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Archive for the ‘Cardiology -Interventional -PCI’ Category

How to rule out critical left main or proximal LAD disease with near 100% specificity without coronary angiogram ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , , , , , , on July 10, 2011| 4 Comments »

Very often in clinical  practice  cardiologists are asked to R/O significant coronary artery disease in asymptomatic persons .This population includes  people with multiple risk factors like diabetes, HT dyslipidemia  and non specific ST/T changes in ECG.

Many of us have lost the confidence of   ruling out CAD   in these population without looking at their  coronary angiogram.

Is it a right way of practicing cardiology ?

What we need to realise is,  we are asked  to rule out any critical lesions that are going to make a impact on these  other wise comfortable patients.  Nothing wrong if you miss a 30% lesion in PDA or OMs or diagonals !

Can we do this without doing coronary angiogram ?

Yes ,  we can .

Step by step  Ask these questions

  1. Ask the patient , if  he /she   can climb three  flight of  stairs  without any difficulty or
  2. Walk briskly for  20 minutes (5km/hr)

If yes , give  a   certificate   that he  has no critical  left main or proximal LAD  disease.

If you do not believe in his words , put him on a tread mill ,  if he crosses   stage  3   Bruce in TMT ( 9 mts)

give the above certificate  “with a frame”  now .

For still suspicious  physicians ,  We have  one more  investigation called  echocardiography !

Echo : The forgotten tool  for screening left main lesion.

Modern day echo machines have a  3mm resolution power (Many have 2mm ) .While ,  we are expected to look for 3mm vegetation to R/O Infective endocarditis , rarely is  a  cardiologist ,  tuned to  look for the left main ostium  in routine echocardiography  which averages 4-5mm is size. (Left main by echo link to another article)

In short axis  view just tilt at the level of pulmonary valves  (Atrio- pulmonary sulcus) one can visualise the left main ostium and the proximal left main emerging from the 4 o clock position. If you are lucky you can see the entire left main.

If nothing satisfies the physician (Or the patient)  ,Refer him for sliced CT scan , catheter coronary angiogram , or a  nuclear Imaging .Be ready for the attendant anxiety, interpretation errors, corporate  pressures , urge to  balloon ,  kick backs etc etc

By the way , how can  one  be happy by ruling out only left main disease ?  Is it not other lesions possible ?

Experience (Not science) has taught us  no  critical coronary obstruction is  possible ,  if  a patient walks for  9 minutes  in treadmill (10METS).

Even if it is there (A remote chance)  there is little documented benefit of any revascularisation procedure.

Counter point ?

Is it not a “crazy idea“  to rely on patients history in ruling out  CAD   in these era , where   angiograms relayed  live  into   cardiologists  ipad  ?

Science has no value if it is not applied  for the patients welfare. Meticulous clinical  examination (And application of mind)  is the foundation stone on which  any medical investigation and therapy  should be based  upon. Most of the inappropriate coronary revascularisation are due to  neglect   of  this vital  component of clinical examination.

(I wonder ,  is it  really possible  these ” acts of omission”   be  deliberate some times  ! )

Final message

Clinical interrogation  may  miss an insignificant  CAD  ,  but it can never miss a critical CAD* .

 

Do not do coronary angiogram routinely to R/O  CAD.

It is not the way cardiology is to be practiced !

If only we apply  those  simple,  time tested concepts in every day practice we not only  save millions of  Rupees ,   but also thousands of futile   diagnostic tests and associated untoward effects can be avoided.

* Senstivity of  ruling out any CAD is about 70% , but it’s capcity to R/O critical CAD approaches 100%.

Reference:

Please refer your own Brain.

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How useful is balloon atrial septostomy in refractory pulmonary hypertension ?

Posted in Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Land mark studies, tagged , , , , , , on July 6, 2011| Leave a Comment »

Management of  severe  pulmonary hypertension continues to be a difficult task .Medical therapy is not definitive, in-spite of the new prostocyclins, endothelin antagonists and  sildenafil analogues.Natural history  depends mainly on  the presence of  any treatable cause ( Especially ,connective tissue disorders)  ,  supportive management along with anticoagulation.

