Posts Tagged ‘atrial fibrillation’

There is a tough ongoing rivalry between drugs and catheters to conquer the commonest electrical chaos in human heart, namely Atrial fibrillation (AF). Mind you,the confusion about the importance of this arrhythmia is huge and real.Bulk of these episodes are transient , paroxysmal and do not require rigorous management.While stroke prevention seems to be the major aim and target , the real world scenario seems to tell  a different story.

The nomenclature conundrum 

AF may be classified as many ways a learned cardiologists can think . Often it’s done with reference to etiology, duration , rate, neural (sympathetic or parasympathetic)  humoral , cardiac or non cardiac , reversible or irreversible ( Endocrine, Electrolytic, hypoxia etc).

Unlike VT , bifurcating  AF with reference to the  presence or absence of structural heart disease is rarely meaningful.Subclinical atrial interstitial fibrosis in elderly is so common especially so in hypertensive individuals making all lone atrial fibrillation as true structural disease.

Classifying AF with reference to atrial enlargement again is problematic as any sustained AF can dilate these thin atrial chambers in few weeks time making  it a sequel to AF rather than a cause to it.

Adding further fuel to the confusion is the  recent man-made (read cardiac scientists!)  problem .Linking the etiology of AF with the presence or absence of valves pathology is definitely not helping us. In the process , we forget a casual fact that valvular AF needs aggressive valvular Intervention and not arrhythmia Intervention !*A patient with dilated cardiomyopathy with mitral regurgitation and LA enlargement with AF is considered non valvular AF in spite of clear pathology in mitral valve apparatus.(Is there myocardial AF by the way ?)

What is the current role for catheter ablation in AF ?

The question of advanced catheter based management boils down to a minority of refractory, fast , troublesome AF which has failed by most available drugs. More Importantly the long-term success of ablation is lowly 20% ( PV reconnection, geographical miss, atrial focus etc) and follow-up medication  is  absolute must even after successful ablation. Its well-known , severe the underlying heart disease more likely is the recurrence .Ironically these are same ones that attract the catheters.

The previous debate of rate control vs rhythm control gave sufficient lessons  that complex modalities to restore sinus rhythm is unwarranted . As scientific  cardiologists we continue to be adamant and don’t learn from our mistakes and blindly adore and adopt technological excessess.

Now, thanks to CABANA* the ablation for AF has proven to be a fruitless  process considering the time ,effort and potential (& real )complications.

*The Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation . Just presented in HRS annual meet at Boston MAy 2018.

The bright spot is even in these commercial medical world the study like CABANA is a silver lining. Mind you it’s partly sponsored by Industry , still went against them. Three cheers to the genuine medical research team of CABANA for bringing out a truth. Now, I am optimistic more such trials in cardiology will be proposed

A companion to CABANA from UK

A 2018 landmark paper from  published in BMJ reveals a dramatic truth that the risk of stroke continues to persist even after resolved Atrial fibrillation,  largely concurring with CABANA.(Nicola J Adderley, Risk of stroke and transient ischaemic attack in patients with a diagnosis of resolved atrial fibrillation: retrospective cohort   studies   BMJ 2018;361:k1717)

So, how to get out of these AF conundrum ?

Practically , an extreme simplification of AF classification is warranted . It should answer these couple of  questions !

1. Will the  AF in a given patient require long-term oral anticoagulants  or not ? (or ok with antiplatelet drug !)

2. Should I make any meaningful attempt to convert the AF to sinus rhythm at all* ?

* You can also redefine the second question , does this AF deserve a EP consult or not ?

Final message

AF is largely a benign arrhythmia in global perspective . However, In those patients were  its troublesome , safe and effective drugs are available to tackle it.We shouldn’t Insist to make it complicated.

Meanwhile . . .the anxious pulmonary veins seems  to enjoy the  moment as they escape from the fire .No wonder they will thank and celebrate the CABANA.



Post-ample and counter point

The RF ablation is a high risk procedure , as we develop less injurious cryo balloons the results of Invasive ablation procedures may score over drugs.Let us wait and don’t prematurely ditch the catheters.

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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.


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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The mechanical atrial function   during atrial fibrillation remain a mystery . In fact , the general  belief  is during  AF  the mechanical function of atria is zero. This is why AF  is promotes stasis and   LA clot formation. It may appear theoretically correct  , still   AF especially coarse  still imparts some amount of  mechanical motion .But this usually does not translate to any useful hemodynamic function .

If atrial booster pump is lost (which is said to be 25 % of  LV filling )  suddenly one expects dramatic symptoms  especially if there is associated LV dysfunction or aortic valve disease .

But in real world AF is well tolerated arrhythmia in most  .  We know by land  mark trials AF  is as good as sinus rhythm  if the rate is  is under control

This is a definite evidence the AF  may not compromise  LV filling   even if   it nullifies  the  atrial contractility .

There is one  more evidence for  retention of atrial mechanical activity in spite of AF .It is well recognised , pre-systolic accentuation is preserved  in many cases of mitral stenosis with AF.

