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Unifying Theory of Atrial Fibrillation

“Rotors are just a way of thinking about and visualising reentry. There is nothing magical or unusual about rotors…the concept of a rotor is just a biophysically more realistic concept of what maintains reentry; you can get multiple circuit reentry in a pure rotor based model.

First of all, if you take a pure mathematical model of the atrium that ‘s highly realistic and induce reentry, which you can do easily, it’s a rotor. It’s not a leading circle in terms of what it looks like and what determines it. It’s a rotor.

If you have something that stabilises the rotor such as a large refractory gradient -which we can reproduce mathematically with acetylcholine distribution or probably what happens with vagal AF – you get stabilisation of a rotor and you can get AF with a single rotor maintaining it.

If you have an anchoring factor, like fibrosis presumably, or something like that, you can get a much more stable rotor. If you don’t have any of those things you need a very big substrate, and when you have a very big substrate then you can reach a situation where you don’t have stable rotors but the rate of rotor production and destruction (balances) –  when a rotor hits a barrier you get two daughters counter rotating rotors which annihilate each other; if the substrate is large enough the rate of daughter rotor formation and daughter rotor annihalation becomes sufficiently equal that you constantly maintain  enough rotors to maintain AF even though none of them are longstanding.

That’s all conceptual.

How that relates to patients with long standing AF or long standing persistent AF I think is that you have factors that anchor the AF in terms of local fibrosis, maybe anatomical features, less likely functional properties, and so you have some degree of stability of rotors and some combination of rotor production and rotor degradation.

The real question, and frankly speaking the disagreement between Sanjiv and Michel and Pierre as i see it, is how stable those rotors how are whether they really are relatively stable enough in space that they last for a long time and you can eliminate them or whether they are less stable but they stay in a relatively constant region.

I think in the end the differences between them are not really so large. It’s just a question of whether you see a single rotor in a region remaining absolutely stable over time, or a region as much more likely to harbor rotors and therefore more rotors sit there. In the end the two ideas may actually converge and come down to the same thing.


From Stan Nattel, discussing rotors and AF at HRS in ?2015.

Notes from Josephson: Indicators of High Risk AV Block

Scraps of paper from years ago. EP is probably under-utilised in the diagnosis of syncope.

This was entitled, ‘Indicators of High Risk AV Block’

  • HV > 80 ms with symptoms
  • HV > 100 ms with/without symptoms
  • alternating BBB with ∆HV
  • block below the His with incremental atrial pacing CL > 400 ms
  • exaggerated ↑HV with procainamide, flecainide etc.

Paroxysmal AV Block

In the setting of a normal resting 12 lead ECG: 

  1. Vagal: PP slows, or PR increases before or around block – pacing may stop you fainting (1, 2 ,3)
  2. Idiopathic: no change in PP or PR interval – pacing will stop you fainting (4)
  3. IntraHisian disease: PAVB begins with a pause (PAC or PVC) – pacing will stop you fainting and may save your life (5, 6)
  1. Brignole, M., Menozzi, C., Moya, A., Andresen, D., Blanc, J. J., Krahn, A. D., et al. (2012). Pacemaker therapy in patients with neurally mediated syncope and documented asystole: Third International Study on Syncope of Uncertain Etiology (ISSUE-3): a randomized trial. Circulation125(21), 2566–2571. doi:10.1161/CIRCULATIONAHA.111.082313
  2. Brignole, M., Donateo, P., Tomaino, M., Massa, R., Iori, M., Beiras, X., et al. (2014). Benefit of pacemaker therapy in patients with presumed neurally mediated syncope and documented asystole is greater when tilt test is negative: an analysis from the third international study on syncope of uncertain etiology (ISSUE-3). Circulation: Arrhythmia and Electrophysiology7(1), 10–16. doi:10.1161/CIRCEP.113.001103
  3. Sutton, R., Ungar, A., Sgobino, P., Russo, V., Massa, R., Melissano, D., et al. (2014). Cardiac pacing in patients with neurally mediated syncope and documented asystole: effectiveness analysis from the Third International Study on Syncope of Uncertain Etiology (ISSUE-3) Registry. Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology16(4), 595–599. doi:10.1093/europace/eut323
  4. Brignole, M., Deharo, J. C., De Roy, L., Menozzi, C., Blommaert, D., Dabiri, L., et al. (2011). Syncope due to idiopathic paroxysmal atrioventricular block: long-term follow-up of a distinct form of atrioventricular block. Journal of the American College of Cardiology, 58(2), 167–173. doi:10.1016/j.jacc.2010.12.045
  5. Lee, S., Wellens, H. J. J., & Josephson, M. E. (2009). Paroxysmal atrioventricular block. Heart Rhythm : the Official Journal of the Heart Rhythm Society, 6(8), 1229–1234. doi:10.1016/j.hrthm.2009.04.001
  6. el-Sherif, N., & Jalife, J. (2009). Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers? Hrthm, 6(10), 1514–1521. doi:10.1016/j.hrthm.2009.06.025 