Ultimate  strategy  would involve a   plan  for a “Lung “or  “Heart -Lung”transplantation  , if feasible. Last decade saw an innovative modality of creating an  artificial inter atrial  shunt to decompress the right heart .This had varied response in the  real world  , still  most  showed some benefit .In fact , in 1998 the world symposium on PHT ,  formulated guidelines for BAS (Balloon atrial septostomy)

Principle of  Balloon atrial septostomy (BAS)  and mechanism of benefit

The symptomatology  of  pulmonary HT  is largely  determined by mean RA pressure .

Puncturing  the  IAS and diverting blood  flow into left atrium would decompress the RA ( or even the RV )  and reduce the Mean RAP.

The resultant  right to left to shunt  can   increase the cardiac output  only  slightly ,  still  good enough to  provide   relief from the fatigue.(Though at the cost of  desaturation.)

What is the risk involved in the BAS.

Procedural risk of  a cath study in a sick  patient with hypertensive lungs (Can be really high !)

In some patients  even a small  fall in systemic  oxygen saturation can be counter productive.

What is the balloon used ?

Mansfield or Tyshak balloons are good choices .

Balloon diameters are between 5 -14 mm

Technique

Involves standard Brockenborough needle /Mullin sheath /Guide wire in pulmonary vein.

Atrial anatomy to  be well  analysed prior to BAS  . (Please note even though it is similar to PTMC , anatomically we encounter a large right atrium rather than left atrium .)

Fluroscopy with  TEE guide optimal

Pulmonary angiogram might help.

Intra-cardiac  Echo may be  ideal.

Blade septostomy may be preferred if hardware is available

The endpoint of procedure

  • Size of ASD > 5mm
  • Fall of arterial saturation < 80 %
  • Sustained atrial fibrillation with hypotension
  • Any  disabling complication

Hemodynamic impact

  • Cardiac output increase by 750 ml to 1 liter
  • It is expected ,  RA  mean pressure  would fall at least 5mmhg from  the baseline value.
  • PA pressure , no significant impact expected.
  • Tricuspid regurgitation regresses.
  • RA,RV size marginal reduction observed.

Follow up and outcome

  1. Greatest  relief is from syncope.
  2. Functional class improvement  in >50% .
  3. One year survival benefit is substantial (75-90%)  .Beats the  natural history (40%) convincingly.
  4. Late deterioration  can occur as ASD gets closed in few.

When  BAS is contraindicated ?

  1. Critical RV failure
  2. Patient in class 4
  3. Mean RA pressure > 20mmhg
  4. Pulmonary vascular resistance index> 55 Wood units / sq.meter

* BAV should not be considered as a  live saving  procedure  in any dying patient with PAH.  It needs to be  selected early and carefully .In fact,  the very high procedural complication  rate is related to late selection of patients.

Natural foramen  PFO better than BAV ?

We do not know yet.It is highly possible  natural opening up of PFO is good thing to happen for patients with severe pulmonary hypertension.

Reference

1 . SS Kothari  et all  Indian heart journal 2002

2. http://content.onlinejacc.org/cgi/reprint/32/2/297.pdf

3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC484602/pdf/heart00028-0066.pdf

  4. http://erj.ersjournals.com/content/early/2011/02/24/09031936.00072210.abstract

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What is the direction of blood flow across patent foramen ovale(PFO ) in otherwise normal adults ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology-Anatomy, tagged , , , , , , , , on June 26, 2011| 1 Comment »

  1. Left to right
  2. Right to left
  3. Can be in both directions
  4. No significant flow at all !

Answer :   Every response can be correct

The patent foramen ovale is a physiological orifice , which  becomes  pathological if persist into  adult hood .The incidence is estimated to be about 20 %  of the population (Amounts to 100 crore PFOs roaming  in our planet!). It makes  no sense  to  believe  just spotting  a  PFO  in routine echocardiography be termed  as pathological . But recently  (Adding much to  interventionist’s  delight ! ) the presence of which is being linked with migraine and stroke in young.

