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Archive for March, 2011

How to misinterpret pericarditis in coronary care unit ?

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , on March 18, 2011| 1 Comment »

For  a police officer who visits a crime site  every one looks like   a culprit. For a cardiologist  sitting in coronary  care unit  all chest pain  will have to look like  an infarct  !  Then only he is a cardiologist !

A rare , but costly mistake occasionally  happens . When a  patient with severe chest pain in the  retro sternal region with ST elevation in ECG , enters the ER  there is little  reason to suspect any condition other than STEMI !

This is how medical  errors takes place

Medicine is an art , we can not take it as granted .Acute MI can present with normal ECG and a dramatic ST elevation need not be MI

Here  was  a patient who presented with this ECG and one our fellows correctly diagnosed the condition .

Most  physicians would have thromolysed this patient or  might have wheeled into cath lab.  We have such events reported from primary  PCI registry .

Key differentiating points

  • Diffuse ST elevation not confining to a arterial territory
  • Absence of reciprocal changes
  • ST  segment with concavity upwards.
  • Echocardiogram and enzymes will be useful

iFAQs  in pericarditis

What is the mechanism of ST elevation  pericarditis ?

It is actually a zone of epicardial or Sub epicardial injury.

What will be the ECG finding if STEMI is associated with fibrinous pericarditis ?

Double dose of ST elevation .Mimics  a re infarction.

What are the dangers of thrombolysing a patient with diffuse pericarditis ?

It can bleed into pericardial  space

What happens

What will be the ECG finding in localised pericarditis ?

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Is the final frontiers in lipid metabolism decoded ? The receptor X in the liver

Posted in Uncategorized, tagged , , , , , , , , on March 18, 2011| Leave a Comment »

LXR are a unique group of nuclear receptor proteins located in liver as well many body tissues where lipid metabolism is active. They are first identified in liver with apparently no ligands ,  they are  hence referred to as  X (Also called orphan receptors ) .Later  these receptors can be termed as a target receptors for cholesterol metabolites like oxysterols .

 

How this nuclear receptors modify  the subsequent events could ultimately determine the toxic effects of cholesterol in human body.

An update in NEJM appeared in 2007

The the science of lipidology  is  confronted by  with  suspicious  ,  false targets .We are  biochemically still pitch blind  beyond a point . . . after cholesterol enters  the cell .

We have been targeting cholesterol synthesis by blocking HMGCOA.

Statins though claimed to be the God sent molecule , genuine researchers would agree statins  have a   huge  limitation  and it  is a  hyped up drug in controlling atherosclerosis. In fact ,  it is  believed  (In private ) nearly 50% of people who take statin  atherosclerosis goes  unabated.

Can we modify how  LDL  cholesterol is going to be utilised inside the cell ?

LXR family of proteins along with  RXR are expected to  break  the  barrier.In knock out mice models  LXR agonists are  able to control  and prevent LDL propagation within vascular cells .

The research is ongoing. Let us believe  the right target  has been identified . Nothing is guaranteed as of now . . . but out journey should continue .

http://en.wikipedia.org/wiki/Liver_X_receptor

http://www.nejm.org/doi/pdf/10.1056/NEJMcibr075951

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The six delicate rims that hold the ASD device together !

Posted in cardiac surgery, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology congenital heart disese, Uncategorized, tagged , , , , , , , , , , , , , on March 14, 2011| 1 Comment »

ASD device closure as a modality is constantly improving  . . . but  the consensus is  , it is  yet to catch up with  of  good old surgical  outcome . The key to success is not only in the device but hugely dependent on the technique and pre-procedure evaluation  .In fact , the pre procedure TEE imaging technique  is as important as the procedure itself.

There are lots of discussion about this particular issue. TEE is mandatory we know  but now we realise it is  still better to have a  Real time 3dimensional  (RT3D ) TEE . Rim  size  and ASD  morphology estimation is  the primary aim.

There are  at least 6 named rims for ASD. For a circular  orifice  it  may not be logical to have a fixed number of  6  rims . Ideally the entire circumference must have a rim .( This happens in  central defects )In many,  the complex anatomy of IAS does not allow this. So we are compelled to fix the number of rims to six.

  1. Aortic (Superoanterior),
  2. Mitral (AV valve/ Inferoaterior)
  3. SVC  (Superoposterior),
  4. IVC  (Inferoposterior),
  5. Posterior ( Atrial free wall ).
  6. Coronary sinus rim

One can realise how important these rims are , as  they are the   foundation tissues on which the device is going to be seated for the rest of the patients life.

When do you call a rim is adequate sized ?

5mm is  considered suffice. But it varies depending upon the device and expertise.

Can we deploy an ASD device  in patients   with deficient rims?

Logically the answer is expected  is   “No” but  , many have liberalized the criteria now , after realizing   one may  not have 5mm rim in all six sites in a given patient. If you follow this criteria strictly   you can’t do more than few devices a year !

What is the resolution power of TEE can it miss a 3mm rim  ?

TEE has a good resolution it should pickup any thing equal to 2mm or more.

Which is most important rim and which is the least important rim ?


What are the potential complications that can arise if ASD device is deployed with a critically low rim ?

Having discussed  that every rim is equally vital  ,  we  need to answer this sort of questions  often .  I am waiting to get the  practical tips for the above issue from  my experienced colleagues .  I shall post it soon .

It is sometimes assumed Aortic rim may not be that important .Here is a   good discussion  for  ASD closure with deficient aortic rim from Saudi Arabia  . http://www.rmsolutions.net/rmfiles/SHA21/028002.pdf

Meanwhile let us learn . . .

