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Archive for the ‘Atrial fibrillation’ Category

Who can answer this unusual query in mitral stenosis?

Posted in Atrial fibrillation, Mitral stenosis, Uncategorized, tagged , , , , on December 20, 2022|

I will go with the last response. As for as I understand, we have never quantified Atrial muscle mass properly even in normality. One may be tempted to think there is no purpose to measure it, other than academic reasons. The fact that the incidence of atrial fibrillation in mitral stenosis is not linearly correlating with LA size makes us think, LA mass (Virtual LAH) may have a say in triggering AF.

This post is meant for cardiology fellows. Maybe someone can do a study on this by measuring LA mass pre and post-PTMC, we might get an idea about regression as well. Meanwhile, we are well versed with infiltrative diseases like atria like amyloidosis that can mimic LAH. Currently, we realize fatty infiltration of LA is the common trigger for AF in varied populations.

By the way, readers are welcome to post any specific formula to measure LA mass if they come across .

Reference

A good review of LA anatomy.

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Why “Isolation of pulmonary veins” and “Arrest of AF” may turn out to be two different events !

Posted in Atrial fibrillation, Uncategorized, tagged , , , , , , , , , on August 19, 2022|

AF is not only the most common cardiac arrhythmia,it is also an extensively researched entity in cardiology literature. We are trying to rein in, this arrhythmia for the past three decades with multiple strategies. Drugs, pacemakers, ICDs devices, surgical cuts, RF catheters, and the latest technique is trying to frostbite the atrial electrical circuits with ICE. ( Karl-Heinz Kuck,N Engl J Med 2016 )

It is believed that up 60% of AF originate from pulmonary veins. What does it mean?  So, when we blindly suggest PV Isolation routinely for all PAF,  there is 40% futility straightaway! Apart from the hugely variable anatomy of the pulmonary veins, there are prohibitive levels of recurrence due to  PV reconnections. Maybe, will find new technical solutions as we are now moving in 2nd or third generation cryo balloons, 4D imaging, contact force sensing, etc. But let us not forget there are other sources of focal electrical activity too  

Importance of non-PV ectopic beats initiating  AF(Ref 1,2)

  1. Superior vena cava (SVC),
  2. left atrial posterior free wall (LPFW),
  3. LA appendage
  4. crista terminalis (CT),
  5. coronary sinus ostium (CSO),
  6. Ligament of Marshall
  7. Interatrial septum (IAS) 

Ablation or no ablation, we need to reflect on two things in the management of AF.

1. AF can be triggered by totally different mechanisms like intermittent hypoxia, adverse electrolytic flux, diffuse atrial interstitial pathology or amyloid, etc. Before calling the appointment desk of the EP guy’s office please rule out all the systemic causes. This could be your last (lost) chance to save the atria from pulmonary burns.

2. This one is more important. Read carefully. It is not a divine protocol that demands us to restore sinus rhythm in all patients with AF. There is an excellent knowledge base, backed up by wonderfully done studies. (Need not mention the trial name, I think) that should effectively neutralize our compulsive &  misplaced urge to bring back sinus rhythm in all chronic AF.

With respect to the overall outcome, It hardly matters whether you treat the AF by rate control or rhythm control. While there is major technological leap in our fight with AF.It is heartening to know simple measures like regular exercise can control or reverse AF by atrial fatty mass regression.

Final message

We have played with fire for quite some time within the innocent lesser chambers of the heart  (RF ablation) and burnt our reputation considerably. Now, silently we have decided to fall for a more friendly weapon ICE. But we must remember our obsession with the pulmonary vein as the only source of initiation of AF is essentially flawed. Further, all these hyper-technology-based combat of AF is indicated only in a fraction of our patients (Maybe 5-10%) 

Reference 

1.Chen SA, Tai CT, Yu WC, Chen YJ,  Right atrial focal atrial fibrillation: electrophysiologic characteristics and radiofrequency catheter ablation. J Cardiovasc Electrophysiol. 1999 Mar;10(3):328-35. doi: 10.1111/j.1540-8167.1999.tb00679.x. PMID: 10210494.

2.Lin, Wei-Shiang, et al. “Catheter ablation of paroxysmal atrial fibrillation initiated by non–pulmonary vein ectopy.” Circulation 107.25 (2003): 3176-3183.