The size of the orifice can be from a single millimeter to one centimeter* . The direction of blood flow in PFO   is determined by the mean gradient across the orifice. It has to be  left to right  as the LA pressure is  generally   higher by few mm mercury  ,hence there is a small  tide of flow entering into RA with each left atrial filling or contractile wave .(v and a ). This  quantum is miniscule and has no hemodynamic significance in most life situations.

* Some call( Wrongly ) 1cm PFO  as small ASD.

When can Right to left to flow occur ?

When the right atrial pressure increase more than LA pressure it is obvious  blood can enter LA . It is well-known this occurs  in any pathological situations like RVOT obstruction severe PHT , tricuspid valve obstructions etc.

Physiological  Right to Left flow :

Forced expiration (Valsalva) can cause transient  right to left flow. This  may happen in many real life situations like straining, heavy isometric exercise, blowers, muscians  etc.

Which is clinically  significant ?

Left to right or right to left  ?

Left to right shunting is rarely an issue as there is no systemic  desaturation.

Right to left  shunting  can be  important for two reasons

  1. Arterial desaturation( transient )
  2. Shifting of venous debris into arterial side  can result  in potential paradoxical embolism .(This can be air, clot fat , amniotic fluid etc)  This is the reason stroke in young is closely linked to presence of PFO.

PFOs during positive pressure ventilation

PEEP is a classical example where a right atrial positive pressure ,  shunts the blood in pulsatile manner into left atrium .

Platyponea  hypoxia  syndrome .

This is  postural right to left shunting  across PFO .It  is a less recognised (but a common entity) where -in ,  when the patient  lies down there is a  right to left PFO shunt and transient hypoxia .This is often corrected as the patient sits up. The reason being  the valve of PFO , the   door like flap  which guards  the orifice  ,  is aligned   in such a fashion , it  opens up in a  lying posture(Aided by gravity ?)  , shuts down in  sitting posture .It should be noted  The PFO valve is not a constant feature  . The size  of this valve , the stiffness , the hinge points , ability to  float  are highly variable .Hence the clinical variation in PFO syndrome.

The IAS septal aneurysm is an  important variation where the valve of PFO balloons out into left atrium  may become a nidus for thrombus or a focus for atrial arrhythmias .

Stroke in young  and PFO  :This  topic  deserves a separate article

Reference

Anatomy

Excellent PFO images from Yale university library  ( http://www.yale.edu/imaging/chd/e_pfo/index.html)

 

http://chestjournal.chestpubs.org/content/100/4/1157.full.pdf+html

http://chestjournal.chestpubs.org/content/118/3/871.long

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

Excellent PFO images from Yale university library

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Doing bad with good intention !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Coronary artery disese, tagged , , , , , , , , , , , on June 24, 2011| Leave a Comment »

Human body is a bundle of mystery.   In an  average  life span of human beings,   millions of   afflictions come and go . Most are benign . Our body has a  full-fledged defense ministry    armed with sufficient weaponry in the form of , immune cells, thousands of regulating enzymes, hormones ,  cell service molecules  etc  .It can tackle most of  the ailments our body encounters  with out a doctors help (Jungle animals rarely die of disease!)  .

Of course , the body  needs  external help  when it’s  intrinsic resources fail . There are few   serious disorders that has to be intervened .However ,a big  fraction of them  will   die  in spite of whatever we do .

Is it not  fascinating to know more than  100s  of chemicals  act day in, and  day out ,  to  prevent our  blood  from clotting and keep it flowing .  If only the natural lytic mechanism fails  for an hour , and  create a  vascular  chaos   we will realise  importance of it !

Even as we debate appropriateness of medical care  in this  21st century   here is startling scenario ,

When a child  presents  with physiological hypertrophy of lymphoid tissue  , as their body begin to  learn and record the micro biological mysteries  of our environment  , it is  often “cross labeled ” as  tonsillitis  or appendicitis and  end up in surgical tables.

This article just released  in  European heart journal , tells us ,  how the rampant use of appendectomy and tonsillectomy in the early child hood  may make them susceptible for CAD in later age group.

The role of medical professionals is identify the trivia ! and prevent unnecessary interventions.

Unfortunately  or (Should I say dangerously)   many of  the   professionals  understood it  in a diagonally  opposite manner . Identify the trivia ,  instill fear in our patients  and intervene ,   in the process injure  our great biological system.This is also applicable to many cardiac  interventions.

