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Archive for the ‘Atrial fibrillation’ Category

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 functionJ Am Coll Cardiol Img 2009 2:11471156

 

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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 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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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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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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Answer  is question is wrong : RAA clot do occur in AF and severe right heart failure.It is less often recognised , since echo views are difficult and clinical events are silent.

RAA right atrial appendage clot tee echocardiographyBrief account of RAA clot formation

  • RAA is broad flat ,thin ,  chamber comparable to elephant’s ear.The ostium is not that distinct as the body as it  blends  with crista  terminalis .
  • Rough pectinate muscles  should make it prone for thrombus.Further , RAA has more sluggish flow than LAA  increasing the propensity for thrombus.However , the flat nature of the chamber , absence of tortuous tracts , constant  SVC flow which is abutting the  RAA can counteract this.
  • RAA clots are  less recognised as echo views are difficult .TEE is often required.
  • Overall RAA clot is 50% less common than LAA.
  • RAA clot should be specifically looked  for  in chronic AF and any severe right heart failure. (Unlike MR jet TR jet has less efficiency in flushing the  Right atrium )
  • Finally,clinical events from RAA clot are less conspicuous as the emboli reaches the pulmonary  bed silently.Unlike its colleague on the left side it  neither triggers TIA nor a stroke !

Reference

right atrial appendage clot raa clot in af atrial fibrillation

1. Buğan B, Baysan O, Demirkol S, Güngör M, Yokuşoğlu M. Right atrial appendage thrombus in a heart failure patient with sinus rhythm. Gulhane Med J. 2011; 53(3): 214-215.

 

2.Subramaniam B, Riley MF, Panzica PJ, Manning WJ. Transesophageal echocardiographic assessment of right atrial appendage anatomy and function: comparison with the left atrial appendage and implications for local thrombus formation. J Am Soc Echocardiogr.; 2006; 19(4):429-33.

3.Sahin T, Ural D, Kilic T, Bildirici U, Kozdag G, Agacdiken A, Ural E. Right atrial appendage function in different etiologies of permanent atrial fibrillation: a transesophageal echocardiography and tissue Doppler imaging study. Echocardiography;2010; 27(4):384-93

4 .Ozer O, Sari I, Davutoglu V. Right atrial appendage: forgotten part of the heart in atrial fibrillation. Clin Appl Thromb Hemost; 2010; 16(2): 218-20

 

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electrical CONDUCTION OF HEART

Image source and courtesy http://www.heart-consult.com

Answer

I am afraid the 4th response is closer to truth .Readers may share their thoughts. If there are three distinct pathways   spreading widely connecting the two spacious chambers and   converging again with  precision at the compact  AV node , it  is a  marvel .

Further , If these pathways are real ,  we must  experience different types of  inter nodal re-entrant  tachycardias.Of-course ,we do come across few macro re-entrant tachycardia in the form of atypical atrial flutters  They need a close  watch .Tracking these arrhythmia may throw light on existence of these pathways.

However, the presence of nodal approaches  with preferential inputs to AV node from different parts of atria would indeed  suggest existence of such pathways !

Further study

What does  sophisticated carto and other electro anatomic mapping say about these inter nodal pathways ?

Reference
An excellent article from imperial college London
Atrial anatomy and inter nodal pathway thorel bachman wenkeback

Heterogeneous three-dimensional anatomical and electrophysiological model of human atria . Seemann G, Höper C, Sachse FB, et al. Institute of Biomedical Engineering, University Karlsruhe (TH), Kaiserstrasse 12, 76128 Karlsruhe, Germany. Transact A Math Phys Eng Sci 2006 Jun 15; 364(1843) :1465-81.

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