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Archive for March, 2011

Anticoagulants are different from  antiplatelet agents. One acts on coagulation cascade  , while  the other acts on platelet aggregation. That’s what ,we have  been taught  for over a century.The reality is , there is a huge functional  overlap between these two .

Some of the questions   which struggle to get  a clear answer  ( Atleast for me !) 

 What will be the bleeding time in patients  who are on  oral anticoagulants ?

Ans :  Since it  affects only clotting mechanism bleeding time will be normal or near normal .(Is this reasoning correct ?)   But ,we clearly know , Warfarin  increases systemic bleeding risk : Does this risk occur without affecting the  platelet  function ?

If bleeing and clotting are two different phenomenon how warfarin increases bleeding risk ?  If warfarin alone increases bleeding risk  heavily   why  Warfarin – Aspirin  combination  is used  in many  patients with prosthetic valve  ?

In a patient who is  receiving full intensity heparin( say in Acute coronary syndrome )  can we afford to withhold aspirin or clopidogrel ?

Heparin is given  for preventing recurrent  STEMI and antiplatelets are given  for preventing recurrent  NSTEMI !  Is that the answer  ?  How solid is the concept of white clots in  Unstable angina and red clots in STEMI ?  Can a  blood  really clot without help from platelets ?  Can a person really bleed with intact platelet function ?

Final message

We are  far . . . far away  from fully understanding   science of   human  coagulation and bleeding   ! Meanwhile it is a common sight  to prescribe  all in one cocktail  (A LMW Heparin* , an aspirin,  clopidogrel    ) to most of our ACS patients believing   at least one of them will take care !

* Remember the original caution message when LMWH was introduced said ,   LMWH   should not be used along with Aspirin !

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Ever since  Barlow reported  this entity , mitral valve prolapse was made  a fascinating disease of  the heart . Cardiologist’s honeymoon with this disorder lasted  for too long   . . .  four  decades ?. It is probably the most  common valvular disease physicians diagnose .The importance of which was  exaggerated  and at one point of time  the term was  getting  abused.

So the criterias  were made strict in later decades . Now unless MR is present along  with valve thickening MVPS should not be diagnosed.

Clinical presentation

  • Atypical chest pain
  • Palpitation
  • VPDS
  • Asymptomatic pre excitation
  • Anxiety state  including  panic attacks (More common after informing the patient about MVPS.) 

 

Here is Monograph with excellent Images.I think this is available  free with Google Books. 

 

MVPS -Auscultation

Classical finding is mid systolic click with late systolic murmur.

But in reality,   It can present with  any of the following

  • Early -mid systolic click,   with  murmur
  • Only murmur
  • Only click
  • No click,  no murmur -Only Echo evidence of MVPS
  • Clinical Click  but no MVPS in echo*

The timing of click and murmur depends on the LV volume and the contractile force.Status of pap muscle is also important.There are studies which  show dehydration can induce MVPS and hydration corrects it  .One can guess the anatomical importance of this entity.

Currently myxamatous  valves with clear prolapse with at least  grade 1 MR (Not the often reported trivial MR !) only be labelled as MVPS.All other  forms increase patient  anxiety , lead to unnecessary echocardiogram and of course promotes   physician    affluence !

*Chordal clicks

This was first described by Reid .A redundant  lengthy chrordae  folds unfolds  making a noise. Mitral valve as such may not  prolapse into LA and hence echocardiogram would be normal.

Origin of chest pain in MVPS

It is still a mystery  out there regarding the origin of chest pain in MVPS.

It is thought to be a  mechanical pain from any of the following

  • Valve
  • Chordae
  • Myocardial stretch
  • Ischemic unlikely

*currently it is  believed  to be a pain perception problem at cortical level.

ECG

  • Non specific T wave inversions in inferior and lateral  leads common
  • Early repolarization patterns are common
  • WPW has a  rare association

TMT

False positives excercise stress tests are  reported  often .

Echo

  • Echo  is to be primarily blamed for the  rampant diagnosis of this entity .
  • In deserving patients Echo is vital to define valve anatomy and MR assessment.
  • TEE will help us the exactly identify  culprit  scallops (Commonly P2 A2)  and facilitate the surgeon during repair.

Coronary angiogram

Many of the MVPS patients end up in inappropriate CAGs ( Decent term for guideline violation !).As a rule  , almost all will have normal coronary angiogram.

Incidence of  Ventricular arrhythmias

VPDs can be common in MVPS. ( Myocardial /Pap muscle Stretch induced ?)

