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Archive for the ‘Cardiology – Clinical’ Category

Diabetes is a systemic disease affecting  almost every cell  that metabolises  glucose .What begins  as  a minor  functional impairment  ,   worsens gradually and ultimately   end up in severe  structural changes.The basement membrane of  cells  face  the brunt of the attack .  (In the strict sense every cell has a basement  but it is well  developed only in kidneys ) . We also  know , diabetes  is able to inflict universal damage by targeting the vascular endothelial cells.

In the kidneys DM makes the  glomerulus  more porous causing protein leak*  and ultimately damages the tubules and end up in CRF. In the retina it excretes the  proteinaceous  material into the vital layers  and result in  retinopathy and progressive visual loss.

* Micro/Macro albuminuria

In fact , there is  a very close link between eyes  and the kidneys  Nephrologists   hesitate to make a diagnosis  of diabetic nephropathy without ocular  changes. The peripheral vascular disease and diabetic foot are  another expression of this microvascular  dysfunction.

What is the impact on cardiac micro-circulation ?

Whenever significant diabetic nephropathy is present there must be a significant cardiac micro- angiopathy as well.This is now  a fact than an assumption. We are not recognizing it rather  ! (If only we have a cardiac  creatinine we can easily identify diabetic myocardial protein leak !)

When kidneys lose protein , cardiac capillaries  lose proteins to interstitial   space  and result  in progressive  fibrotic reaction . We know  extravasaation   of high osmolar  proteins   can play havoc  in cardiac interstitium  !

Proteins are the particles of life   . . . but in wrong places  it can  transform into deadly  molecules  in a fraction of time !

Hence ,  the cardiac protein leak in diabetes can cause  any of the following clinico -pathologic entities.

  • A mild left ventricular  hypertrophy .
  • Increase global  cardiac  mass (Similar to bulky kidneys  seen in early diabetic nephropathy )
  • Simple diastolic dysfunction.
  • Severe restrictive features
  • NDCM (Non dilated cardiomyopathy )
  • Finally a DCM  like  transformation

How to recognize cardiac protein leak ?

  • Clinically it presents either as  angina or early heart failure symptoms ( not both usually ) .Diastolic dysfunction  in echo,  positive stress test , patchy thallium uptake abnormality  often with  features  of   syndrome X  is also recognised.
  • Many of the low flow or slow flow phenomenon  in coronary angiograms  might reflect micro-circulatory dysfunction .
  • This is recognised by prolonged TIMI frame counts  and  prolonged  coronary sinus filling and emptying time .

What about macro-vascular  complications  in diabetes ?  How is it different from micro-vascular complications ?

Though we expect a direct  link between  micro and macro  vascular complication ,   the later  appears  to a  patho-genetically  independent  process . This will be addressed later.

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Read with caution . This  may either injure or cure your patient !

Click on the ECG to view what happend !

 

How does  verapamil  terminate a  VT  ?

Physicians  often  debate  vigorously before   labeling  a cardiac arrhythmia as ventricular , atrial junctional  , abberant or not etc etc .  But  for  an arrhythmia   it matters little  from what  chamber it is going to to originate . After all ,  any cell in the heart if excited can generate an arrhythmia .  The ion channel abnormality and the influx and efflux of ions  that determines how a drug is going to terminate an arrhythmia.

In fact , way back  in 1989 the Sicilian Gambit stressed this concept when classifying anti-arrhythmic drugs .This classification taught us  , even though there is a  huge list of  clinical cardiac arrhythmias  , from the therapeutic point of view there are only a handful of receptors  (scattered  all around ) to target  !

When we look at this angle , we realise  , many of  ventricular action potentials  have  important slow  calcium currents  similarly  junctional action  potentials do have some  sodium currents.  Calcium current  is present in every  myocardial cell  more so in the vicinity of AV junction.  Further , at times of ischemic or hemodyanmic stress these ion channels  may  take a different avatar altogether.Slow sodium channels and fast calcium channels etc !  (A wild imagination or is it a fact ?) Other important targets are potassium channels

Heart is a complex structure both macro and microscopically  .  In the three dimensional  histopathologic   interface between atrium  and ventricle (Especially in the  basal areas , outflow tracts  , around the AV grooves ) there  are  lot of sharing  and overlap of  different morphology  of cells . A high septal VT can behave  exactly like an SVT  which  includes the  tendency to get terminated by calcium channel blockers.

