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Archive for the ‘Cardiology -Interventional -PCI’ Category

Surprisingly it is common !

A .Abandon the procedure call the surgeon for an emergency CABG

B. Open the most critical lesion.*

C.Attempt to open and stent all possible lesions.

D.Send the patient back to CCU for a conventional  thrombolysis or attempt a intracoronary thrombolysis.

Answer : All  can be a right response depending upon the available expertise ,  time window, associated complication and hemodynamic stability etc .

* Please note ,the most tight lesion may not be the culprit artery. Though there is high chance for that  being the culprit , it  can be very deceiving   especially when  there is multi-vessel  CAD with  chaotic collaterals.

The site of lesion and site of infarct can unimaginably remote.  (A traffic snarl at remote flyover  can have its impact  right on the busy commercial street due to diversions ! ).

What will happen if you open  a non culprit artery first mistaking it for a culprit ?

This could lead to  dangerous turn of events as whatever little perfusion the patient was getting through the ill-fated  IRA will be challenged by the fresh diversion  facilitated by non IRA angioplasty. Extreme caution is required.

Emergency CABG  within 3 hours  of MI even though advocated  by few ,  is still considered a risky  way to reperfuse  the heart.(In India  there  is  nothing called primary CABG!)

An energetic interventional  cardiologist would vouch for opening all lesions . Only thing  , he has  to  make sure is  , the patient also has enough energy to withstand  his  onslaught. Never   non culprit lesion if a patient is stable . 0ur aim is not that.If the patient  is in shock or impending LVF one can justify opening  few more lesions  that improve total muscle function which can be vital.

What about fall back on thrombolysis?

This may be seen a defeatist attitudebut  when the aim is  in the  well being of patient ,  there is no defeat or success. If severe  CAD is encountered and both  CABG / PCI  or not an option,  the cardiologist need not feel guilty or  humiliated to refer him back for thrombolysis. (Of course , Intracoronary thrombolysis  is  an option !)

Final message

Primary  PCI  is often made  to  appear ” As  a  kids play”  by many modern  day cardiologists . It is not so.  It requires a team effort. It is  race against time.   Feasibility depends largely on the coronary anatomy. The failure rate of  primary  PCI is often camouflaged .(Currently Success of pPCI is boasted at 95%)   Logically it should include pPCI ineligible anatomy as well . Many still do not understand the real purpose of pPCI.   The aim is to salvage the myocardium  at risk , sure and fast. Never attempt for total revascularisation in an emergency situation however tempting it is !

In young persons with discrete single vessel disease  the procedure is simple and outcome is straight forward. In elderly , diabetic , STEMI on  preexisting CAD,  diffuse  multivessel disease  ,   complex main left,  bifurcation lesions , one requires  lot of brain sense  to provide optimal outcome . Many times that sense includes abandoning the procedure !

Please read a related article in this site  Primary CABG

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Patent foramen ovale (PFO) is the new generation hole in the heart for  21st century  cardiologist. Present in about 20% of population  , would correspond to 140 crore  “man holes”  as  on  2012   in this planet. PFOs are embryological remnants across the inter atrial septum.

These minute  holes measuring few mm  are largely a  benign finding .In the recent  decades , it is being increasingly debated these holes  may  not  be innocent after all .Extensive  use of echocardiography in recent times   has contributed to  the awareness  as well as anxiety.

Evidence  is mounting  linking PFO to

  • Migraine,
  • Stroke and
  • Peripheral embolism.

While the above   observation may be true  ,  the  fact that >100 crore people have this entity   , raises  a serious question ,  as labeling  all of  them as heart disease will create chaos among the already health obsessed   population .

So , the main purpose should be ,  to identify the high risk subsets* of PFO population .(This will be a <5 %  at the most). People with PFO may  carry  a mental  stigma because it is referred to as a hole in  the heart by the  general  public .For many  the sense of living with a hole in heart is often more damaging than the hole itself ! (Incidentally , many develop  migraine only after reporting about this hole !)In a strict sense  PFO  is not a hole , rather  it is a communication it may be tunnel  or  slit like .It is argued physician should avoid calling PFO as a hole .

*What is a significant PFO ?

  • Large PFOs >5mm
  • PFOs that shunt blood
  • PFOs with septal aneurysms
  • PFOs with documented stroke or embolism
  • PFOs with atrial chiary network
  • PFO in  persons with systemic pro-coagulant states (Except probably in  pregnancy )

Final message 

PFO is a common residual congenital  atrial septal  anomaly . Usually  benign  . One can  live with it perfect harmony. Only occasional patients  are  at risk.