Final message

Heavens sake ,  youngsters  , please  remember  , medical  profession is all about removing suffering from patients  . Do not fish out “non -existing” illness from your patients  body !   Let me remind you ,  professional approach means  , whatever you do it should be in the  interest of our patients . The moment  you deviate ,  you cease to be professional .

Also realise  ,  good   intentions can never be an excuse for  inappropriateness !

Reference

http://eurheartj.oxfordjournals.org/content/early/2011/05/27/eurheartj.ehr137.abstract

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Catheter whip + Calcium in aortic valve = Stroke . . . but TAVI is safe !

Posted in cardiac surgery, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology journals, cardiology-ethics, tagged , , , , , on June 19, 2011| 1 Comment »

There was a time  , even  cardiac catheterisation was contraindicated if the aortic valve  is  significantly calcified. LV angiogram was judiciously  avoided in all such patients . Why ? A significant increase in disabling strokes were witnessed .Those were the time  a sense of  fear (common sense ?)   prevailed . Every one was following this dictum with sanctity .

Now in 2010 .TAVI has  arrived with great fanfare . We not only cross the calcific valve , we literally play  a violent contact sport   in the aortic root  for over two hours with all sorts of pushes  and passes  on  a  fragile valve.And  we are happy to  claim that  stroke rate is comparable to aortic valve surgery and TAVI is not-inferior to AVR in high risk surgeries .

How is this possible ? As the times  changed ?  Is it true , our stroke  fears are just imaginations  or have we lost our  faculty of  reasoning and  sense ? (Will it be logical to  fund a research  if someone claims a  surgical  technique  to replace  aortic valve in  a beating heart without aortic cross clamping !)

Data shows  even if  distal protection devices are  used the stroke rates  can reach to  objectionable levels .It remained  a mystery ,  at least to me how no body was  questioning this ? I was happy to find this editorial in NEJM which  just stopped  short  of   banishing  this modality in its current form.

http://www.nejm.org/doi/full/10.1056/NEJMe1103978

What price it asks ?  and leaves the readers to guess  the answer ? NEJM wants to be too decent and polite , but in science politeness is generally not required  ,  as long as  your  observations are  correct !

For all those enthusiastic  interventional cardiologists  here is  a positive message .

Nothing comes easy in science.Great  inventions do have problems  initially .  Without  major hurdles  there can be no progress ! It is  because of   you  modern cardiology is making giant strides . Remember  the early days of angioplasty , early days of pacemaker  .  But  please realise  the most important issue  is ,  whatever  we   innovate or discover it  should be shown   superior to the  best  existing modality in all aspects(Technique,  procedural  complications, long term  outcome ,costs, side effects etc  ) .It is awful  to note   new drugs or devices  are  rarely compared with  the best treatment that is currently available .

A  new  treatment that simply  complements  or proves  non-inferiority  can never be considered an invention. How can we   portray radio frequency  renal denervation (  a complex  lab procedure ) for controlling blood pressure   as a great innovation for man kind  while we  have   so many drugs and  modalities  available  at a fraction of the cost  with  little  consequence .

Reference

http://www.escardio.org/congresses/esc-2009/news/Pages/Transcatheter-Aortic-Valve-Implantation.aspx

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In the management of CAD , cardiologists attack the lesion , surgeons avoid the lesion . . . who is the winner ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged , , , , , , , , on June 18, 2011| 2 Comments »

Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !

Reference:

http://www.thelancet.it/journals/lancet/article/PII0140-6736(90)92230-F/fulltext

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

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How does thrombus look like in coronary angiogram ?

Posted in Cardiology -Interventional -PCI, tagged , , , on June 17, 2011| Leave a Comment »

It is a fashionable topic  in  cath meetings and workshops  to discuss  about thrombus loaded coronary arteries. Still  visualizing a  thrombus  in coronary angiogram is  never a  mean  task !  It needs  lots of  visual  acuity  and  imagination to recognise   intra coronary thrombus.

