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Archive for October, 2012

This man enters your cath lab  every morning !  . . .  He is Mr Stent !

Endo-prothe`ses coronariennes autoexpansives.”

    “Endo-prothe`ses coronariennes autoexpansives.”  This is the official name given to coronary stents  when it was first used in man in 1986 in France . The first  stent in human coronary artery was implanted by Puel . Followed by Sigwart  ,Puel combine .

Later on  , the name Stent came into vogue . Surprisingly stent is not a technical name . It is a name of British dentist. To know more about the historical aspects of coronary stents read the following review from Circulation.

References

http://www.fauchard.org/history/articles/jdh/v49n2_July01/charles_stent_49_2.html

1 .Puel  J, Joffre  F, Rousseau  H;  et al.  Endo-protheses coronariennes auto-expansives dans le prevention des restenoses apres angioplastie transluminale, Arch Mal Coeur 8 1987 1311-131

2. Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L. Intravascular stents to prevent occlusion and restenosis after
transluminal angioplasty. N Engl J Med. 1987; 316: 701-706.

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DES is  a revolutionary coronary support device ,   but it was always a suspect  when it came to STEMI and primary PCI .

How good and safe is DES in STEMI ?

Cardiologist were always beating around the bush for a specific answer to this question.

The general  principles and background

DES was thought to be unsafe in a thrombotic milieu .(DES was notorious for acute stent thrombosis) .Still ,first generation DES ( Sirolimus and Paclitaxel ) were thought to be unsafe in STEMI .However anecdotal evidence suggested DES reduced stent thrombosis  . .Then came the 2nd generation DES (Zotarolimus and Everolimus ) . There was a  excitement every where .The logic  was   “If first generation of DES is not good . 2nd generation  must be good”   What a way to think scientifically .Wisdom  did not prevail  . Many started using ZOTA /EVERO  in STEMI  .(Medtronic and Abbot were silently enjoying the scenario !)  And now finally Everolimus was tested with BMS in  STEMI .

That is EXAMINATION trial for you  . . . Published in Lancet  September 2012

It  has found  2nd Generation DES are not superior to BMS in STEMI in terms of  patient outcome . The study broadly concluded  that  the patient related parameter did not show any significant difference  while  stent related outcome seemed  fare better.

Why this patient – stent dissociation ?

How can large group of patient who  have more stent thrombosis and TVR ,  still  no correspondingly increased ACS or deaths

Does this mean  these stent thrombosis are safe events ?

The answer lies in the fundamentals. The  stents  represent  anatomical  correction  , while  the patient  outcome depend   more on physiology ( flow )  so we are back to square one  to the fundamental  coronary conflict  ie  improving anatomy need not impact physiology.

Critical comments

After reading the EXAMINATION  trial  I asked my third year fellow .

What was  the re-stenosis rate  in DES vs BMS  at 6 months ?

He said this study never analysed the issue of re-stenosis  .

I asked him , Are you sure ?

He confirmed it with a firm Yes.   And then , I found this

                                   A shocking omission for a study which is supposed to answer a   critical question whether
                                   DES is good for   STEMI in the long term
Final message
What a way to conduct a large  land mark study ?
This  study   never bothered to find out the re-stenosis rate  with DES  after  primary PCI and compare it with BMS  .
In fact they have conveniently mentioned ,  follow up angiogram was not part of the study protocol .
I concluded  at the end of journal  review meet   , that  this  EXAMINATION  was not properly conducted   and DES may come back with a vengeance   in the near future !

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This is a true story  . . . happened  many years  ago under my direct  vision.

A  48 year old women came with significant breathlessness and catchy  sub -sternal chest pain .

“I  was exerting too much in recent days  doctor” , she said .

Her ECG  showed  a tachycardia and dramatic ST depression in most leads .

The ER in charge promptly texted the cardiologist .

The moment he saw the ECG ,he  had no hesitation , to order for an emergency angioplasty  (  How can he plan a angioplasty  , without even  knowing the coroanry anatomy . some one murmured  . May be   . . what he probably  meant was emergency angiogram   the other explained )    Further , he was telling his    fellows  . . . that  this is going top be  tough case and a possible  left main PCI .

An emergency  angiogram was done .  On table  it was a huge  surprise for every one ,  it was a  a classical  text book   look alike normal coronary arteries !

The moment normal CAG was  visualized  the consultant  concealed his momentary  surprise    and went on to say  it is classical case of syndrome  X   with severe micro- vascular disease causing ECG changes !

As  the patient did not give any opportunity to poke her coronaries   she was wheeled out of  wheeled out of cath lab.

Meanwhile ,  first year  fellow came rushing with the blood reports and biochemistry .

Is everything  alright ?   Yeh sir ,  except her Hb %  . . .  it is  5.6  Grams !

The bewildered  consultant *  realized   the  high  coronary drama , that is  been enacted  over the  past 2 hours !  and  learnt  (and taught) a most important  lesson to their fellows !

