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Carvajal Syndrome : A new form of Intercellular cardiomyopathy with electrical instabilty .

March 9, 2011 by dr s venkatesan

Mystery  surrounding  the Inherited cardiomyopathies are  getting  unraveled . Now ,we have  a unique entity of cardiac muscle disease due to  Desmoplakin mutations which affects the  cardiac intercalated disks.  They are Naxos disease and Carvajal syndrome.

Source : Wikipedia

Heart has a skeleton too

We know skeletal muscles   need  a bone for its attachment   . If  we  think cardiac  muscle can work independently . . . we are mistaken !

Heart is not a simple mass of muscle.It has a fibrous skeleton around which the muscle is spun around. Myocytes  not only  need to stick with one another,  it has to  be packed over the cardiac fibrous skeleton systematically.

The cardiac  gums that do this job need to  be under strict quality control . After all ,  these muscle sticking proteins  need to be serviced constantly  throughout life span of heart. It is  simple to understand ,when there is  breakdown of this process  , protein  to protein disconnection  takes place  . It results in  cardiomyopathy.

Thus many of the  cardiomyopathies are  not  primary  disorder of cardiac  myocytes as such . They can be termed as disorder  of myocyte adhesion to cytoskelton.

These  present as cardio cutaneous syndromes .(Skin share similar adhesion molecules)

Carvajal syndrome

This is due to mutations of plakoglobin  family of protein . Involves desmoplakin ,  a defective desmosomes and disruption in myocyte adhesion  which  promote  abnormal myocardial stretch ,  dilatation  later fibrosis  and progressive cardiac failure. Non compacted LV can be a feature in carvajal syndrome. Recurrent VT/VF demands an early ICD therapy.

Natural history

  • Woolly hair at birth
  • Cutaneous changes at appear at  the age  of one year.
  • Cardiac involvement  occur in adolescence
  • Can overlap with ARVD

How  is Carvajal syndrome   different from Naxos disease.

It has

  • Predominant LV involvement.
  • Fatty infiltration uncommon

Reference

http://www.ncbi.nlm.nih.gov/pubmed/14761782

http://circ.ahajournals.org/cgi/reprint/116/20/e524.pdf

From cell biology to Inter cellular biology

For over a century biologists were concentrating  research inside the  human cells .Now we are more interested in the inter cellular planes. It  remains an ultimate mystery how the zillions of  cells are sticked together in an orderly fashion  without fighting each other with a  perfect anatomical and physiological harmony.

Understanding the molecular  basis of cell adhesion will  help us decode the pathological states   in which  inter cellular  disintegration  is the hall mark !

A review article on the topic.



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Is plain balloon angiopasty(POBA) a dead concept ? If so who killed it ?

March 8, 2011 by dr s venkatesan

When  PTCA was introduced  by Gruntzig  in 1977 the whole world was awestruck. All he did was . . . to dilate a coronary stenosis with a balloon. No scaffolding  was ever thought off at that time.  It was a huge achievement .   PCI version 1 was  performed for over  20  years in nearly a million  patients   . Till his death stenting  was  an unknown concept.

When the stents first came in,  it was first used with extreme caution .  From the days of  bail out stenting, it  has evolved  into provisional  stenting, elective stenting ,and  now  what is called  “mandatory stenting”

When  Greuentzig was able to  perfuse the obstructed coronary arteries  successfully  in thousands  of patients  in the 1980s,    with a simple balloon

. . . what is the difficulty for us  to replicate it  in 2011 ?

Unfortunately  advocates of POBA (Plain old balloon angioplasty) are considered  to be  un-scientiifc cardiologists or even carry a risk of labeled as quacks.

But please remember . . . POBA   is alive and doing well  too ,  in spite of the serious threat  it faces from the current generation interventionists  . It  will continue to have an  important role in  many  situations.

1.In patients with multivessel  disease while the  proximal lesion  deserve a stent  , POBA is preferred in distal lesions  to reduce the overall metal load .

2.POBA has a major role to play in Primary PCI .We need to realise  dying myocardium does not demand  for stents. It simply requires  quick and prompt restoration of  blood flow. POBA can achieve this with flying colors in most situations.

3. Further , stenting  may be  difficult in complex lesions   during primary PCI .Experience tells us , it  is  dangerous to prolong the primary PCI  procedure time. Here POBA is the only choice ,  may be assisted by thrombus aspiration. Stenting may be delayed or even avoided in many STEMI patients. . We know there is huge STEMI population with  pure thrombus with no atherosclerosis.

4.Patients  with  co morbid conditions , who are  likely to have a non cardiac surgery in the near future  and those who  can not take antiplatelet  drugs  POBA will score over BMS/DES.

5.Finally a POBA costs nothing . .All it requires is a stiff  balloon . In this recession prone world  and ever increasing incidence of  CAD  , POBA  could be the  answer.

6. Acute recoil in POBA (Sudden deaths in POBA is  a rare event !) are more of a perceived fear rather than a reality. It can be argued stents  are  primarily used  to make  cardiologists job easy and  comfortable.

7.Cost effectiveness of plain balloon verses stenting was never  properly tested .

Final message

When sudden deaths  due to subacute   thrombois in DES population   is accepted with all those attendant  pride . . . why not we accept a risk of  less sinister event  namely the  late onset restenosis with POBA.