  • A lesion which looks fresh with multiple layers of  irregularity within the lumen is  often assumed to be thrombus.
  • An   intra luminal filling defect   is the  most often  used  “criteria  to suspect” a  thrombus

A long segment thombus with dye penetrating and coating the thrombus all around

Thrombus  vs plaque ?

Both are  radiolucent .  But a thrombus  or a plaque coated  with  dye  will make it radio opaque. The radio opacity of a thrombus is determined by extent of dye coating ,  the thickness of the dye layer, obliqueness to the x-ray beam . A thrombus plaque  interface can have two different  planes  of densities.

Theoretically dye can not encircle  a plaque  in its entire circumference as it will be attached to vessel wall (Unless  circumferential  dissection is present  )  Hence , dye can not coat a plaque fully ,  at best it can give  an appearance of eccentric filing defect  with over hanging edges .  While a  thrombus  can manifest with a  complete filling defect

Thrombus vs dissection

This is  still more complex   . Both can have a filling defect  .A  flap is a  line like  filling defect To complicate the issues further,  both thrombus and dissection occur together in the same spot .

How confidently  one can  identify a thrombus in coronary angiogram ?

During acute MI there is no difficulty in identifying it ,  as every acute  obstruction  must contain some thrombus* . Some interventionists  have special  ocular   sense   to   detect thrombus. Few others rely  on their intuition  rather than  solid evidence.

Sucking out a thrombus during primary angioplasty  has now become standard concept and is indeed  feasible  in most situations. It is obvious we have a task  on hand to identify thrombus correctly and quickly during primary PCI /UA .

Blind suction,  even though rewarding should be avoided.  Caution is required as blind  suction pulls a plaque with force !

A plaque debri  with a  thrombus, a dissected flap  all can combine together   to produce a complex  “masala”  of  coronary lesion especially after a difficult guidewire cross . This is refereed to as a battered coronary artery .These are the lesions which are prone for recurrent acute or sub acute thrombosis even if the lesion is  stented  properly.

During  primary PCI   thrombus coated dissected plaque  is just tucked  and  opposed behind the  gentle stent struts.The thin layers of thrombus between stent struts and the vessel wall is  missed  , 100 out of 100 times   by coronary angiogram . (IVUS very good in detecting this) .Because of this risk , Intensive anti -coagulation in complex PCI becomes mandatory

* Diagnosing thrombus in a chronic lesion is  much . . .much  difficult !

What are specific  modalities available  to  confirm thrombus

IVUS, Angioscopy, OCT are  hi tech tools to identify intra coronary  thrombus .(Which i feel  have little practical  value in real emergency situations)

Final message

Thrombus  may be a  key  finding  in acute coronary syndrome (Of course  the contribution of fissure, injured ,  plaques to the lesion can never be underestimated . ) Still , we have no simple , accurate method to identify it  ( Forget quantifying it) . Lots of assumption , guess work and gut feeling is at play in the cath lab .

We  expect better online , real time tools to improve out tentativeness inside the coronary artery  .

//

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Stenting can convert a stable plaque into a vulnerable plaque . . . True or False ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , , , on June 15, 2011| Leave a Comment »

An atherosclerotic  plaque is termed  vulnerable when it’s  future behavior is unpredictable .A vulnerable  plaque has a  tendency to get occluded at any time.

Anatomically  a  vulnerable  is  present  , if the lipid core is more , fibrous cap is  thin  and  a  large lipid  core hanging eccentrically. A plaque with high temperature (Hot plaques ,febrile plaques)detected by OCT/Raman spectroscopy or thermography

Note the T cells and macrophages wage a losing battle against a metal monster !

What is the best method to calm down these vulnerable , hot ,inflamed plaques ?

A stent which scaffolds a plaque is believed to stabilse it  and  make it less vulnerable to rupture. This is the most optimistic view on coronary stenting .

Here comes  a pessimistic view !

A metal inside a coronary artery covering is  additional  threat .A metal  is   perennially  thrombogenic  ,especially the drug eluting stents which suppress the normal endothelial  function .

What  is the realistic view  ?

A stent should be used cautiously and judiciously in coronary plaques  with   high risk features  .Here  a  stent  in all probability  converts a vulnerable plaque  into a  relatively stable plaque

When stenting is done indiscriminately( without application of mind )  in stable non flow limiting lesions  stability is replaced with vulnerability.