Pauses. Mechanism?

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All you need to know

For the diagnosis:


It may have been epilepsy…

It may have been epilepsy, but I’d like to see the ECGs.

“In a tragic mirroring of his father’s death, Hugh drowned in 2000 when he had an epileptic seizure while fishing. Kate said the family always believed Kenneth had suffered from undiagnosed epilepsy and had drowned after a seizure. Elisabeth Mackenzie, now 77, lives in northern NSW.”

“Letter from the heart inspired Mackenzie’s ‘nearly perfect’ novel”

August 17, 2013

The Australian (sub required)

Would you place a pacemaker?

I am reporting Holter recordings this evening. This patient was referred for tachycardia – no history of syncope to my knowledge.

My questions:

  • where is the block
  • would you place a pacemaker, ignore this asymptomatic finding, or perform an EPS?

AV Block


My first observation is that this occurs during waking hours. All sorts of funny business happens at night which can be ignored in the absence of symptoms.

My second observation is the presence of a narrow QRS – confirmed on the 12 lead ECG. Therefore block will be either intraHisian or AV nodal.

The third observation for the ‘dropped p wave’ in the upper panel is that the difference between the longest PR interval and the shortest PR interval is < 100 ms. In AV nodal block the difference is usually > 100 ms.

The last observation is that the conducted p waves on the lower panel during 2:1 AV block have PR intervals ~ 200-210 ms. The PR interval is usually > 200 ms in AV nodal block. Intervals < 160 favour infranodal block.

Therefore it is unclear if the block is in the AV node or His bundle. I would perform an EP study with careful attention to placement of the His catheter. It should be drawn back as far as possible so as not to miss a split His. If HV ≥ 100 ms – PPM; symptoms and an HV ≥ 80 ms: PPM; block during incremental (not burst!) atrial pacing at cycle lengths ≥ 400 ms: PPM.

35 yo male with syncope (or victory of the physical examination!)

This young man presented to emergency with syncope. He was walking up a slight incline, became dizzy and lost consciousness. His rhythm in hospital was sinus, a TTE showed normal left and right ventricular function with no valvular heart disease, and normal pulmonary pressures. A CTPA was negative. What would you do next?

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I did not mention some important information. I examined him on the day of admission and noted a loud P2 (palpable when sitting forward). On the basis of the ECG and physical examination I diagnosed pulmonary hypertension but was surprised that the pulmonary pressures were normal on TTE.

A couple of weeks later he presented to my rooms. Doubting the original diagnosis I repeated the TTE and obtained a TR jet suggesting pulmonary pressures of at least 60 mmHg. This was confirmed on a right heart catheter and the final diagnosis after further investigation was primary pulmonary hypertension.

The physical examination remains important, and not all syncope is arrhythmic.

75 year old lady with vertigo

I saw this lady because of her abnormal ECG. For many years she had suffered ‘vertigo’, variously diagnosed as an inner-ear problem. She had in fact been admitted to hospital on one occasion for 4 weeks and discharged on prochlorperazine for ‘vestibular neuronitis’.

At the time of my review she was symptom free and in normal sinus rhythm.

She carried an ECG from a time when she was symptomatic, and the rhythm was identical to that during her extended hospital stay (pictured).

What do you think this rhythm is?


Wenckebach or is it?

Here is an interesting case of apparent Wenckebach…or is it? I would appreciate your help on this one. A recognised form of heart block?


Update: This strip shows a Wenckebach pattern with increasing PR intervals before block. The point of interest is the second blocked P wave at the end of the Wenckebach cycle. I do not know the mechanism of this. But this patient has a PRKAG2 mutation associated with severe conduction disorders of the AV node (± preexcitation ± hypertrophy).