So the prime job of cardiologists is to not diagnose and create panic about  this entity. rather reassure  them (Is it better do not reveal to them if it is found incidentally ? Patient empowerment group would call  this a  foul !  I do not support blind empowerment  )

At the same time our main  aim is to identify the  high  risk subsets who are prone for events.

Closure of   PFO with device is required in a fraction . (*By the way ,  if   PFO is really dangerous ,  why It is never an indication for surgical closure ?  )

Reference

Your  search for best information  on PFO  would end here .  Here is  land mark   article  in JACC  by  Hara   also contributed by  Renu Virmani . A US  Japan  combines initiative  : A must read by every cardiologists

http://content.onlinejacc.org/cgi/reprint/46/9/1768.pdf

http://www.anesthesia-analgesia.org/content/93/5/1137.full

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Atherosclerosis is an  inflammatory and degenerative disease of blood vessel.The common  belief is  (Of course , it is a fact ) it  mainly causes vascular obstruction and compromise vital organ function(heart, Brain, Kidney etc)

Here is a different facet of atherosclerosis , A middle aged man  surprised us with this  coronary angiogram .   Instead of obstructing the flow the  coronary vessel begins to dilate. This is due to a medial weakness .(The media for some reason begins to give way rather than proliferate to the atherogenic  stimuli.)

Same patient's RCA

One may wonder why he underwent CAG when obstruction is least expected in such a vessel   !  It was paradox of sorts , this man  in spite of his  wide bore coronary artery ,   was prone for coronary thrombus and one such episode landed him in our CCU . ( Please note both faces of atherosclerosis “obstructive and dilatory” can manifest in the same  vessel in different combination.)

This angiogram may be reported  as any one of the following

  • Diffuse atherosclerosis
  • Diffuse atherosclerosis with focal dilatation  and aneurysm formation
  • Coronary  ectasia

These patients should get life long  medium  intensity  (INR 2-2.5) oral  anti coagulants  for preventing coronary thrombosis.

Watch out for similar aneurysmal changes elsewhere (Renal, Cerebral, Aorta etc )

Counter point

How are so sure it is is due to atherosclerosis ?  Can it be a  congenital coronary medial weakness ?

Your guess is not my guess . . . My vote is for atherosclerosis .

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In this politically and scientifically  uncertain world nothing is  in black and white. How can you  expect  EST to behave differently ?

Even as  we  are fully  aware of the  limitations  of EST  ,  it  does not make sense   to categorize  EST result into either positive or negative .

In fact , our  estimate suggests  a significant bulk of the patient would fall in the grey zone  .

It is referred  in various terms by  the reporters of EST .

  • Borderline positive
  • Mildly positive
  • Equivocal
  • Inconclusive

What does all these terms mean to the patient ?

It mans only one thing . . .

Physician  who reports  the  EST    is unable to  conclude whether  his patient has  significant  CAD  or not . It is a dignified way of  expressing  the  limitations .

Many factors may play a role. (See the illustration above )

  • Patient factors : Poor exercise stress levels and conditioning
  • Lesion factors:  Collateralised CAD, treated CAD  can result in partial or mild  changes.
  • Machine factors :Caliberation errors.
  • Interpreter : (Physician ) factors

Error in measurement of ST segment . What is borderline  for  one doctor may indeed be true positive  for the other and vice versa .

How will be the  EST in  a  revascularised  or  medically treated CAD ?

If revascularization is a complete success ,  stress test  would  revert back to normal or it can be a borderline as we have just mentioned.

To our  surprise ,  it may  remain  positive in spite of apparently successful procedure.(Residual wall motion defects , scar mediated  ?)

How to proceed  after this borderline EST/TMT ?

Few options are available for the physician/patient

Talk  with the patient again  , assess the  baseline risk  of CAD   if it is low ignore the TMT result and reassure.

  • Repeat  stress test after  a month.
  • Stress thallium
  • Doubutamine  stress
  • CT angiogram
  • Regular Cath  angiogram* (May be the best , of course it also carries a  risk of labeling  the condition as  mild  CAD / non critical CAD etc )

For the  patient  the  easiest  option  may be ,   self  referral to a different cardiologist .   (Also called second opinion )

Final message

There is indeed an entity called   borderline  EST  . Do not dare to  ignore it  or else  face the consequences .

Read  related articles in this site .

1.Can medical management convert EST positive to negative ?

2. Should every one with positive EST should undergo CAG ?

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Atherosclerosis follows a general hemodynamic  rule.

It has a predilection for medium and small  sized vessels and love to  home in  on the  branch points .

We know coronary  artery disease  mainly involve the proximal tree. We get occasional patient  with mid or distal CAD.

