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What are the “Nine” vulnerable points in the atria for focal atrial tachycardias ?

March 4, 2011 by dr s venkatesan

Human atria is a rough terrain infested with peaks and  troughs like the  Himalayan range . The two atria together has a minimum of ten entry or exit points . Cardiac arrhythmias are   something similar to the  uneven  earth plates  triggering an  earth quake.  Like the earth surface there are  areas in the atria  with high seismic activity !

It is now discovered there are nine vulnerable points in human atria that can initiate focal electrical activity at times of hemodynamic/ischemic/metabolic stress .

The common causes for Focal /Ectopic atrial tachycardia are

  • Hypoxic AT -COPD ( Probably the most common cause .If persistent it will degenerate to MAT- AF )
  • Structural atrial disease
  • Hypertensive heart
  • CAD
  • Valvular heart disease
  • Drug induced

Note ,  all these  vulnerable points are located either in the  junction of  an anastomosis  with a venous structure or valve or septum.

Further, these sites are often the  embryological fusion points making it still more vulnerable due to tissue defects.

Why free wall of atrium  is  a less common  focus ?

They are relatively smooth, lack ridges and joints. Unless the walls of atria are diseased  focal tachycardias are less common from these sites .

Other forms of Focal atrial tachycardias

Indian perspective  and Rheumatic atrial tachycardia.

In developing  countries  focal atrial tachycardia in rheumatic heart  differ very much from the tachycardia described above. In fact many of the rheumatic atria present straight away  to atrial flutter or fibrillation.

Pulmonary vein focus should rarely be considered in atrial tachycardia that occur in RHD.

Post operative tachycardias

Surgical scars can result in what  is called  Incisional tachycardia.(Especially after complex atrial  surgeries like Sennings, Glean/TCPC  etc )

Multi focal atrial tachycardia .

This is nothing but a focal tachycardia which tend to fire from different angles towards different targets  often lead to a chaotic atrial rhythm .  Digoxin and DC shock paradoxically aggravate this arrhytmia.

Atrial epicardium/pericardium interface as a focus

When pericarditis is the predisposing  event  then it can emanate from anywhere from  epicardial surface .

Since left atrium is only  partially covered by pericardium it is not logical to assume pericarditis related AT arise from RA epicardium.

Atrial tachycardias in congenital heart disease.

Complex atrial anomalies, SVC type ASDs, PAPVCs can  give raise to abnormal  electrical focus

Reference

An excellent original work from  Royal Melbourne Hospital, Melbourne  Australia.

A must read  . . . http://content.onlinejacc.org/cgi/reprint/48/5/1010.pdf

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Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias | Tagged , , , , | Leave a Comment »

Post syncope Giant T wave inversion

March 3, 2011 by dr s venkatesan

Is there a ECG marker for recent syncope ?

Yes . This was classically described many  decades ago. Following a Stokes -Adam attack  when the patient recovers from the loss of consciousness a peculiar ECG pattern was observed.

A typical ECG from our CCU

The mechanism is not clear.It can be due to

1. Repolarisation abnormalities due to ischemia.

2.Acute adenergic surge triggered  due to  transient   cessation of circulation* .

3.CNS  injury  and extreme  vagal with drawl

4.Hypokalemia

* Thought to be the major mechanism

Out come

The ECG is more dramatic .The physician is usually more tense than the patient !

It  is often  benign .Prompt pace maker implantation is required.

Reference

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What is the effect of systemic hypertension on Aortic stenosis gradient ?

March 2, 2011 by dr s venkatesan

Aortic stenosis is the commonest valvular heart disease  in elderly. Severe aortic stenosis  requires early  aortic valve replacement . Severity of aortic stenosis is  best assessed by   echocardiogram. ( Cath studies are rarely indicated  now) Mean Doppler gradient across  the aortic valve (dPm) is the widely used  parameter to assess severity.Americans believe  in  a cut off value of  40mmhg  while  Europeans  want it  to be at  50 mmhg . Obviously, these  numbers 40/50   become  vital  as it determines the  critical decision of replacing the  aortic valve which carries up to 4-10 % mortality.

Even as we realize ,   Doppler gradients are so important , we also need to  know ,  how fragile  ( and  vulnerable  ! )  are the Doppler equations ,  especially when it is critically dependent on the angle , flow,  heart rate  , the LV  contractile  force  and associated MR etc. These errors are over and above the  the  technical simplification of Bernoulli equation  which ignores many accessories like viscous  friction ,  proximal velocity etc  .Mind you  . . .with this battered Doppler modality we make a critical operative decision !