Is it not curious to know  any angina  in a patient  who  had   PCI  for chronic  stable angina  is labeled  as unstable angina. 

Vulnerable stents

Following are typical  clinical scenarios   where stents could  carry a vulnerability  tag . 

  1. Poorly deployed  stents
  2. Properly deployed (but unnecessarily deployed especially in chronic stable angina )
  3. All Bifurcation stents
  4. Distal left main stents
  5. Stents with plaque prolapse
  6. Finally and most importantly all  drug eluting stents are considered  vulnerable ! (That’s why  our patients has to  live at the mercy of dual platelet blockers , life long.  Of course , there is no life time warranty   that  drugs do their  job properly)

And now . . .  you answer my  question !

Can  stenting convert a stable plaque  into vulnerable plaque ?

  • If  “yes’ is your answer your patients are in safe hands .
  • If  ” No”   is  your  answer ,  you are  fit to become a leading  interventional cardiologist !

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Double blinded , prospective , multicentre , randomised nonsense !

Posted in bio ethics, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged , , , , , , , , , , on June 5, 2011| Leave a Comment »

Medical  research can be divided into few  broad  categories

  1. Basic science  research  in animal models
  2. Basic science  research   in Human
  3. Clinical : Bedside-  observational
  4. Clinical:  Epidemiological
  5. Community based long term data analysis
  6. Interventional -Drug /Device/Surgical

*Logically the  top 5  should  constitute  the bulk of research  ,  in reality    last one wins the race with considerable ease . Why ?

The important issues that  confront  today’s medical research  starts  right from the  “Aim” of the research ,  methods , materials statistics,  and  goes on  to   ethical issues , conflicts, futility ,  gimmicks  0f  publication  ,  marketing and ultimately left  for human assimilation .

(Read a related article in this blog   can  Aim of a study be wrong ?)

Data(s)  won’t  lie  . . .humans do  !

Science is nothing but collection of  facts ,  rechecking  the facts , and  finally confirming ,  they are indeed  facts. So medical  data collection becomes vital .  Data,  if  properly collected ,  wont lie.   Bias is always an issue in prospective trials. Further ,  and whenever and wherever  scientifically  motivated  human  beings interact with  data  the later   becomes a vulnerable  target and  get manipulated   for various reasons . (Read the famous article on data torturing  in  NEJM : I will link it soon  ) So blinding  becomes  mandatory   and it should  be total as some studies  tend  to  gain vision half way through !

Image courtesey : Jupeter images

Simplicity of observational studies.

We  give undue importance to RCTs . What we fail to understand is RCTs are required only  in selected situations in medical research (New drugs and interventions ) Meanwhile , we can do wonders with retrospective observational  data. These  data  can not be  manipulated  as the events  have occurred already and those people who collect or record the data  wouldn’t know this data is going to be utilized  for a study (This  , in fact  is  equivalent  to 100 % natural blinding and constitute a  real world study )

Observational  study can involve  patient behavior ,    disease behavior  , community impact, drug action, investigation modality , etc  . . .etc  . Your mind is the limit . Cost of doing a observational study is less but the impact on the society can be great .

Observing skills are the  biggest causality in modern medical times , This was  only scientific weapon of  our ancestors had , which they  used in an exemplary fashion .( Recall how Heberden described angina and Harvey taught us about circulation without even ECG and X RAY chest )

Fraud in medical research

Wherever big money is flowing corruption and fraud is unavoidable . . .at the  least . . .  we  should recognize it

( Many journals  just point out this possibility by simply displaying message of conflicts .They do not bother more than that  . . . just a warning message  )

Now in the modern scientific world  ,   even as the   genuine contributions   from our ancestors  left to  stare  the back of us  , we try to indulge in all sort  of unpleasant things.

In an audit against fraud in medical  research ,  it was found most of the fraudulent research happened with drug and device trials and few in basic science involving genetics and molecular medicine . It  was  rare to identify fraud in research involving purely clinical and  epidemiological  analysis .