*Crazy hemodynamics : For an attached LA clot to  dislodge ,   one needs some amount of LA contraction isn’t ?  Unfortunately  a fibrillating  atria always  tend to  have this one ! This again is a senseless  proof for some  mechanical activity of LA during AF !

How is this possible ?

Is it a  purely volume dependent filling   ? ( Or )  is it  the  Intrinsic LA starling forces that do not depend electrical atrial activation .

This is definitely an  issue to ponder over . A good LV contraction makes the atria empty more completely . This would  somehow  mean , LV relaxation  is facilitating atrial function . During  AF the LV  handles effectively  the additional burden  imposed by the loss of   25  %  booster pump of atria ( Accelerated LV relaxation ? )  A  constantly  changing  RR interval makes LV diastolic function a more complex event .

Final message

Atrial fibrillation is  a well tolerated  arrhythmia in vast  majority of patients  . This  implies either of the two things.

  1. The so called  physiological atrial  booster pump is redundant  or dispensable in otherwise healthy heart
  2. The booster pump is indeed important  . . . but it is less  affected by AF as long as the rate is under control !

It is to be  strongly emphasized , Heart rate and  LV function  will ultimately determine  , how one is going to tolerate the AF  !

It is  a small gesture  from LV  to LA  at it’s hour of crisis  . . . in return  for  it’s lifetime assistance  as a booster pump ! 


How  rate control  prevails over rhythm control in spite  zero atrial contractility in the  former  ?

Comments welcome !


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RR interval in Atrial fibrillation is irregular because . . .

  1. The Atria  fires irregularly
  2. AV node conducts irregularly
  3. Atria confuses the AV node  with  its random firing  and varying penetration *
  4. The ventricle just reflects  irregular  response of atria .

The answer is all of the above. Response 3  explains  best.

*Please note , the AV nodal property is predominantly  responsible for the irregular RR interval in AF  . Atria confuses the AV node  with its random firing .The varying penetration into different depths of AV nodal structure and  the resultant concealed conduction make the   the AV nodal refractory period into continuous oscillation .This  random delays in AV node  is reflected in RR interval as irregularity   )

The response we get in ventricles  in AF  can be summed up as  “A filtered atrial rhythm”

Paradoxically,  amidst the chaos in atria  the rate  is fairly constant within the atria (Fibrillatory   wave firing  at up-to 600/mt )  Of course  , the FF interval in the atria will also be varying  .  At a rate of 450-600 this is difficult to quantitate  especially in fine AF.

When does RR interval becomes regular in AF ?

  • When the patient develops complete heart  block.
  • Digoxin toxicity
  • Associated Sinus node dysfunction

For advanced readers in EP : A mystery explanation for irregular  rhythm in AF  in the offing ?

AV node is a physiological and electrical sink .

When atria fires at 600/mt it absorbs about 60-70  % of the atrial response .Whether it releases the original impulse or initiate a new rhythm in the junction  is not clear.

There is some evidence to suggest the rhythm that control the ventricle in AF may not be  filtered original rhythm from the atria .Instead it could be a fast junctional  escape rhythm (Is that a junctional fibrillation ?)


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Dronedarone is a drug which was developed to replace the very effective  , (but side effect prone ) antiarrhythmic drug Amiodarone.

After years of study ,  Dronedarone has been  approved for use in some* of  our  patients with atrial  fibrillation

* Who are they ?

That is the only thing  , we are  unclear about Dronedarone  ! ! !

The recent studies on Dronedarone DIONYSOS have  clearly  proven it , to be  a  less effective  agent in controlling  AF  , but has a  advantage of fewer adverse effects.

Hence ,  for preventing the potential  side effects  of Amiodarone , let our patients  take an inefficient drug ! This is  how we are inclined  to think ! But the medical industry can not be blamed altogether  , after years of research they develop  a molecule and they would like to  have at least a small pie in the atrial fibrillation market place !

It again proves the centuries old adage,  that all drugs are poisons .If a drug lacks side effects it ceases to have the desired effect also . If you want a drug with zero side effect  a sugar coated placebo  is the best choice !

Is there  really a  role for Dronedarone ?

  • Yes , may be in patients  who have recurrent AF in spite  of stabilising  the underlying conditions that perpetuate AF( Hypertension, CAD, COPD etc)
  • When Amiodarone is contraindicated or withdrawn due to side effects
  • Remember ,  Digoxin, Beta blockers, or even calcium blockers  , can have an  important role in the  chronic management  of AF. But they are unpopular  for many reasons other than academics!

Final message

Dronedarone is power-less antiarrhythmic  drug  ( “Less- powerful ” could be a more  polite  and decent  word !) that has a specific role in the management of AF when  efficient rate or rhythm  control is  deemed unnecessary !

Why don’t  we have study  with  one to one comparison of Digoxin ,Beta blocker and Dronedarone  in the chronic management of   atrial fibrillation !

