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Posts Tagged ‘atrial cardiomyopathy’

(This is supposed to be a poll. Sorry, readers, you can’t select the answer. WordPress is not kind enough and suddenly made the poll service payable extra. I am already paying nearly a $100 fee to maintain this site. I can’t afford any more.)

We have been taught Bi-Atrial enlargement is the rule in AF .It is still true in most situations. But, we rarely dispute it , & ask which atrium dilates more in AF ?

Let us see few factors.

  • Both atria develop from a combination of the primitive atrium, sinus venous, and pulmonary veins.It is logical to presume there must be a hidden morpho-electrical continuity.
  • The baseline RA dimension is a few mm more than LA. Further, it is thin-walled, more compliant and can distend depending on volemic status.
  • When atrial fibrillation (AF) begins, it can start with a single focus, degenerating to multiple wavelets, and it spreads throughout the entire surface area of both atria. A fibrillatory wave that occurs at a rate of more than 600 beats per minute can cause fatigue in the long run, leading to atrial dilation.
  • In all probability, this dilation is a form of atrial tachycardia and atrial cardiomyopathy. However, underlying lesions such as hypertension, mitral valve disease, COPD, ASD, and TR greatly influence the degree of atrial enlargement.
Spatial relationship of sites for atrial fibrillation drivers and atrial tachycardia in patients with both arrhythmias July 2017 International Journal of Cardiology 248(3)
  • AF begets AF. This is similar to MR begets MR. Atrial functional MR occurs when the lower part of the atria stretches the mitral annulus. It is important to recall that a small area of the posterior aspect of the LA is a part of the mitral valve apparatus. Therefore, AF begetting MR and MR begetting AF should not be considered a funny rhyme, but rather a realistic possibility.
  • Histopathological specimens of atrial tissue in chronic AF can present with surprising results. The atrial muscle can be entirely normal, or the interstitium can be infiltrated with lipids, fibroblasts, amyloid, etc.
  • Regarding the issue at hand, it is widely known that in cases of mitral stenosis with AF, the left atrium (LA) is larger than the right atrium (RA) due to the obvious reason that the baseline LA was larger at the onset of AF. However, in cases of lone AF, AF in hypertension, or chronic AF, both atria tend to dilate equally..

Implications for electrophysiologists.

In contrast to other tachycardias, with atrial fibrillation (AF), the focus is often speculative, and ablation attempts are made accordingly. Pulmonary veins have been the primary target for ablation for many years, yet the success rates remain inconsistent. To determine if the AF focus is non-pulmonary venous, such as right atrial, septal, or involving the inferior vena cava (IVC) or superior vena cava (SVC), several techniques are employed to provoke and localize these non-pulmonary vein triggers

Localized atrial fibrosis and interatrial blocks can result in differential fibrillatory counts across the atria. (RA fib-rate can be more than LA, and vice versa.) Is there proof for this, or just an academic gossip? We know atrial flutters can be confined to one atrium. (Pierre Jaïs Circulation 2000) When such flutters transform into fibrillation, how does the spillover of signals occur to the contralateral atrium? On a personal note, we have recorded good E & A Doppler signals across the tricuspid valve, in RHD mitral stenosis, and AF. No published proof as such. I strongly suspect the right atrium can resist the tsunami of approaching fibrillatory waves from engulfing its chamber in at least some patients. An appeal to the new generation EPs who have special flair in AF should look into this and either prove or disprove it.

Final message

My answer to the question is either D or E. Atrial size in AF is not a trivial thing to ignore. This question pushes a simple idea. In primary or lone AF, just by having a look at the RA to LA size ratio, one might get a reasonable guess,about the Initial focus, trigger & pathology of the AF.

A request to all the high profile stake holders involved in the science of PV ablation (either with Ice or fire). Think about all the possible right-sided or septal focuses, before going overzealously for the jugulars of Pulmonary veins, especially if the RA significantly larger than LA . This will save time, effort & of course our reputation.

References

Nil

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A brief learning session with cardiology fellow about a possible new concept in Left heart failure.

What is the commmest cause for acute pulmonary edema?

Left sided heart failure”

“Can you be more specific , Left sided means ?

“I meant LV failure , typically DCM of any cause or Severe un-controlled HT”

“Ok .good. Does Left Heart failure include mitral valve dysfunction also ?

“Yes sir, very much. Classical mitral stenosis and Isolated MR can cause pulmonary edema. In fact, acute AR Iis also part of left heart disease”

So far, so good, now coming to the complex part of left heart

Can LA fail in isolation independent of LV , ie I mean with normal Left ventricle ?

I am not sure. Can we call new onset atrial fibrillation as a primary atrial failure that can result in pulmonary edema?

Excellent. You are absolutely right. But I am talking about mechanical atrial failure, not electrical. Are you aware that most of the time AF is a well tolerated arrhythmia , it can even be silent in many cases. This is because the pumping function of the atria contributes only 20-25% to LV filling. This can easily be compensated by augmented LV suction force , provided the baseline LV function is normal.

Have you heard about ACM. Atial cardiomyopathy?

“No sir”,

“You will hear more about it soon” (Ref 1) Scientists, especially Echo guys are closing in on this concept. We know, the atria has three functional components, namely conduit, reservoir, and pumping. Curiously, we have realized that the pumping function of LA may not be that critical from indirect observations from some land mark studies . (Rate control vs rhythm control studies in AF are a powerful proof on the atrial pumping function .(AFFIRM/RACE etc ) I don’t know, whether I am right in saying the above statement.

It is tempting to conclude , only if all the three functional components of atria gets affected , then only primary atrial dysfunction can be diagnosed. The concept is more complex than we realise. In diastole , pulmonary vein, LA , LV all work as single functional unit. Only in systole, we see them as different things.

Atrial DCM

Like LV systolic function, which is coupled with RV in parallel , LA function is closely knitted to LV in series during diastole. The key to suspect or diagnose this entity is to demonstrate dissociation of LVEDP with LA mean pressure & PCWP. This is not an easy job in bedside. Isolated Increase in LA volume without any reason , is one clue. LA ejection fraction is possible marker. (Kanagala P, . Int J Cardiovasc Imaging. 2020)

Final message

We are in the early days of understanding primary atrial mechanical failure, Atrial cardiomyopathy (ACM) or atrial DCM is being proposed as separate entity. It is very likely, some subsets of HFpEF might turn out to be primary atrial disease, depending on the level of investigation we do.

Reference

1.Li M, Ning Y, Tse G, Saguner AM, Wei M, Day JD, Luo G, Li G. Atrial cardiomyopathy: from cell to bedside. ESC Heart Fail. 2022 Dec;9(6):3768-3784. doi: 10.1002/ehf2.14089.

2.Patel, R.B., Lam, C.S.P., Svedlund, S. et al. Disproportionate left atrial myopathy in heart failure with preserved ejection fraction among participants of the PROMIS-HFpEF study. Sci Rep 11, 4885 (2021). https://doi.org/10.1038/s41598-021-84133-9

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