricles.


Cardiomyocyte Remodeling in Atrial Fibrillation and Hibernating Myocardium: Shared Pathophysiologic Traits Identify Novel Treatment Strategies?

Weil BR, Ozcan C - Biomed Res Int (2015)

Surface electrocardiogram shows sinus rhythm (a) with organized atrial electrical activity and contraction following impulse formation from the sinus node. There is a one-to-one relationship between atrial (p wave) and ventricular depolarization (QRS) with normal electrical conduction. However, atrial fibrillation (b) is associated with rapid, chaotic atrial electrical activity with variable ventricular conduction. Intracardiac recording of atria (c) shows disorganized electrical activity.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499626&req=5

fig1: Surface electrocardiogram shows sinus rhythm (a) with organized atrial electrical activity and contraction following impulse formation from the sinus node. There is a one-to-one relationship between atrial (p wave) and ventricular depolarization (QRS) with normal electrical conduction. However, atrial fibrillation (b) is associated with rapid, chaotic atrial electrical activity with variable ventricular conduction. Intracardiac recording of atria (c) shows disorganized electrical activity.
Mentions: Atrial fibrillation (AF) is the most common sustained arrhythmia, affecting about 1% of the general US population [1]. It is an abnormal heart rhythm characterized by rapid, irregular, and heterogeneous atrial electrical activity that is associated with ineffective atrial contraction (Figure 1) [1]. There is variable and irregular conduction of atrial electrical activity to the distal electrical system and ventricles.

Bottom Line: Development of novel therapies for primary and secondary prevention of AF is critical and requires improved understanding of the cellular and molecular mechanisms underlying the AF disease process.These shared features, which include an array of structural, metabolic, and electrophysiologic changes, appear to represent a conserved adaptive myocyte response to chronic stress that involves dedifferentiation towards a fetal phenotype to promote survival.In this review, we discuss the pathophysiology of AF, summarize studies supporting a common remodeling program in AF and hibernating myocardium, and propose future therapeutic implications of this emerging paradigm.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiovascular Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY, USA.

ABSTRACT
Atrial fibrillation (AF) is the most common arrhythmia and is associated with a high risk of morbidity and mortality. However, there are limited treatment strategies for prevention of disease onset and progression. Development of novel therapies for primary and secondary prevention of AF is critical and requires improved understanding of the cellular and molecular mechanisms underlying the AF disease process. Translational and clinical studies conducted over the past twenty years have revealed that atrial remodeling in AF shares several important pathophysiologic traits with the remodeling processes exhibited by hibernating myocardium that develop in response to chronic ischemia. These shared features, which include an array of structural, metabolic, and electrophysiologic changes, appear to represent a conserved adaptive myocyte response to chronic stress that involves dedifferentiation towards a fetal phenotype to promote survival. In this review, we discuss the pathophysiology of AF, summarize studies supporting a common remodeling program in AF and hibernating myocardium, and propose future therapeutic implications of this emerging paradigm. Ultimately, better understanding of the molecular mechanisms of atrial myocyte remodeling during the onset of AF and the transition from paroxysmal to persistent stages of the disease may facilitate discovery of new therapeutic targets.

No MeSH data available.


Related in: MedlinePlus