How to perform the “all important” pre- procedure TEE ?

The following article which also  includes video clippings will be immensely useful for all those enthusiastic cardiologists.Thanks to JACC  for making this link free .

Three cheers to AMRITA team from India

http://imaging.onlinejacc.org/cgi/content-nw/full/2/10/1238/

A stylish article on the topic

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ACCORD study :Diabetic wars can not be conquered by Aggression !

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , , , , on March 13, 2011| Leave a Comment »

Action to  control cardiovascular risks in diabetes (ACCORD ) : The accord long-term follow-up results are just out  in NEJM  March 2011   http://www.nejm.org/doi/full/10.1056/NEJMoa1001286

The ACCORD study which created a huge buzz in 2008 when it was prematurely terminated  for fear of  bad outcome ,  with aggressive blood sugar lowering (Hb A1 c <6 %)  .The  negative  trend was confirmed in the aggressive* group even after switching to non aggressive group  at further 1.7 years follow-up  till late 2009.

*Intensive /Aggressive is used interchangeably in this article .

Why should aggressive glucose lowering be harmful ?

This  question is  struggling to get  a  logical answer for over 5 decades. To answer this question,  it  need to realised  our  fundamental understanding of  diabetes  itself  is  flawed ,   as  we have equated it with high blood sugar.

                                                    A  persistent state of  high blood sugar   can never be  used  as a  synonym for diabetes melites.  There is much . . . much  more , to it  !    Patients ,  lay persons and pharma industry  may  think  like  that   but  it is unfortunate many  physicians  have the same thinking   pattern .  The fault lies there .

Diabetes is a systemic metabolic disorder  apparently due to lack of insulin( or relative excess of it ! as in insulin resistance ) in which hyperglycemia is one of  grossly visible abnormality.

It is estimated there can be at least 100 invisible or less visible  biochemical abnormality in every diabetic individual.In fact , DM has more profound effect on lipid metabolism  than carbohydrate metabolism. Almost every microproteins   in our body  gets glycated . That  can be either be  reversible or irreversible .We know how difficult it to reverse diabetic nephropathy or retinopathy

If we realise the above reality there is absolutely no surprise why lowering blood sugar alone  does not reverse diabetic complications !

The second major issue is the modalities we  use  to target the  blood sugar 

Right from the days of early sulphonyl ureas  and biguanides ( of  Tolbutmide and Phenphormin etc ) one thing was very clear (or unclear  ! ) vigorous control of blood sugar has always been a doubtful intervention in controlling  diabetic complications .

                                                If  high blood sugar causes  excess mortality,   why  bringing it to  normal levels  does not reduce long-term mortality convincingly  ?

Is the Madness  lie in the methods ?

It seems so.  ACCORD study has strong reasons to suggest the  worse outcome in aggressive management is due to multiple , drugs used in a random fashion.

Then there  is always this  question  . . .How good is HB A1c  to assess the adequacy of DM control.  ? Biochemically this molecule still has lots of issues regarding its reproducibility.

Individuals who control blood sugar  by  natural means and by minimal drugs seem to do well. Early diabetics and  pre diabetics  should be our targets.

One should also remember the drugs we have today to control DM  have yet to prove the long-term safety records (Say for a span of 30-40 years)

Modern medicine  usually does not bother about the future  . . . it simply shrugs of the issue  with a caution statement . . . that the ” Drugs  you take  are well-tested and  thought to be  safe and useful with the current level of research !”

What is aggression in DM management ?

No one has defined it so far. But the any of the following may fit in with the  definition

  • Any DM patients prescribed more than  two drugs and Insulin
  • Premature start of Insulin
  • Lack of diet and exercise management  and  trying to substitute them with  incremental drugs and insulin 
  • Finally ,any patient who is always tensed up about his HBA1C and switches his physician  frequently  end up in  early complication   than the ones who follow simple non pharmacological approach.

 

How good is the idea  ,   to define aggressive thrapy  with reference to HBA1  levels ?

ACCORD defines aggressive approach  with HBA1C   as less than 6 %  and   Non aggressive as  7-8%  ( or  is it 6-7 %)

Not withstanding the limitations of HBA1C , there can be many patients who will require multiple drugs and insulin to maintain the HBA1C  even  at  7-8 %

How do yo label  them ?  Aggression by  number of  drug used   . . .  but still  considered  Non aggresive control  by HBA1c  criteria .

If ACCORD study fixes the indiscriminate use of drugs as a cause for bad outcome ,  then the very definition of aggressive approach need to be changed !

 Final message

ACCORD says it all . Never be aggressive on diabetic patients. The aggression we show with drugs can be more dangerous than the deadly diabetes itself.

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Is Aspirin’s role become reduntant once the patient is started on oral anticoagulants or Heparin ?

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , on March 13, 2011| Leave a Comment »

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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Mitral valve prolapse : Finally . . . facts are trying to prevail over fiction !

Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics, tagged , , , , , on March 12, 2011| 4 Comments »

 

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 Aneurysm vs Ectasia : Semantics at play !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology-Anatomy, tagged , , , , on March 11, 2011| 1 Comment »

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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For Primary PCI to be most effective . . . Do it before the Troponin appear in blood !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , on March 9, 2011| Leave a Comment »

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

Posted in Uncategorized, tagged , , , , , , , on March 9, 2011| Leave a Comment »

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 ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on March 8, 2011| Leave a Comment »

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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