Here comes  the ace . . . Shall we  term it as  as negligence  in clinical echocardiography ?

Apart from  the above factors  ,  a single  important  critical determinant of  pressure gradient across AV is the mean pressure in the Aorta itself .  The mean  LVOT gradient = LV cavity pressure -Systemic blood pressure.Echo derived gradient tells us only the pressure difference across the valve.It does not reveal how much is contributed by raise in LV cavity pressure and how much is contributed by the change in systemic pressure.

How many  cardiologists would  measure the simultaneous  blood pressure while recording LVOT  gradient in AS ?  ( To be precise it should be measured in the same cycle  )

If  Aortic mean pressure is high  as in systemic hypertension  LV pressure must raise considerably higher . The contractile capacity of LV is tested here. A hypertrophied LV  easily achieves this.  If the LV fails to elevate it’s intra -cavitory   pressure sufficiently high the LVOT gradient may never reach  the 40 /50 mmhg range  that is required to label  aortic stenosis as  severe.

Many hypertensive patients exactly experience  this situation . The left ventricle of  many  of the hypertensive patients  fail this stress test  and result in low gradient AS.  Note , this happens in spite of   having  normal EF.

The link between systemic hypertension and aortic stenosis is a complex one. The after load becomes double here.There is a strong vascular valvular interaction. The following effects  are seen.

The effect of SHT on AS

It is well known HT  initiates the Aortic stenotic  process by damaging the valve and  also  result in progression.

Transient elevation of systolic pressure  can result in increase aortic orifice , and a fall in gradient.

The effect of  AS on SHT

Once the AS becomes severe , the systolic blood pressure may be reduced. (This not a rule ) If the mechanism of HT is increased  vascular  tone (Which often is the case ) systolic BP will remain high .

Effect of AVR

Surprisingly ,  many times the blood pressure normalises after AVR.The mechanism is not known.

Role of Anti HT drugs.

Fixed vasodilators are thought to be contraindicated as sudden fall in systolic blood pressure against a fixed obstruction is detrimental.  ACEI may be tried cautiously.(SCOPE AS study )

Reference

The following are the excellent article on the topics .All provided free by the  “Heart” Journal

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Final message

In the evaluation of  Aortic stenosis   ignorance continue to prevail over our  knowledge. The Gorlin’s  the  Hakki’s, and the Hatle’s formulas  have made the  calculation of aortic valve area  look like a   child’s  game  (Which is not !)

Referring  all patients  with a  mean gradient > 50mmhg to the surgeon for AVR (or now a  TAVI)   may be the  easiest option  for the cardiologists  (but definitely not an intelligent one ). Even  as we struggle to decode the intricacies of isolated  AS  ,  one can guess  the complexity  when SHT adds on to AS .

Understanding the hemo-dynamics in  AS in association with prevailing blood pressure is vital.  It is a more scientific way of doing  echocardiography . Every cardiologist should give their input as they encounter hypertensive patients with AS.

It  would appear  ,  an AS patient developing HT at a  later  age  and a HT patient developing AS later are two different poles in the hemodynamic spectrum.

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Why prasugrel is heavily indebted to aspirin for it’s glory ? . . . The curious case of human platelet business !

February 28, 2011 by dr s venkatesan

Platelets  are the major culprits in initiating arterial thrombus.Platelet  inhibition is  the key  modality  to treat /prevent  acute and chronic coronary syndromes. It is  an approved indication for primary and secondary prevention of CAD.

Anti platelet  agents are the biggest drug  market among the cardiac drugs. It is  a billion dollar  medical game  played  with two  million  human  platelets !

Aspirin is the best anti-platelet agent known .It is not only most effective but also  available at a fraction of the cost other  drugs. Unfortunately  it is  a generic and not a patented one .Being cheap  ,   good safety profile  is the biggest  disadvantage of aspirin  !  So ,  consistent efforts were made to make this drug appear weaker. Hence came many new anti-platelet agents .

After analyzing  the available literature ,  I have compiled the following conclusions ( Mostly biased observation ! but I strongly believe the  bias is more  towards truth . . . )

All of the following statements can be termed either  true ,were true , believed to be true ,  may  be  true ,  at some point of time  (Between the  last decade and today !)