Postamble

If you think this write-up is too biased, please read the CABANA trial fully before ditching this post into the dustbin.

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In AF why the ventricular rate is irregular?

Posted in Atrial fibrillation, Cardiology Patho physiology, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , on January 14, 2022|

Here is a case report from Dr. Brugada’s group. What is your diagnosis?

Source & Courtesy Sergio Richter, Joseph Brugada et all , 100(1), 154–156. doi:10.1016/j.amjcard.2007.02.067

Whoever diagnosed AF in the above ECG need not feel bad. The rhythm is not AF, though it mimics very closely. In cardiology, especially in electrophysiology, we can get surprises on a daily basis. (Read below)

Why the ventricular rate is irregular in AF?

Atrial fibrillation (AF)  may sound like a  simple clinical arrhythmia until we ask this delicate question. The traditional and fairly accepted answer is that, AV node with all its collective decremental property filters the incoming atrial impulses (Which varies 400-600/mt) in a random fashion and allows only about 1/3rd of impulses. So, technically it is  AV block of various degrees that makes the ventricular response irregular.

Any other explanation possible?

How about AV node playing out a silent game with Atria, deciding to block everything and start its own fast escape rhythm, rather than leaking out selectively atrial impulses. Some think this is fictional, some others feel it can be real too. When this happens it can be referred to as irregular junctional tachycardia or AF with varying AV blocks. It has been tough, to prove it is only the atrial impulses penetrating through the AV node complex and exiting on the ventricular side unscathed?

Understanding AV node is not easy 

AV node morphology and function still remain a mystery.( Katritsis DG.  Arrhythm Electrophysiol Rev. 2020)The AV node shows huge variation in its size, shape, orientation with LV long axis and AV plane in short axis. The approach to slow pathways with multiple inferior nodal extensions makes a dual (or even poly ) AV pathway in any human being real. How common is dualism or multilateralism within the AV node in the general population? (More than 30-40 % ?) . Let us also mind the traffic in this busy & complex AV flyover can change on a moment-to-moment basis based on neurohormonal and autonomic tone.

Any tachycardia can become irregular if the AV node wishes so !

Though rare ,multiple physiological splits in the AV node make it possible for a single atrial impulse can generate 2 or 3, even more, ventricular impulses. (1: 2 or 3  AV conduction) Since these pathways are dynamic they can make the ventricular response irregular as well (Unlike the regularly coupled Echo beats in classical AVNRT substrate ). Hence, any supraventricular tachycardia can masquerade as AF if AV nodal pathways decide to split and share the impulses this way. It is also interesting to note there has been a documented link between AVNRT and AF (.Ref 2) . Also, adenosine-induced AF is known (James E. Ip et al Circulation: Arrhythmia and Electrophysiology. 2013;6:e34–e37)

Final message

Irregular RR interval with absent/or invisible P waves is not always AF. It can be due to the aberrant behavior of the AV node.( anatomical or functional) It is termed Pseudo Atrial fibrillation as in the above case report. Why do we need to be aware of this entity? We need to be cautious, as any overzealous efforts to ablate the pulmonary veins in such patients will go in vain.

Reference

1.Sergio Richter; Antonio Berruezo; Lluis Mont; Tim Boussy; Andrea Sarkozy; Pedro Brugada; Josep Brugada (2007). Pseudo–Atrial Fibrillation, Rare Manifestation of Multiple Anterograde Atrioventricular Nodal Pathways. , 100(1), 154–156. doi:10.1016/j.amjcard.2007.02.067 

2.Schernthaner C, Danmayr F, Strohmer B. Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias. Med Princ Pract. 2014;23(6):543-50. doi: 10.1159/000365418. Epub 2014 Sep 3. PMID: 25196716; PMCID: PMC5586929.