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It is a well known  cardiac auscultatory  sign,   S 1  becomes  variable in intensity with the onset of atrial fibrillation.

In physiology , the intensity of S 1 is determined by many factors.

  1. The valve morphology(Thickness, Calcium , Rigidity )
  2. Valve mobility
  3. PR interval
  4. Force of LV contraction
  5. Preceding RR interval (4 and 5 are inter related)
  6. Insulation and auditory factors (Thick chest wall  etc)

How does atrial fibrillation modify the intensity of  S1 ?

It is to be noted , atrial fibrillation alters only one  of the above factors, namely the RR interval which becomes irregular.

The mix of short and long RR intervals  occurs at random  . A short RR interval, results in a relatively softer S1  and vice versa . The mechanism is directly attributable  to the degree of LV filling and subsequent change in force of contraction .

Many times , at fast ventricular  rates (Say >150) the distinction between short- long cycles is  negligible in terms of net cardiac cycle.

If  the RR interval , is too prolonged there can be an  inverse relationship  with s 1 intensity .It gets  muffled as the  mitral valve floats back  to it’s  orifice and a partial or even complete  closure occurs , making  force of LV contraction irrelevant in the genesis of S1 .

The vanishing act of PR interval  in atrial fibrillation.

It does not require great brains  to  understand ,  if P waves are absent ,  PR interval must also be absent !

If PR interval is absent ,  there  can be no  influence of it on the first heart sound. Logic demands  absence of PR interval must have some sort of  influence on the intensity of S1. As far as i know cardiology  literature has not answered this query.

What are the two types of S 1 variation ?

Experince  has shown us , the variation of S1 can be of two types*.

Sequence 1 : Varying between , Loud -Louder- Loudest -pounding

Sequence 2: Varying between , Loud -Normal – soft -Muffled

* Applicable only for those with shrewed ears !

S 1 intensity with reference to underlying pathology : Valvular vs Non valvular atrial fibrillation

It is obvious the impact of  varying RR interval on  the intensity of S1 will directly depend upon the underlying pathology. The  intensity of   S1  in  non valvular AF (Like , lone AF, Thyrotoxic AF, Hypoxic  AF ,Ischemic AF etc)  are  more vulnerable to  changing   RR interval .

In rheumatic heart disease , the influence of valve morphology , rigidness, calcification and presence  of MR  generally prevail over the  impact  of changing RR interval .So,  in a case of tight mitral stenosis  and AF  it  is expected the sequence 1 is more common .

In lone AF or AF due to CAD , sequence  2 is more likely *  Associated LV dysfunction , and ischemic   MR may further dampen the intensity of  S1 .

Clinical implication

Hearing  few occasional  loud  S1 in AF , is an indirect indication that underlying LV function is good,  as it reflects the force of  LV contraction .

Silent AF

Some hearts are notoriously silent even in the midst of AF. If  the silence is not  due to obesity  or  other insulation defects,  it suggests a sinister diagnosis ,  like severely  dysfunctional ventricle  like  DCM etc.

As a corollary, it is often noticed ,  palpitations* are , often not  felt  by patients with dysfunctional  ventricles  in spite of atrial fibrillation. (As loud S 1 is rare with dysfunctional ventricle)

*Palpitation is a symptom that equates to Dp/Dt of ventricles.

What  happens to mid diastolic murmur in AF ?

The murmur length  varies  linearly with reference  to RR interval. The pre systolic  accentuation disappears ,but   pre-systolic component may persist .

Final message

Simple, bed side auscultation during atrial fibrillation can give us vital clues about the etiology, and the  underlying LV function .  Let us not be ashamed to talk about clinical cardiology  . . .at least in the bed side !

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Management of  atrial fibrillation has been a  big puzzle for cardiologists  for many  decades  till  it became a corporate game , and  now in the era of recession it has become  medicare’s  night mare !

So , we  were  made to dance to the tunes of the so called evidence based cardiology . . .

  • From only rhythm control to . . . in 1990s
  • Either rhythm or rate control  . . .       in early  late 1990s
  • Then cost control  was found  more important than rate control  . . .
  • . . . So rate control became superior to rhythm control in early 2000s

In 2010 , even the  rate control  became  a luxury ,  here comes the  real ace !   ” Casual rate control may be  suffice in most cases of AF “

Read this article  from  NEJM , which tries to  make  sense out of nonsense  and judge for yourself

Probably the most influential  article  in electrophysiology over  the  next decade

Click  below to reach Nejm article



Gist of the trial

Technically and literally it  means a  “Take it easy attitude” as long as patient is comfortable , even a rate  of  more than 100 is allowed . Few years back the above concept could be termed a “non sense”

Final message

In this  perennial  management issue  of AF  ,  Whether ,   we were successful in  restoring   sinus rhythm or not , we have restored  the common sense*  Thanks to RACE 2 investigators.

* Do not unnecessarily trouble a  asymptomatic  patient with those powerful  and costly  antiarrhythmic drugs .

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