  1. Aspirin alone is good enough in both  ACS and chronic CAD
  2. Clopidogrel is   equally effective like aspirin in ACS.
  3. Aspirin alone is dangerous in ACS.
  4. Clopidogrel alone is more  dangerous than aspirin alone in ACS,
  5. Aspirin + Clopidogrel  provides the best anti-platelet  action.
  6. Aspirin + Clopidogrel combination is still dangerous .
  7. Prasugrel is more effective than clopidogrel
  8. Prasugrel can never be as effective as aspirin *
  9. Never use clopidogrel alone in DES patient.
  10. Aspirin can be safe in most stented patients
  11. Mono platelet inhibition is a crime !
  12. Risk of  sudden death continues to be significant in spite of dual antiplatelet agents in many with DES.
  13. For prasugrel to be  really useful  it should always be prescribed with aspirin.
  14. Prasugrel alone can be dangerous in stented patients.
  15. If the patient is  getting heparin  simultaneously none of the above seems to be  really  important (Of course all patients with ACS will be getting this )

Above are my inferences in all those trials on platelets in the last three decades

What do you infer  ?

To  a discerned reader all of the above statements  may appear wrong   !

*Finally , it looks to me  both clopidogrel and prasugrel ride  a fake  ride on the shoulders of trusted war horse called Aspirin . There is  a strong basis for this  suspicion  as none of the researchers are ready to do a one to one direct comparison between aspirin and prasugrel  or clopidogrel !

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Eccentric plaques : Another grey area in interventional cardiology !

February 27, 2011 by dr s venkatesan

Reporting a coronary  angiogram  may look like child’s play  for most cardiologists. Many do it in less than a minute. (It goes something like this  90 % LAD , 30 % ostial OM1, 50 % mid RCA etc etc ) The famous and meticulous  classification of Ellis and Ambrose proposed  two  decades ago appear largely redundant.

In this review we shall  briefly  debate an eccentric plaque or lesion .

Pathological definition

Pathologically  an eccentric lesion  will have a disease free arc  within an  atherosclerotic lesion.If we apply this criteria most of the plaques appear to be eccentric.

Angiographic definition

In simple terms  eccentricity is  said to be present when the plaque  volume is three times more on one side when compared  to opposite side .

The incidence of eccentric lesion is largely under estimated.  It can be up to 40 % of all lesions.

It has histological  as well as  hemodynamic  significance.

How to measure eccentricity index ?

Ratio between maximum plaque thickness and minimum plaque thickness (Including the media )

Image courtesy modified from Circulation. 1996;93:924-931

In the above figure : The eccentricity index is measured  as the ratio of the maximum  to minimum plaque plus media thicknesses. In the eccentric lesion  the maximum wall thickness measures 2.6 mm, minimum wall thickness measures 0.2 mm, and eccentricity index is calculated to be 5.2.  In the  concentric lesion  the maximum wall thickness measures 2.2 mm, minimum wall thickness measures 1.6 mm, and eccentricity index is calculated to be 1.4.

What are the associations of eccentric plaque ?

Calcification and hard plaques are more common in eccentrically placed plaques.The  most vulnerable point for plaque  rupture or disruption is  the shoulder region between normal and plaque segment.

A long eccentric lesion with over hanging plaque

 

Clinical implications

  • Acute recoil
  • Coronary spasm
  • Mechanical effects : Asymmetric expansion of stent
  • Drug eluting stents

An arc of normal plaque circumference predispose to acute recoil and spasm.this is logical as the normal  arc will have a fully functional  medial smooth muscle  which are prone for spasm.

Does stenting reverse  the eccentricity of plaque ?

It may not .  The drag effect of major plaque mass may either result in plaque prolapse or  asymmetric stent approximation  or even stent crushing effect.

How does the  the stents  elute in an eccentric lesion ?

Stents are not intelligent enough to  differentiate  the plaque surface and normal surface. We  also know these drugs are  toxic to  normal endothelium  and hence  are not welcome in the normal arcs of an eccentric lesion.

Since the drug secretion   is uniform throughout the circumference   it makes the   DES a perfect misfit in eccentric lesions  As  we  realise most of the lesions are pathologically eccentric one can guess the long term  consequences .

Final message

The more we think we know . . . the less  is understood .