Amiodarone is a most popular  drug for VT termination ? Are we clear about the mechanism of it’s  action in terminating VT ?

It is  more of a perception and belief  that  class 3 action   may be   responsible for termination of VT by Amiodarone . In reality it is very difficult   to prove this point.  As Amiodarone  has all the  4 classes  action that includes beta and calcium blocking properties.. In fact ,  now  there is evidence  to  suggest   beta or calcium blocking action  may be more important in terminating  VT when  it is administered  IV  . (While  the class 3 action predominates in long term oral therapy )

A verapamil sensitive   VT may  successfully  be terminated by  Amiodarone  not by its  unique  action  instead it   may simply represent  its  calcium blocking  property.

Final message

Many  of the  VTs terminated by Amiodarone   could  also be verapamil sensitive . Since verapamil is never tried first we will never ever know the incidence of such phenomenon that gives pseudo credit  to Amiodarone

It may not be big crime to try injection verapamil in some of  the  stable ventricular tachycardias( As my fellow did ) especially  when we we know there is an entity called verapamil sensitive VT !


Q for the readers :

How many deaths are reported in cardiology  literature  regarding    fatality  following   verapamil  in   VT ?

I am trying to find  the answer the  data is very hard to come by !

Critical comments welcome.

 

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Ever since Brugada found the unique pattern of ECG on right pre- cardial leads and its  association with  premature electrical death ,cardiac electro-physiology got a new impetus. Hundreds of articles(May be thousands !) on Brugada are  available . Many criterias  were proposed.  Brugada  and his colleagues should be credited for bringing  in such an interest in the  field of inherited ventricular arrhythmias.

On the down side ,  as we have a habit of  prematurely formulating criterias  ,  it brings  an artificial academic  barrier  Funnily , in medical  science  deviating   from a criteria (However hastily it  was  proposed  )   is a considered  big  offense Further . the hype surrounding  any new scientific  entity makes it difficult  for others  to overwrite  it .

Brugada recognized a ECG pattern with  a genetic predisposition for VT and VF  . Now , we know there are many etiologies  with a similar pattern  of ECG . What Brugada did was ,  he  exposed the tip of Iceberg called inherited ventricular arrhythmia . But the essential criteria –  Absence of structural heart disease ,  to diagnose Brugada   was  always questionable.

(Please realize , presence  or  absence of structural  heart disease depends , more  on  how advanced  our  imaging modalities are . If you can map a virtual histology of RV epicardium one may detect some  microscopic abnormality in every case of Brugada. In human biological system , God  usually bonds  structure and function too  closely  and hence  functional  abnormality rarely occur  in isolation )

Brugada is  not  a new disease ,   it is  a  recognition  of a  pattern of ECG  related  to sudden deaths . Subsequently , we  realized any dispersion in repolarisation in RV epicardial surface  , the   risk of sudden death  is increased. From the days of  Brugada  we  have  come  a long way.

What is new in Brugada syndrome  ?

(Not exactly new . . .  it is  known  for many years )

Brugada is no more an exclusive  functional disorder of  sodium channels of RV  epicardium .It can have structural defect (known & unknown ) .It may  have infective , degenerative etiology as well .

How does these structural changes appear ?

Chronic sodium channel malfunction  can result in cell membrane defects which can augment   Idio-osmole   inside  the cell and result in  apoptosis   etc .

Which comes first ,  electrical or structural abnormality ?

It is an  another  chicken- egg tale  waiting to be decoded   within the RV epicardial cells

Can wall motion defect occur in Brugada ?

Early observations done in out hospital (MMC Chennai ) has found anterior  RV free wall motion defects. Tissue Doppler studies are  being undertaken.

Final Message

The  following paper  wonderfully documents  the structural and histo-pathological  changes in RV epicardium .  This  implies ,  our belief   about this  unique electrical  disorder  is  bound to take a beating  and  we  expect a major perception makeover regarding Brugada  in the years to come .