This again ,  in  combination with atleast one  proximal  lesion. Decision making  is easy if there is critical proximal lesion.

Here is a patient who has isolated  critical distal CAD . He created a heated debate in our cath meet

His LV function  was normal , He had TMT  borderline  positive , but no angina ,

What has to be done for him ?

A fellow suggested  a thallium

It was countered by other  ,  we can take it as granted   there is  cold spot in  thallium in a small  posterior segment , then how will you proceed ?

  • PCI, medical , CABG ?
  • CABG definitely  not ,
  • PCI  . . . may be . . .Medical  may be !

When you are confused about  the choice and outcome  . . .confuse the patient* as well ! And , let him decide after a mini  , (but exhaustive ) lecture on coronary blood flow , risk of heart attacks etc .

So in this modern  era of pseudo   empowerment , it is ironical  patients will prevail over doctors after learning   half or quarter  truths  from their android powered smart phones and i pads  !

By the way finally  what  was decided ?

The patient and overwhelming majority voted for a drug eluting stent for  the OM lesion event  as  it appears technically a bifurcation lesion ! This is how cardiology is practiced.

Reference:

Isolated distal coronary artery disease. Presented in cardiological society of  India meet 2005

A clarification .

** One  definition for “confusion” is  being in a  “unclear”  state of mind !

**The aim of this blog is never to confuse the patient. The  above statement is necessary because many patients do believe(or rather want to)  they  understand every thing about their illness even as doctors are baffling with the  great uncertainties and intricacies of  most medical conditions.

Can medical management convert TMT positive into negative ?

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  • How do you classify  stent thrombosis ?

  • What is target vessel revascularisation ?

  • How do  you define  peri-procedural MI ?  Is  troponin elevation alone  enough ?

Want answers for all these ? Your search ends here  . . . The academic research consortium criteria committee provides everything free .

A must read for both  mature and immature  cardiologists . http://circ.ahajournals.org/content/115/17/2344.full.pdf+html

Here is a cartoon for classifying  stent thrombosis (Time based )

There is another etio-pathological /Geographical classification for  stent thrombosis  that will be discussed later.

( Entry block , exit block  , diffuse thrombosis  etc  Read -Geographical miss.)

A word about Academic research consortium

ARC is a consortium of clinical research  from the  Harvard medical school and their associates . The aim of which is  to bring clarity in the  definition of  medical  terminologies and study endpoints.A universal  criteria is being prepared  so that  the study results are comparable which currently use  different criteria  and end points.

For cardiology ARC came out with standardized definition in the year 2007.

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“Limitations of a study”   column appear in scientific articles  because . . .

  1. It  offers   lame excuses
  2. It  informs us  ,  not to get  fooled by  their  finding  .It could  be terribly wrong
  3. The editors won’t publish the paper  without this customary paragraph!
  4. Judge yourself . . . we are transparent !
  5. No study is 100% perfect . Just to make sure the readers are aware of it.

I fail to understand , why even  good articles are rejected for minor  errors  in methodology by many   journals.

Meanwhile ,  how on this earth it’ s  possible  ?   for  some articles to  appear in  top journals ( with questionable conclusions )  embellished
with   major errors in methodology ,  but has  a proud declaration and confession about the  flaws  of the study  in the “Limitations of study” column !

So , in this  modern scientific world  ,  it suggests to me ,  one can  can write whatever  you think as science , as long as  you  declare it and able to impress the editors  to  shift the errors into  limitations column ,  you  are likely to be excused  and also  rewarded !

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Landing an aircraft is a high precision job. A pilot and co pilot with the help of air traffic control  must  do this job meticulously every time .They   are not  afford to make any mistake .Number of lives are at stake.

In cath lab something similar happens every day  although a single life is at stake !   We call this coronary stent landing  . If  it lands  wrongly  it is referred to as  geographical miss ,  a descriptive  terminology for a poorly deployed coronary stent !  ( In strict terms it  should be called as  failed PCI !)

But there are few vital differences   between the two . . .

If an aircraft overshoots  the  runway   it is visible to every body and it becomes a national news next day !

If you deploy a stent away from a lesion it is usually a  silent  event  . Only a few alert fellows and staffs know it ! Patient  often gets discharged  next day (of course after paying the bills )  and  the consequence is often delayed  by weeks  or months  when he comes back knocking  the  ER doors with an ACS !

Final message

The stent -plaque  dissociation is  much more common than we perceive ,  for the simple reason cardiologists have  learnt  to accept   luminal shadows  as surrogate markers for plaques . ( Coronary blindness !)