Drug trials  need to be prospective . Vested interest can play  havoc in prospective data .There is a  thing called steering committee in all major studies   . . . we do not know what does the  word  steering really   mean .

There has been many  occasions  even well conducted studies turn out be  fraudulent . Now we realise many such studies are struggling to prove its worthiness .

In fact  it is argued every study before getting published   should undergo a  global ,  independent  trial   monitoring  board for genuineness  of the study . (Not the customary  peer review !)

Final message ( Sorry its  a  long one !)

We have a huge problem  here . I am afraid  we  haven’t even  understood ,  what  we  mean by medical  research !

For today’s   youngsters  medical  research means doing sophisticated  tests in nano- labs  , human genome  mapping ,  space age imaging modalities  or  involving a multi- billion dolor drug trials . This is absolute  falsehood.

What we need to do is   “search” , ” search”  ,  search again (That is   why it is called re-search )  for all those elusive  problems  our patients   face .Not only in their body , in their  home , in their community,  etc . Every  patient  teach us  few points,    observing and learning new things  and  publishing is  also an important aspect of  research .One can do  a instant   research in the crowded  OPD of a hospital   , in the wards , (What is the profile  of fever pattern in a winter season in your hospital ? does it reveal a new viral epidemic ?)

An ideal research  should  identify a problem and suggest a practical solution to a given problem .There are millions of such issue waiting for our attention in the bed side.  But what is happening  currently ? Current medical research is largely direction less ,  fueled by vested interest ,  makes  sure it avoids  all genuine problem areas !

Many studies  happen  based on  flimsy scientific   basis  .We are still  wasting our time to increase human HDL levels. ( Not with standing  the famous Torcetrapib fiasco  )   .Hundreds  of thousand of dollars   are pumped into this  research even after realising  only the  endogenous HDLs generated by natural methods like  exercise   are  the really  good HDL !)

While we do million dollar research   with a dubious risk factor called  high sensitive C reactive protein  ,   there is  no takers against number one killer disease of human kind  namely  “The  poverty” (WHO ICD codeZ59.5 )*

Let us prey   God  to instill common sense to all of us  . Patients  suffer with disease and we suffer from irresponsibility  or reduced responsibility ! It  makes us happy at-least few forces  like Lancet  , British medical journal etc are fighting lone war  against this  ailment  medical science is suffering .

*Please note :  http://www.icd10data.com   WHO labeled poverty as disease many years  back without much fanfare ! It is rarely mentioned in  any  graduate student**  medical text  in whom our future lies .  I do not know whether  Wars  and terrorist acts  been included as disease  or not !

**Our students  rattle about  about the  exotic  tick borne  Lyme disease happening once a year in remote hills ,    while  most will stare blank   when asked  how to diagnose and  treat  nutritional  anemia with  which millions suffer  every day !

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What is PAMI 3 coronary flow ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , on June 4, 2011| Leave a Comment »

While anatomical  grading of obstructive  coronary lesions are  quiet easy ,functionalc assessment is always difficult.The famous TIMI grading system had one unique problem .TIMI 1 and 2 grades are relatively easy to grade. TIMI 3 flow  which corresponds to normal penetration  and normal  distal perfusion  . This distal perfusion was entirely optical .

This was an important issue , in assessing post  PCI or thromolysis patients . It was realised much later , TIMI 3 flow is  stunningly  heterogenous group  .It was  ironical  ,  even after a successful PCI ,  restoration of TMI3 flow  could not be relied upon as an index of successful PCI  .

So , the PAMI study group included time as additional factor in grading TIMI 3 flow. PAMI 3 is  essentailly same as  TIMI 3  flow but  with a  condition , complete  distal vessel filling  must  occur within 3 cardiac cycle . PAMI 3 can be termed as a   refined version of TIMI 3 introduced in the evaluation of success of primary PCI . This helps us  define  or  diagnose   slow filling .

What are the other ways  to grade TIMI 3 flow

  • Myocardial blush index
  • TIMI frame count ( < 25 frames )

PAMI : Primary angioplasty in myocardial infarction

TIMI :  thromolysis in acute myocardial infarction

Reference:

http://circ.ahajournals.org/cgi/content/full/circulationaha;104/6/624

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