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A presentation on atrial fibrillation : Old wine in Old bottle

Posted in Atrial fibrillation, tagged , , , on December 12, 2021|

Link to PDF download 

Good news: Nothing much has changed since 2008

  • Recognizing the clinical importance of AF and the need to rule out a systemic cause is the key, Further, a genuine bedside debate about the pros and cons of simple vs aggressive treatment discussion is welcome.
  • The nomenclature issue of valvular vs non-valvular has finally seemed to have settled. The latter is banished for good reason. (Funny to note Aortic valve  was considered as not a valve for  so long !)
  • The rate vs rhythm control debate still favors the former. (AFFIRM/RACE)
  • Stroke prevention is the concern  &  anticoagulation is the mainstay. OAC/DAPT /triple therapy has evolved a little more in the last decade. Though stoke is a major concern, we rarely see neurologists & cardiologists debate closely on risk profiling issues of such patients. (at least in this part of the world.)
  • Whether we have conquered AF or not we have become experts in creating an unlimited number of bleeding risk scores. Understanding and applying them at the bedside need special memory and expertise.
  • On the combative front, ablation strategies, however, advanced they look, are vested with the risk of injuring the surrounding structures. My biased opinion is that the risks are prohibitive except in very refractory and troublesome AFs. (with all these 4D, contact, cryo, etc)  Recall the CABANA study. We are beginning to understand, the true embryological face of pulmonary veins insertion points is so variable, and residual sleeves are very rampant that will sustain the AF even after an apparently successful ablation.
  • LAA appendage closure studies again don’t look rosy as the device itself is prone to thrombus at least in the early periprocedural period. (Watchman requires more security and protection than the Inmates !)

Final message 

AF is a simple arrhythmia in 9/10 patients. Please, let us not complicate it. We must ensure, systemic and non-permanent forms of AF should not drain our cardiac resources. We shall follow basic principles of managing a cardiac arrhythmia that will suffice in the majority. An occasional patient needs to be referred to an EP specialist.  

A new look at AF risk estimation for stroke

doi:10.1001/jamacardio.2021.3709

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Why AF is often well tolerated in Hypertrophic cardiomyopathy ?

Posted in Atrial fibrillation, tagged , , , , , , , on November 29, 2020|

Up to 25 % of LV filling is done by atrial contraction. Atrial booster function is important in LV outflow lesions. This can be critical in patients who have diastolic deformities of LV. ( an audible or even palpable S4 confirms the atrial kick in these situations )  This is how we were taught for decades right. Still, it may hold good in many left-sided condtions, but in HCM it definitely seems to be not true. 

A succinct review of this topic makes a good read.

Incidence if AF in HCM is about 20% (Mostly paroxysmal 70 % , Persistent /Permanent 30 %)

Mechanism of AF IN HCM

  • Increased atrial wall strain(Proven by strain echo studies)
  • Atrial dilatation
  • Atrial pathology (Atrial myocyte  disarray,  myosin is present in atria too. )
  • Unrelated to HCM (SHT etc)

We can confirm with large observatory data, left ventricle handles AF so well. (Ref 1)The onset of AF, (at the least), is, expected to cause some new worsening dyspnea. Even that is not universal (very surprising isn’t it ?)

Does AF correlate with syncope?  again no is the answer. So it’s the LV outflow behavior that determines the hemodynamics not what is happening at the inflow. Even hard outcomes like heart failure, sudden death, net mortality was not found to be altered much by the lesser chamber fibrillation. But, the only issue relevant here is thromboembolism that has to be taken care of.

How is that AF make little hemodynamic Impact in HCM ?

It is difficult to comprehend this scenario. For this to happen the mean LA pressure should remain within the physiological range even when the atria goes to fibrillation. But it seems distinctly possible as many patients with HCM are not aware of this arrhythmia. The LA pressure-volume loop is an enigma. It is likely LA “v” wave loop can adjust to “a” wave deficiency in an exemplary manner.

Further, the hyper-contractile left ventricle can assist itself by sucking blood in very late diastole (to be precise with the onset of systole )and so it need not really depend on the atrial kick.  A similar phenomenon explains the persistence of presystolic accentuation in the murmur of mitral stenosis. The fact that rate control in AF is able to compete with rhythm control in  AFFIRM/RACE study vouch for the negligible hemodynamic impact between SR/AF.

Clinical implication

  • A well-tolerated AF doesn’t preclude the need for thromboprophylaxis. We must ensure  NOAC/Warfarin in all those with persistent AF.
  • Attempts to convert AF to sinus rhythm with all those Invasive LA mapping and Pulmonary vein is unwarranted if not contraindicated.
  • When ICD is indicated additional  Atrial leads to reduce AF is again becomes reductant. 

