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Posts Tagged ‘atrial fibrillation’

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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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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No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  

 

Reference

1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 

 

 

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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.Circulation2017136:2420–2436. 

 

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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.

Reference

http://www.acc.org/latest-in-cardiology/clinical-trials/2018/05/10/15/57/cabana

Post-amble 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.

https://1drv.ms/v/s!Ahm_xjThT-nXgY5EtHnqjxFkb_PWtQ

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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.

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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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 ! 

Postamble

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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