Hi Agustinus,

I really does not sure about my answers to fulfill your expectation. But there are various modalities for assessment of atrial remodelling;

1. ECG--simplest and most commonly used one

2. Echocardiography--used as a routine during clinical practice  

3. Computed tomography

4. Cardiac magnetic resonance imaging--by using DE-MRI--most valuable non-invasive technique, but has still many drawbacks

5. PET/CT--newer one

6. SA-ECG--ancient one

7. Histological examination---invasive technique

Hi Reynold, have you ever heard of CARTO3 electroanatomic mapping system? After positioning the navigating catheter into either left or right atrium, you can check activation maps and have an idea of wavefronts and depolarization phenomena of the entire chamber. Slow activation is a sign of remodeling.

Thank you very much for responding.

I have further question regarding your answer.

For non invasive modality such as ECG, ECHO, CT, MRI or PET, how could we differentiate that the atrial remodelling process already occur or not? Any atrial size enlargement was associated with atrial remodelling?

For CARTO 3, how could we differentiate between scarred tissue and true atrial remodeling?

Fibrotic areas do block conduction; in fact,  you see different voltage maps (scale of colours). Non invasive assessments cannot differentiate accurately.

You may consult an expert in Left Atrium volumetry such as Jørgen Tobias Kühl at Rigshospitalet, University of Copenhagen (ResearchGate member). His team uses a 320-CT scanner and some automated software for left atrium volumetry (Vitrea) designed in my company. for a multimodality comparison of LA measurement technique, you can check his recent paper: "Assessment of left atrial volume and function in patients with permanent atrial fibrillation: comparison of cardiac magnetic resonance imaging, 320-slice multi-detector computed tomography, and transthoracic echocardiography" (European Heart Journal – Cardiovascular Imaging (2014) 15, 532–540)

His team observed LA enlargment in the patient group.

open access: http://ehjcimaging.oxfordjournals.org/content/15/5/532

Thank you for the info Pascal. How could i contact Jorgen? do you have his email?

Why not using ResearchGate? search: Jørgen Tobias Kühl

Are you  interested in bed-side evaluation of the atria?

By surface ECG you can measure P-wave duration (and P-wave morphology in inferior leads) to identify (partial and advanced) Inter-atrial block.

it's simple and effective !

Let me know if you need further explanation

I think the easiest way to measure /detect atrial remodeling is by the size of the atria.

You can measure atrial volumes in Echo, cardiac MRI or CT

we prefer cardiac MRI.

You can see atrial volumes increase comparing paroxysmal, persistent and permanent atrial fibrillation with decreasing ejection fraction and you can even see decreasing volumes after successful therapy (e.g. ablation).

The exact measurement of fibrosis in the atrial myocardium is not at all easy

I think the goal is to measure the time course of recovery from one state to the other in respect to the atrial dimensions or volumes or P-wave duration after conversion of atrial fibrillation into sinus rhythm. Delayed recovery to normal states is due to electro-mechanical remodeling process and this can be improved using Ca++ antagonists or newly tested late sodium channel inhibitors (experimentally investigations). 

PS. Very interesting field of research.

"For non invasive modality such as ECG, ECHO, CT, MRI or PET, how could we differentiate that the atrial remodeling process already occur or not? Any atrial size enlargement was associated with atrial remodeling?"

It is possible to compare the volume of the atria, typically normalized by the body surface area, to various studies that have compared normal versus diseased populations.  However, you raise a significant point about how to differentiate between arrhythmia induced remodeling, and remodeling caused by other comorbidities, such as mitral valve regurgitation, hypertension, etc.  Because of the complex manner in which all of these factors intertwine, I don't think post-hoc attribution of causality is possible for any feature of atrial structural remodeling.  Fortunately, measurement of these features, e.g. fibrosis, or atrial volume, can help determine the best treatment options to pursue.

If you are looking for tools that can help you measure atrial volumes from image data, check out Seg3D.  It is a free image segmentation package that is quite stable and has releases for most major operating systems.  

"For CARTO 3, how could we differentiate between scarred tissue and true atrial remodeling?"

I am not certain what you are looking for here.  If a patient has an atrial arrhythmia (AF), and no prior ablation therapy, I would assume that any abnormal tissue is atrial remodeling.  If the patient has previously undergone an ablation procedure, then there may be a difference between scarred tissue, and remodeled tissues.  If you are interested in trying to classify these tissue types, I would look at work that has been done with voltage mapping.   Marchlinski et al. looked at the amplitude of intracardiac electrograms as a means of classifying different types of cardiac pathology.  Their work has largely focused on ventricular scarring, but I would start there anyway.

Good luck!

http://sci.utah.edu/cibc-software/seg3d.html

http://circ.ahajournals.org/content/101/11/1288.short

The easiest way to detect atrial remodelling is with ECHO, however there are several measurements that can be found in the literature, which somehow denotes relatively low sensitivity and reproducibility. The following measurements can be done: LA diameter, LA volume, improvement of LA function (LA emptying fraction), LA global longitudinal strain.

Experimentally seems somehow easier to detect remodeling using atrial monophasic action potential recordings. 15 min tachypaced atria led to significant shortening of the atrial action potential and refractoriness, facilitating the inducibility of atrial tachyarrhythmias. In clinical settings all parameters that may indicate deranged atrial wall contractility post a longstanding AF episode are certainly useful.

The major question is the molecular mechanisms involving membrane and intracellular ion channels in electro-mechanical remodeling. For example the role of L-type Ca++ induced K+ channel activation resulting in action potential abbreviation and Ca++ mediated afterdepolarizations.

thank you very much for answering my question. You have given me great advices. If you do not mind, i would like to ask a couple of question related with suggestions :

To Isaac Aidonidis : Your suggestions were good. My question is, should we ask the patient to undergo EP sinus node function test or EAM ? and my other question, how can we analyze the cellular mechanism these channel?through biopsy or animal study?

To Joshua Blauer : Thank you for the software links. My following question Is it applicable only for non invasive or invasive? in my country ( i am in south east asia country), mostly i use echo assessment

To March Bracht : Thank you for your advise. I would like to know more, In using MRI, do we need to contrast ? How to interpret that MRI assessment? should we have to attend and finished the course before doing it? Is there any opportunity for me to do the course?

Thanks