Final message

Many of the hemodynamic concepts we have learned over the years could be based on logical perceptions that may not manifest at the bedside. Constant flux in our understanding of cardiovascular physiology is required. 

Reference

1.Rowin EJ, Hausvater A, Link MS, Abt P, Gionfriddo W, Wang W, Rastegar H, Estes NAM, Maron MS, Maron BJ. Clinical profile and consequences of atrial fibrillation in hypertrophic cardiomyopathy.Circulation. 2017; 136:2420–2436. 

 

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How to assess diastolic function in patients with atrial fibrillation by Echocardiography ?

Posted in Atrial fibrillation, tagged , , , , , , , on October 23, 2019|

Assessment of LV diastolic function primarily depends on the Doppler flow profile across the mitral valve and also to be noted are the 2D features of LA and LV for associated abnormality like LVH, LAE etc.

Why diastolic dysfunction assessment difficult in AF ?

Since most diastolic doppler mitral inflow parameters involve analysis of atrial contraction A wave, atrial fibrillation makes it difficult to assess diastolic dysfunction. Since we have only early diastolic velocity to assess, the changes confined to this E velocity is of paramount importance. This E velocity again is subjected to cycle length dependent alteration in both its acceleration and deceleration time , making things still more complex.

However, the following features help diagnose diastolic dysfunction in AF

  1. Lack of significant  E velocity variation (<20%)  Inspite of significant RR interval change.(This implies mean LAP is kept high irrespective of cycle length suggesting elevated baseline LAP)
  2. E deceleration time (<140ms) (In long cycle)
  3. Propagation velocity in color M Mode(Vp)  <45cm/sec might help (RR interval dependent, measure in the long cycle)
  4. E/e” in a single beat by dual doppler probe (Ref 1)  > 10 indicate diastolic dysfunction that correlate with PCWP> 15mmhg (Ref 1)
  5. Finally (and curiously ) presence of AF by itself may imply significant LV diastolic dysfunction. It could be due to an increase in atrial strain and afterload of LA (ie pre A-LVEDP) (Of course, It should be in the absence of mitral valve disease)
  6. LA dimension in AF*

*LA dimension is a very good sign of chronic elevation of LAP and diastolic dysfunction in the absence of mitral valve disease. However, AF can dilate the LA making it a less useful parameter. But, it should be noted in AF both RA and LA dilate together.So,  a disproportionate LA>RA (or if RA is normal size ) could still be a marker of baseline LV diastolic dysfunction.

 

Reference

  1. Kusunose K., Yamada H.,  Nishio S., et al.  Clinical utility of single-beat E/e′ obtained by simultaneous recording of flow and tissue Doppler velocities in atrial fibrillation with preserved systolic function. J Am Coll Cardiol Img 2009 2:1147–1156

 

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Pulmonary vein isolation in AF : Seems, it’s Just not adequate !

Posted in Atrial fibrillation, pulmonary vein ablation, rf ablation, tagged , , on August 21, 2015| 2 Comments »

A land mark concept , that changed our understanding about the mechansim of genesis of Atrial fibrillation happened  in the year 1998 .( Haïssaguerre ,Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins N Engl J Med 1998; 339:659-666). He proved AF originates in specific focal points from the pulmonary vein ostia at its draining point in LA.Even though there only few selected focal points it was difficult identify those and hence empirical RF ablation of all 4 pulmonary vein became a standard practice. 100s of thousand of these invasive procedure were carried out in patients with chronic AF.

Now, in a span of 10 years , we realise many of these patients require second or third siting of ablation.The irony is , there are many non pulmonary connections  that require repeat ablation.

Common mechanism for recurrences are

  1. Inadequate first ablation
  2. Reconnections
  3. Inflammation and fresh scars
  4. Additional venous focal  sites (coronary sinus  ,SVC, Vien of marshall)
  5. Multiple mechanisms /*Non- focal , systemi AF mediated by neurohumoral triggers ?