The images we see daily in cath labs are too simplistic to make vital decisions .There are  constant innovations coming up but none seems succeed in  imparting  common sense to  majority  us.(Namely  direct plaque intervention can never succeed over a diffuse medical  disease called atherosclerosis  )

A good reference article

http://circ.ahajournals.org/cgi/content/full/93/5/924

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Low flow -Low gradient Aortic stenosis : Clarity replaced with confusion !

February 27, 2011 by dr s venkatesan

New concepts are created to clear confusion and bring clarity. We know all along low gradient AS is a hall mark of severe LV dysfunction. Now we suddenly invented normally contracting  LV can also cause  low gradient due to low flow when the aortic valve orifice becomes very critically narrow .

How can it occur ?  . . . few  suspect  it  to be  semantics  !

The terminology  that is  often used in recent times when describing severe aortic stenosis.This is called Low gradient severe AS with preserved LV function .

But logic would say blood flow is required to produce gradient .If it falls extremely low the gradient is likely to fall.

If that is the case every severe  AS patient will experience low flow at least in  few beats . Is this the reason why we find it very difficult to reproduce the exact gradient  ?

Low flow ,Low gradient aortic stenosis is not a  new entity .It is the way we look at the data. It  remains a fact  ,  severe  AS can be diagnosed with 2D features alone ,  without the help of Doppler.We also know  Doppler is less reliable than 2D in many situations for various  reasons .The most important being it’s dependence on angle of  doppler  intercept  and LV contractile force.

Read  the  argument by   Nikolaus Jander from Germany

http://eurheartjsupp.oxfordjournals.org/content/10/suppl_E/E11.full.pdf+html

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Outflow tract ventricular tachycardias : Best review articles.

February 24, 2011 by dr s venkatesan

A well researched article on a difficult topic. By Kim et all from Cornell university , New york.

A must read by all cardiologists . The link is placed with the courtesy of Jacconline

http://content.onlinejacc.org/cgi/reprint/49/20/2035.pdf

After reading this article   one  should be able to answer the following questions.

  1. What is Gallavardin VT ?
  2. Classification of RVOT VT
  3. How a non sustained VT becomes a sustained one ?
  4. Why some VTs cause syncope ?
  5. What is the association  between idiopathic VT and Idiopathic VF ?
  6. How does exercise  trigger a  VT ?
  7. What do we mean by structurally normal heart ?

Readers are encouraged to post link to good articles on this topic.

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology-Arrhythmias, Cardiology-Land mark studies | Tagged , , , , | Leave a Comment »

Man made confusions in labelling ventricular tachycardia !

February 24, 2011 by dr s venkatesan

How to name  a ventricular tachycardia ?

This  continues to be a  favorite past & present  time of  modern-day cardiologists. Especially ,  VTs associated with structurally normal heart  suffers with this  protracted problem .Widespread use of  EP study has not solved the issue as yet.

The   VTs that arise from the left ventricle in an apparently normal heart   has been referred  by  various terms.

  • VT with structurally  normal heart
  • Idiopathic left ventricular tachycardia
  • Verapamil sensitive  VT
  • Septal VT (It can be either myocardial /non myocardial origin)
  • Narrow qrs VT
  • Fasicular VT
  • LVOT tachycardia
  • Hemodynamically stable VT
  • Belhassen VT

Now we have still more exotic VTs like Cuspal , mitral annular , etc . All of the above can mean anything , or same thing   in different centers  ,  different cardiologists in different times .

* RVOT tachycardias also have  many synonyms.( Adenosine sensitive, Adrenergic,  Gallavardin, Parkinson Pop, etc )

VTs associated with CAD , valvular , myocardial diseases generally devoid of  nomenclature problems. Ischemic VT  is yet to be classified in a proper fashion.

The confusion in classifying VT is  not due to the complexity of heart disease. It is due to  the general  comprehension failure as  every VT can be described with reference to clinical , ECG morphology, hemodynamics and presence or absence of underlying heart disease. A simplified and clinically useful VT classification is being prepared in this forum .Will be published shortly .

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A brief lecture on tandem coronary lesions!

February 23, 2011 by dr s venkatesan

Coronary artery lesions can be classified by many types . The popular ones are by Ambrose and Ellis  .They are adopted by ACC and SCAI  .While various  terms  are  used to   describe a lesion. (diffuse, discreet , eccentric , long , tubular  etc) A tandem lesion is the one which has special significance , but is not well discussed in the literature .

