The epicardial fat pad image on chest x-rays was long regarded as nothing more than a barely interesting incidental finding of no clinical importance. That no longer appears to be the case.
The epidemiologic data having established a sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes, and more recently detailed scrutiny of the role or roles of epicardial fat to which has been assigned the ironic designation, of EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.
At least as early as 2003 cardiac fat acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.
Now EAT is accused of playing a role in the genesis of AF.
Dr, Mahajan and co-workers from Australia studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left atrium adjacent to EAT.
Author quotes:
" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "
"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"
1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.
2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128
The epidemiologic data having established a sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes, and more recently detailed scrutiny of the role or roles of epicardial fat to which has been assigned the ironic designation, of EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.
At least as early as 2003 cardiac fat acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.
Now EAT is accused of playing a role in the genesis of AF.
Dr, Mahajan and co-workers from Australia studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left atrium adjacent to EAT.
Author quotes:
" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "
"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"
1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.
2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128
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