A study from the prestigious JCE in May issue of 2015, reveals a starling fact , that about 50% of AF patients  have additional connections  other than pulmonary vein that require ablations at a future date.

If proven right ,  just wonder how much of knowledge and its dissemination  , efforts from  EP industry , technology transfer  over the years is threatening to become redundant .Let us hope,we will somehow conquer the AF either electrically or pharmacologically.

pulmonary vien ablatioan atrial fibrillation carto non pulmonary vien connection

A strong message comes out from this. In modern science, one need not be unduly excited about a new breakthrough.Proof of concept will have to overcome the ultimate test , ie time .

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Atrial fibrillation during STEMI : Don’t get alarmed

Posted in Atrial fibrillation, Infrequently asked questions in cardiology (iFAQs), tagged , , on February 25, 2015| Leave a Comment »

Atrial fibrillation is the most  common arrhythmia we encounter in clinical cardiology .Ironically it is  uncommon during ACS and extremely rare in association with UA/NSTEMI. Surprisingly , an entity ” Ischemic AF” is not to be found in cardiology literature.

The incidence of AF in STEMI is less than 5%. Occurs more often due to factors other than primary ischemia of atrial musculature. Of-course , AF in association with Infero posterio MI and RVMI is an important trigger for AF.LCX disease is more often associated with AF as it gives up a consistent branch to left atrium.

Though it is tempting to implicate ischemia as a trigger for AF ,most often it occurs , in elderly ,associated COPD ,hypoxia preexisting atrial disease .Acute elevation of LVEDP and stretch of left atrium could be a more logical mechanism.

Hemodynamic impact

  • AF can bring down the blood pressure.
  • Worsen ischemia by increasing the MVO2
  • Could be very destabilising in RV infarction
  • Surprisingly it is well tolerated in many STEMI patients.

AF in STEMI- Is it an emergency  ?

It would appear so. But , if hemodyanmicaly stable one need not panic.Many times they are transient .Correcting  hypoxia, optimizing beta blocker would help.

Role of DC Shock  , Precautions before shocking  & Post shock events

  • DC shock is done only if there is hemodynamic instability  or ongoing ischemia .(Very difficult to rule out the later )
  • Mural LV clots can form even within 24 hours and DC shock embolic strokes may ensue .
  • Hence it is mandatory to do an echocardiogram prior to shocking.

Drug of choice

  • Betablocker
  • Class 1c -Flecanide.
  • Class 3 -Amiodarone./Ibutilide/

Role of Digoxin

There used to be a concern about usage of Digoxin in the setting of ACS as it pro-arrhythmic , but it remains useful in the management of AF .There is no other  anti-arrhymic drug available to control, the heart rate without depression of  the LV  function

Rate control vs rhythm control

Always aim for rhythm control in the setting  of ACS.Rate control is may not be a  logical concept in acute settings though Amiodarone does both.

Wide QRS Atrial fibrillation

As we know , AF in STEMI can conduct with aberrancy , and we have a traditional teaching all wide qrs tachycardia are VT in the setting of MI making our patients statistically vulnerable.

After all , both entities lack discernible p waves. At high rates it may be difficult  to identify irregularity  RR interval. However , one would shock such patients  and both AF and VT would respond .All is well that ends well.

Summary

AF during STEMI is a risky arrhythmia and needs urgent intervention , but one need  not be alarmed .There is a set of protocol . Only hemodynamically unstable AF require DC shock .Many times it is just transient.There has been instances of  physician panicky that has resulted in more adverse events .

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How did rate control in atrial fibrillation easily tamed rhythm control ?

Posted in Atrial fibrillation, tagged , on February 8, 2015| Leave a Comment »

We have two options to manage AF.Rate or rhythm control .(Of course , in the strict sense , rhythm control also confers  rate control that is built in-situ with SR ) .There was an initial confusion which strategy would fare better .For a decade or so rhythm control was thought to be supreme. That’s logical to expect as we restore physiology in the later .” We know, medical science  often disrespects logic , and  scientists reinvent this harsh fact in regular fashion” Now , we have clear, consistent data that proved  rate control is a better strategy in most situations of AF .(AFFIRM, RACE 1 and 2 studies). The aim of treatment of AF are the following .