It is imperative to  apply all our senses properly  in the cath lab ,  like  our  pilots  do while they land  . Be prepared  for  turbulent weather which  is common in cath lab as well !

http://www.sciencedirect.com/science/article/pii/S0735109701011123

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It was  the year 1812 ,  exactly 100 years before the Titanic sank  over the Atlantic  , a  small bulletin from  Massachusetts General Hospital was  released .  It  later on became  the  single most  important  journal  for the medical community.  The appearance of  an article about  angina pectoris in the inaugural issue ,   reiterates the  importance of cardiology  even in those   days of primitive  medical care .

The volume. 1  : No. 1  issue of NEJM egan with a classical and critical observation of angina pectoris written  by Jhon Warren .

http://www.nejm.org/doi/pdf/10.1056/NEJM181201010010101

The first issue of NEJM . . . Witness to 200 years of medical excellence

Those were the days  when angina  was treated with tincture  opium and Fowler solution (Arsenic  potash ) .They  can be  termed as  height  of  inappropriateness  and  also  condemnable acts  . . .  is it not  ? 

200 years  later   . . .  in 2012  what  do you think has changed ,  in terms   of  appropriateness  of management   of angina pectoris  ?

What a surprise ,  two centuries  later ,  even as we are  treating  angina  in hi-tech cath labs  with bio-degradable stents and metabolic modulators   ,   bulk of our  population is  grappling with inappropriate therapy for angina pectoris .

Today ,patients are subjected to  questionable modalities  in the management of CAD ,  which the following paper   tries to expose !

Keeping the inappropriate flag high . . .200 years later in 2012


What a way to progress in Medicine !  The reason for this  “200 year  old ailment”  is  attributed to  extreme scarcity of common sense !

( A study , which says regular exercise  can be  as good as PTCA in multivessel CAD ,  would  sound  as a  “nonsense article”  for most  cardiologists  of  current  generation  !)

Finale

When we look  at human history , where billions  lived ( and continue to live ) in this  age old planet , it  would appear  a trivial matter  whether you treat angina pectoris with Tincture opium / Arsenical potash or  Prasugrel  / Rosuvsatin . . .

Whatever be the scientific advancement  the ultimate outcome on human health will depend on how we apply it. So, all young  medical fellows beware of this   !

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Laws of fluid dynamics dictate there is a pressure drop across   a point of narrowing  and recovery  thereafter  . At  recovery point if the vessel wall is weak it tends to balloon out .This is called post- stenotic dilatation .This is  the anatomical equivalent of Bernoulli or venturi  effect. This theoretically  occur only distal to obstruction .

How do you explain the common observation of pre- stenotic dilatation?

  • Intimal weakening due to disease process is the prime  suspect.
  • Pre stenotic  increment in mean pressure  also play a role .
  • Mechanical distention due to stagnated blood  proximal to  critical obstruction  is  a  logical explanation.
  • Finally and most importantly ,contagious , sub – angiographic  atherosclerosis.

How is  dilatation  different from ectasia ?

May be they are all related phenomenon. The definitions  of ectasia ,  dilatation, aneurysm are  more to do  with semantics than with academics.

Clinical and hemodynamic implication in cath lab

  • Sluggish  flow prone for thrombus
  • Stent selection errors likely
  • Stent dislodgment  and migration

Long term effects

  • In stent re-stenosis is more common if adjacent segment show dilatation.

Finale

Enlargement of vessel wall in both pre and post stenotic segments are possible . In small vessels pre- stenotic dilatation is  more common , while in large vessels post stenotic dilatation is  more prevalent .(Aorta, Pulmonary artery)  The mechanisms are slightly different. Apart from the lesion tightness ,  hemodynamic  and genetic factors are also responsible These dilatations are  often labeled as ectasia in coronary artery  and  most cardiologists  tend to   ignore this finding especially if  the margins are smooth.

But , newer imaging modalities like IVUS, OCT have given   better  insight about these dilatations.These   are  actually an  expression  of the  contagious  atherosclerosis .  Pre-  stenotic segments are prone for extensive disease  than even the diseased segment due to  more hemodynamic turbulence. There is some evidence atherosclerosis progresses  proximally more than distally.Smooth margins within the  pre -stenotic dilatation  does  not guarantee  disease free status.

During PCI  there could be  an  argument for covering the dilated  pre- and post stenotic segments  as well* . (We vouch for endovascular stenting when aorta is dilated why  do we hesitate  in coronary  ?)  .Careful selection of  coronary stent size  is  recommended  and  allowance should be given  for these two (Pre and post coronary dilatation ) patho -anatomic phenomenon.

* Stent missing a lesion is stylishly called geographical  miss ! This should logically include dilated segments also.

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