A tandem lesion is  diagnosed when  two lesions  closely abut  each other one behind the other  with an  intervening normal segment. (Like the bullets loaded in a  tandem fashion  in a  gun )

Generally there will be at least  few millimeters of normal intervening  coronary segment.This is  referred to  as  connecting segment.

Clinical importance of tandem lesion

Tandem lesions  carry  the  same significance  like  any other lesion. But ,the primary aim is to tackle the two lesions with a single stent. We know stent edges are rheological culprits.  Two stents  have   4 edges. It is better to cover  the tandem lesions with one long stent* even if we have a sufficient  connecting segment.Geographical miss is less likely with a long stent.  In the strict sense one wold require an IVUS (Intra vascular  ultra sound ) to confirm the normality of the connecting segment. Tandem lesion is  a  marker  of diffuse atherosclerosis  and  the connecting segments often   show ectatic changes.

* This is a ironical as  the conventional wisdom would  tell us , lesser the  metal load it is better for our coronary arteries.But once we embark on a complex  intervention we just can’t restrict the use of stents. The more you put the more it will demand.There are some interventional cardiologists who convert the entire coronary artery in to a metal tube (With or without realising the consequences !)

Illusions of  tandem lesion.

Many  times ,  spiral folds  from a single  atherosclerotic   lesion mimics  a double lesion .This need to be differentiated from true tandem lesion.

What is the hemodynamic significance of  tandem lesions ?

Rules of hemodynamics  would  dictate ,  in a linear and laminar flow  model across a tube ,   immediately after an obstruction there will be a significant  drop in resistance.

This  forms the fundamental   phenomenon  within the coronary artery  . This explains the biggest mystery in cardiology . . .  How  the  TIMI flow is  maintained till 90 % of the  lumen is narrowed. This  also  explains the concept of flow limiting lesion .(Why  a coronary lesion do not obstruct the flow  till late stages  ?)

Does this rule on  hemodynamics  apply in tandem lesions ?

When a lesion is followed  by a lesion with little normal segment in between what happens ?

The blood gets a double jolt every time it traverses a tandem lesion. There  may not be sufficient time and anatomy for the mandatory pressure drop to occur. So for a  given degree of obstruction ,  tandem lesions  is likely to be   more thermodynamically significant than a single lesion.

Pressure recovery after  an obstruction is also incomplete , as the forward head of blood column encounters another hurdle even before it recovers from the initial turbulence.

Which lesion is more important   in tandem proximal  or  distal  ?

The distal lesion determines the thermodynamics of proximal lesion while the distal lesion as  such is  less influenced by proximal.

Long lesion vs tandem lesions




Some times it may appear ,  it is better to have a long lesion than  a two lesion  in tandem. This is because the stent will approximate more evenly .Further there is less likely hood of in -stent restenosis in long lesions as the   edge effect can occur  right in the middle of  the stent in tandem lesions .

Now it is increasingly realised, many of the sub acute thrombosis  are due to po0r stent approximation in tandem lesions or long lesion.


http://www.springerlink.com/content/g063752436617n51/

http://www.ncbi.nlm.nih.gov/pubmed/8789675

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One more cause for dynamic LVOT obstruction : Abnormal Aortic angle ?

February 23, 2011 by dr s venkatesan

Inter-ventricular septum is generally in parallel alignment with Anterior aspect of root of aorta.

Have a look at this echo form a 65year old man

Note the classical bend of basal IVS encroaching the LVOT. Aortic valve opens normally.

 

The basal septum Projecting into LVOT

Pseudo LVOT gradient. It was about 25mmhg which is not significant.

 

 

  • Sigmoid shaped IVS can  cause a unique  LVOT  profile .
  • Present in elderly . The exact mechanism and  mechanical and hemodynamic   implications are not known .
  • It can rarely cause  dynamic LVOT obstruction.
  • When these patients develop Infero posterior MI there could be further collapse of IVS into LVOT .

Relationship between Aortic angle , Hypertension, HCM

Many of the HCM patients may show similar features .When ASH is confined only to basal IVS. HCM should not be diagnosed instead it is  often a defect of aorta /IVS alignment .

Abnormal  aortic angle  with that of IVS  may  make the IVS appear sigmoid.

If  patients  with abnormally angled aorta develop hypertension ASH and sigmoid septum is  more pronounced .

IVS dragging by mass effect  on aortic root is possible and Aortic regurgitation may ensue

Reference

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