  1. Improve symptoms of palpitation
  2. Improve hemodynamics
  3. Reduce MVO2 and hence avoid ischemia
  4. Prevent tachycardic cardiomyopathy in the long-term
  5. Avoid stroke .

Unfortunately or fortunately rate control strategy was able to fulfill all these aims with fair degree of success. There are at-leaset  3 reasons why rhythm control fared poorly .

  1. Rhythm control is actually a myth. Only about 35 % patients  remained in SR at any time in rhythm control .Runs of transient AF can occur at  any given day* and make a mockery of the much hyped rhythm control !(*Due to heightened adrenergic tone or adverse biochemistry/ hypoxia)
  2. The drugs used to maintain SR are far more toxic . The complex EP procedures to convert to SR has not helped either.
  3. Most importantly , rate control with anticoagulants were able to achieve better  stroke reduction than rhythm control group.The reason being stroke risk was unabated even if rhythm is back to sinus,  as risk of ischemic stroke continue to emanate  from as many  sites like aorta, aortic arch and carotid. Hence, in a stroke prone population with AF  , it is the meticulous anticoagulant that’s is going to prevent strokes  rather than rhythm control .Since the rhythm  control patients would  need  to  continue anticoagulants , they lose  a  presumed logical therapeutic advantage.

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Destiny of a cardiac embolus !

Posted in Atrial fibrillation, cardiac source of embolism, stroke, tagged , , , , , , , on October 31, 2014| 2 Comments »

One of my patients with atrial fibrillation  recently developed a  fairly  moderate  sized right MCA stroke that resulted in dense left sided hemiplegia .He was on warfarin , but the stroke was confirmed to be ischemic,the etiology was fixed as cardio embolic .After a  smart  recovery he asked this question.

Why did the clot  from  my  heart preferred  to enter the  brain doctor ?  Is there no other place for it  to go ?

I  told him in simple terms , “It is  your destiny and  the clot’s wish”.  In fact , you are some what blessed as the clot did not enter  the left side of the brain .If it had gone, your speech would have severely affected and you may  not be asking this question to me ! It is true the clot do have other options to  embolise ,  however they are still  trouble some !

cardiac source of emboli embolus ischemic stroke animation embolic

What is the diameter of internal carotid artery , and cerebral artery ? The common size of LA appendage clot almost match with this !

It can go straight down to your leg , kidney , intestines or upper limbs .All are equally dangerous  and present dramatically . Very rarely  it can enter  coronary  arteries  bringing a heart attack rather than a brain attack .If it is going to the legs you are at risk of acute monoplegia instead of chronic hemiplegia .Peripheral embolism are very painful .Intestinal ischemia evokes a most excruciating pain one can  ever encounter !  Luckily  stroke is not painful.God is kind enough ,he foresaw  cerebral ischemia to be more common and hence  made it pain-free ! (There is no cerebral angina equivalent  !)

Having said that , I felt we should get a scientific answer to my patients query .

What determines  the destination  of these emboli in transit from heart ?

 

cardiac source of emboli embolus ischemic stroke animation embolic peripheral renal mesentric lerish syndrome 002

A large clot often fails to traverse the Aortic arch branches and invariably reach the periphery .

The dynamics of a cardiac emboli hitting the cerebral arteries can never be known in live human vascular tree. The following factors might play a role.

  • Clot size and morphology
  • Anatomy of aortic arch -Right MCA is in immediate capture  zone .
  • Arch type and curvature radius
  • Arch  branch ostial size , shape
  • Vertebral arterial embolism is rare because it  is a second order branch.
  • Dessication and disintegration of clot in  transit is possible leading to multiple destination.
  • Most shaggy looking large clots fail to enter carotid instead reach the peripheral circulation.
  • Vegetations, tumor debri behaves differently as the density and mass of emboli has a some effect on the transit velocity and momentum.

Variations in Aortic arch anatomy

aortic arch branching pattern A to Z

Image courtesy : Anatomy Atlases by Michael P. D’Alessandro, and Ronald A. Bergman, from university of Iowa. http://www.anatomyatlases.com

It is  surprising, human beings can have as many types of Aortic arch as  English  alphabets . Then,there are innumerable ways for cardiac clots to embolise too  !

 

 

 

 

 

 

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