This is a funny world . The DES fiasco is driving us towards stent less world and a bio degradable stent is already being projected as new savior.

Meanwhile no  one can kill POBA thats for sure !  It  will  ultimately   be reinvented  with another exotic study  soon !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , , | Leave a Comment »

Glagovian Phenomenon : Why it is one of the vital concepts in cardiology ?

March 6, 2011 by dr s venkatesan

Atherosclerosis  probably ranks first among all  human diseases that cause maximum suffering  to  mankind.Since it is a disorder of blood vessel  it has an easy  access to every  vital organ  in our body to inflict the damages . Histo pathologically , atherosclerosis is an all in one disorder where inflammatory , degenerative and lipid injury  collectively  contribute to the disease progression. Diabetes and hypertension play a vital amplification role.

Atherosclerosis begins very early in life as fatty streaks in every individual and takes different avatars ( or remain indolent)   depending upon the risk factors and life style.

How to estimate plaque burden ?

It has  always been a difficult task to estimate the  atherosclerotic  plaque burden inside the  coronary  arteries.The fundamental flaw for many years is ,  we always thought  if there is a plaque it must  encroach  into the lumen.

Coronary angiogram  , has become the  default investigation  in clinical cardiology . Since it   can  visualize  only the coronary lumen ,  this  flaw  got further  curious  with skewed  interpretation as well.

When things were as it is . . .  Glagov suggested , what  could  possibly be   the  most important  concept in the interpretation of coronary  angiogram .

The concept  suggested  the  atherosclerotic  process  could  actually spread  within the  vessel wall  in a predictable manner .

What determines a plaque to either grow into the lumen or grow away from the lumen?

If we could decode the mechanism of direction of plaque growth we will probably conquer the atherosclerosis  at least by mechanical means . The implications are too many.

A stented coronary artery may be re-engineered to grow the atherosclerosis  towards  the adventia .This could grossly reduce  the incidence of restenosis.

Further , in post Glagov days we realised  mechanical factors like plaque stiffness, eccentricity , plaque mass effect, drifting , lipid core density, medial lysis , elasticity of elastic lamina all could determine the   plaque  movement.

Why compensatory lumen enlargement does not occur in some lesions ?

We do not know the exact reasons . We may call it a fate . . . shall we ?

Curious blessing  : Atherosclerosis  for  some unknown  reason  blesses a  few with coronary artery  dilatation rather than narrowing .

This is called coronary  ectasia . Medial necrosis , weakness of internal elastic lamina or  destruction paves way for plaque shift towards the adventia . It is estimated , if the medial necrosis occurs in at least  50 %  of  circumference of vessel wall   it will  result in ectasia .And  paradoxically if  the media  shows resistance   the plaque grows into the vessel wall.

Endoleak  and Glagovian phenomenon.

Endo leak is the Achilles heel of   endovascular intervention . In fact , many would  consider  it as  a dignified terminology  for graft failure . Endo Leak   occurs when  the artery outgrows the stent  graft and bllood starts  collecting  in the graft vessel -wall interface . When the  scaffold is  placed  within the lumen ,  one may wonder how it is going to prevent  the  artery  dilatation . (Which is basic defect in any aneurysm}In fact , the aneurysm does continue to grow  along with   centrifugal  atherosclerotic  forces ,  possibly by  Glagovian phenomenon .

This makes it obvious  endo- leak is a distinct threat in every vascular  intervention.


Final  message

Most cardiologists  think their ultimate  job  in this world is to  deploy  a stent deep inside a LAD  or RCA.  While a few others indulge in more exotic  adventure of  crushing a plaque ,  trap the debris and  catch it with a  with  a basket .

There  are bigger and bigger   blind areas  in the vessel wall ,  infiltrated with  deadly atherosclerosis which is conveniently ignored  .If only we realize   this fact  , we  can move forward in our war against coronary atherosclerosis.

Of course the good old   medical  interventions  . . .  exactly try  to address  these issues . Let us  think  straight , and  not succumb to glamor  in cardiology !

http://heart.bmj.com/content/84/5/461.extract

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If inapproprite stenting is to be prevented . . . most cardiologists may need to be sued and banned !

March 5, 2011 by dr s venkatesan

Coronary artery stenting  , many consider  as the 2nd revolution in cardiology after   the invention of  cardiac catheterisation .  Millions of angioplasties  take  place  world wide every year .  Suddenly it would appear that medical therapy  was forcibly  thrown  out into the  bin .This in spite of  the fact there is no  major difference in ultimate CAD outcome in the long term between PCI and medical  therapy in chronic CAD.

The COURAGE trial which gave a renewed lease of life to medical therapy , was  severely criticized by the interventionists. 5 years after the COURAGE  the inappropriate stent usage continues unabated.

The term inappropriate usage ,  some how undermines the seriousness of the issue.  Few realise  the fact , inappropriate usage  actually amounts to  mal-practice or  an act of  medical  negligence (Guideline  violation)   which deserve  a strong  condemnation .

The general media is just been exposed to the tip of the Iceberg  (Not even the tip !) At least in USA and other developed countries  they  have systematic data  about  the usage of stents. In a country like India  . . .less said is better. There are many  like  Dr Mark  Midei  camouflaged  in every country.

More pro active Media is required like the ones below.

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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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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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