Sudden cardiac death is no more common than general population .So no worries .

IE prophylaxis

Generally not required unless significant MR present

Management

Most( 99.9%) will require no treatment . Only reassurance .This , if properly done shall be a one time process.There are many young persons  who report to the physicians  periodically to get reassured (Each time  spending 500 Rs !) This is called reassurance failure .Here , the  physician needs  to be urgently  changed.

Many times , parents , spouse and relatives  will  require more  counselling  than the victim  of mvps !

Few with progressive MR will need close monitoring  (Eg Associated Marfan )

Tall,  thin individuals will require aortic size monitoring as well.

Highly anxious persons will do well with beta blockers. Panicky individuals require sedatives as well.

Very severe MR needs surgery .Surgeons   are encouraged  to repair a  myxamatous valve than to replace it .

Secondary MVPS

(MVPS in association with other structural disease  like Ischemic, RHD, Infective endocarditis are important pathological entities that need to be discussed separately )

Final message

MVPS is a benign disorder (Rather it can be called as  a variation in mitral valve morphology  ).  Only  In  a  fraction of  population it  can take a true  pathological course. Cardiologist and physicians should  disseminate this message widely to their draining population.Unfortunately  in the current state of affairs , MVPS  seem to be  less dangerous for human community than the  events  that   follow  the  misplaced diagnosis of this entity. In the name of health awareness  huge costs , time and resources are wasted in dealing with this almost  . . .non entity !

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Coronary artery dilatation is a less discussed entity in clinical cardiology .It is important to realise  coronary artery has one more behavioral pattern in response to atherosclerosis .  Atherosclerosis not necessarily means obstructive disease . Dilatation is also  a common  expression of coronary atherosclerosis .

It all depends upon the medial weakness and resistance.If the medial weakness  is more plaque grows inwards ,  if the resistance  is more plaque grows out.(Read the related topic -Glagovian phenomenon )

What is the difference between aneurysm and ectasia?

The difference between ectasia, aneurysm are often subtle and  mainly  semantic. . If the length of the dilated segment is more than 50 % of diameter it is called ectasia. When  the diameter is more than 50 % of length it is termed aneurysm .( With a  minimal enlargement of 150 % of the reference segment.  To add to the  complexity both can occur in the same vessel.

Here is the patient from our institute  who has an Aneurysm in LAD and ectasia in RCA.



Clinical Implication

  • Ectasia generally do not limit blood flow.
  • Thrombus formation in the walls can be  common.

*Obstructive Ectasia.This can happen  either when ectasia develops in  an obstructive  lesion or a ectatic lesion getting obstructed .

Stenting and ectasia .

Ectasia creates special  challenges in the Interventional era. Stenting an ectatic segment confers  a real danger ,   as  these stents are prone for  dislodgement   or  even collapse  into the lumen or  migrate downstream   triggering an  ACS. In fact , such complications of PCI are never recognised  and hence not  reported.

Final message

Coronary artery dilatation is also an  important pathological state like coronary  stenosis . Since it rarely limits the blood flow  in  isolation  , it is a less respected lesion.

But , interventional cardiologists beware :  PCI in a ectatic vessels can give you (And your patients too !)  sleepless nights .

Treatment of isolated ectatic segments is controversial .Less aggression is always better . CAD risk factor profile management  is adviced . If severe ectatic changes  are present   it is a good practice to add  oral anticoagulants like Warfarin. Surgical excision of aneurysm is rarely required.

Kawasaki disease is a distinct entity that need to be addressed separately in pediatric population.

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Is there a bio chemical way to measure time window in STEMI ?


It seems so. In this era of hyperacute PCIs  , we are supposed to diagnose STEMI very early .If you wait for troponin  to assit you in diagnosis it  implies  one has missed the golden hour already (At least Three  golden hours to be precise !)

Cardiac enzymes have a unique value in timing a STEMI as  time of   onset of  chest pain is   unrealiable

as the patient (Even the physician !)  may not be able to differentiate pre infarction angina from infarct pain.

In these situation cardiac enzymes provide us a clue.

The time of realse of these molecules are fairly predictable.

  • Myoglobin -2 -3hours
  • Troponin elvation -3 -6 hours
  • CPK –  8 -12hours

Remember  ECG  rarely show a  time lag   in diagnosing STEMI  !

Message

For  maximum benefit . . . try to perform the  primary PCI before the troponin  appear in blood .

Does this  sound a crazy   tip ? What to do . . . truths are very often crazy .

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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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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 !

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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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