Probably the most important paper on Brugada syndrome was published in circulation in 2005

*http://circ.ahajournals.org/cgi/content/full/112/24/3680

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We  are at the mercy  of  the three major coronary arteries (LAD,LCX,RCA) that sustain our life . Their  job is clear cut  .It has to perfuse   about 300 Grams of   live bundle of energy  for  an average of 6-7 decades.

What are the hurdles it  faces ,  how it overcomes these obstacles  forms the fascinating story of   “survival  of  human heart”

When coronary blood supply is confronted with a sudden compromise  as in ACS  ,  often the heart has little  time to respond . Hence the damage  and risk of death is  more. Even here there are lots of safety mechanisms and natural lytic process that limit the loss of life to less than 30 %  of all STEMIs. This implies nature protects against the death in 70 % of individuals and help  them  to reach hospital.*

*Among those  who reach hospital , we  the cardiologists  try to reduce the  mortality to about 6-7 % (20% without treatment ) with all  those hi-tech gadgets .It is a  different story and will be addressed elsewhere .

When it comes to  chronic insults ,  the heart has a unique potential to  stage  long haul battles. It has many tricks  under its  sleeves when challenged in a slow fashion.

The main weapons are two

1. Coronary collateral circulation.

2. Ischemic preconditioning.

Here is a patient who fights his life even after all his  three coronary arteries   totally blocked and surviving with one of the branches of left main -Ramus intermedius .

If you have thought his RCA was the savior  you are  mistaken  .

To every one’s   surprise  his  RCA was awful  as well !

He had angina which was  troublesome  but manageable .Was able to live a life with acceptable standards (Indian standard )  After the angiogram he  received  CABG.  A turbulent post operative course ensued  due to various reasons . He  struggled but   fully recovered  . . .  and  ultimately  reached the  previous  standard  of life !

Final message

Modern cardiology is all about not trusting  powers of nature .

But youngsters should realise the enormous potential of those invisible powers.It may sound philosophical , but please  remember  . . .after all . . .  philosophy  is nothing but  search for truths. Atleast believe in them  once in a while !

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Heart has three layers

  • Epicardium
  • Myocardium
  • Endocardium
  • Epicardium is same as visceral pericardium . If pericardial inflammation dissusely occurs ,  it is bound to injure  the epicardium and subepicardium .

    Does  the  troponins  located deep inside the  myocardium  ?

No .It  can  even be present just few microns below the visceral pericardium  . Hence  severe forms of pericarditis can elevate the troponin levels without any issues .

Is troponin  release related to ST elevation ?

 Ideally  most forms of  pericarditis can be termed as epicarditis. The mechanism of ST elvation in pericarditis is actually a sign of  epicardial injury.In fact ,  there is no easy way to  differentiate  a  slice of epicardial infarct from an   inflammatory pericarditis accurately .

Is there any form of pericarditis which invlove only parietal pericardium ?

We do not know as yet ,  about  existance of such  an entity. It is distinctly possible. However , if present it is unlikely to result in significant  ST elevation in ECG.

In pericarditis ,  troponin release is due to inflammation  or necrosis  ?

Both are possible .Even transient wall motion defects are reported in isolated pericarditis.

What is myopericarditis ?

It is  a general term used  to indicate the above situation . In practical terms Pericarditis + Troponin positivity can be termed as myopericardits. It is well known pericardits can extend to endo- myocardium but it is rare other way  around( ie endocarditis extending to pericardium )

What is pancarditis ?

It is the carditis  involving all three layers of heart ,Cassically occura in rheumatic fever. Fulminant carditis is known to raise the troponin to significant levels.

Does troponin elevation  in pericarditis  occur in all  ?

We are yet to collect adequate data about this .  Diffuse , extensive pericarditis ,gross ST elevation ,  and associated pericardial effusion  correlate with troponin.

Crazy questions in pericardiology

What is the pericardial blood supply ? Is there  an entity called ischemic pericarditis ?

Final message

Do not ever underestimate the  importance of  pericardium  whenever you encounter unexplained ST elevation in ECG.

Reference

Here is an article which has   meticulously studied this issue

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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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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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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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