Hi guys , this is neither  a NSTEMI nor  a microvascular syndrome X  . . . this is simply anemia related  extreme  ECG changes !  We have erred in our reasoning and  our pre cath clinical scrutiny has  gone awry ! 

He went on to say  ,  don’t worry  many times medicine is learnt in  hard ways  . After all nothing adverse has  happened here .

The women was subsequently investigated and handed over to  gynecologist for a probable hysterectomy .

Final message

Please be reminded  , anemia  can produce  variety  of  ECG changes.  In extreme anemia  global ST depression is  common especially if  tachycardia is associated .

The lesson here  is ,  whenever  gross  ST depression is witnessed  with vague chest pain  check the hemoglobin first . This is an unusual story of a women  ,  with simple  anemia  (due to   chronic mennorhagia )   landed in cath table in an acute fashion .  Luckily  she  did not have any  incidental coronary  lesions  that prevented her becoming a  greater cath lab  victim !

* The bewildered consultant is none other than the author  of this blog.

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Fractional flow reserve is  a new coronary hemo-dynamic para meter used to assess physiological impact of border line lesions in coronary artery disease. The calculation is simple

FFR is  a terrible concept * for two reasons .

One ,  it never bothers about flow * across   a lesion. It simply  relies upon  pressure drop. We  know  there  is an intricate relationship   between pressure and flow . Simple pressure drop can never be  expected to translate into incremental flow in biological systems .

(FFR anology  in co-arctation of aorta . Can you take difference between upper limb  BP and lower  limb BP as a most accurate   Index of severity of co-arctation of aorta ?  )

How crude it would be   . . .  to  believe so ?

Two   it  ignores the  morphology of the lesion . We know an eccentric soft  lesion with a  good distal   FFR  is  live  coronary explosive .

The  FAME 1 and FAME 2 studies  glorified  FFR  !  I differ in many ways .

Some of  the  observations made about FFR.

  • FFR is to be  done only in discrete ,  safe looking  , intermediate lesions .(Do not ever attempt it in a eccentric lesion )
  • FFR wire is a  stiff ( stainless steel ) wire .  Careful maneuvering is necessary . Lesion crossing  and pull back  FFR wire require some expertise.
  • FFR / OCT  combo,   increase  not only the  fluroscopy time  ,  this procedure can be  more complex than  the intended   PCI .
  • My colleagues tell me FFR measurements are not often  reproducible .(I have little experience in this )
  • Adenosine induced vasodilatation  is not natural physiological model . Further it has  a potential for  a coronary steal if there is near critical lesion in contra lateral artery.
  • There are many occasions   FFR wire has caused  dissection  and  subsequent stenting was necessary  .(The very thing  the cardiologist wanted to avoid !)
  • Bifurcation lesion FFR measurement is prone for errors
  • FFR in two tandem lesions cannot be assessed   accurately
  • Post PCI FFR is not practiced routinely in may centers  the fear of  status quo of FFR.

Final message

This post is not to defame the FFR as a concept . Just to make you think  . . .  how often ,  we  are entrapped  in a  pseudo -intellectual  game in  the cath lab ! FFR  as a tool , can still  be valuable to assess coronary hemo-dynamics in a selected lesion population especially,  discrete,  single vessel ,  or left main disease  with around 70 % narrowing . But never go with FFR alone .Consider the morphology , location   of the lesion .

Finally do not forget  ,  the   good old  EST  can  give a stiff  fight  for supremacy over FFR  in terms of assessing physiological impact of a coronary stenosis (Especially in single vessel disease ) 

Reference

Fractional Flow Reserve versus Angiography for Guiding Percutaneous Coronary Intervention . http://www.nejm.org/doi/full/10.1056/NEJMoa0807611

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Hi all ,

I get frequent comments about my blog. I do try to answer many of them . This is a very unique one , and it is making me think further.Since he has specifically wished his clinical data could be eye opener for others ,  I am jut posting it here . The comment was in response to my article  Who said coronary collateral circulation will not support exercise ?   here is  the extract

Dr. Venkatesan,

I read your blog with great interest and I think I may have something useful to contribute from my own personal experience. I am a 68 year old male with a long history of smoking (for fifty years), and a history of uncorrected hypertension over the years (it has been corrected to normal with medication for many years now). I am a non-smoker now for the past 18 months. I have PAD and a moderate aortic aneurysm of about 3.5CM (ascending and descending) which is being watched with regular vascular scans.
The common femoral arteries in both of my legs are nearly 100% occluded between my thighs and my knees, and yet my ankle and toe blood pressures (and my circulation in my ankles and feet) is almost normal. The reason for that is that according to the vascular scan, my deep femoral arteries are much larger caliber than normal with extensive vascular collateralization by passing the common femoral occlusions.
About twenty years ago before the PAD diagnosis, I realized that I had claudication in both of my calves when I walked a short distance. I expected this was being caused by an arterial blockage in my legs, so I went to the gym every day for about three years, and walked through the pain every day. I believe this contributed to the formation of the collaterals that have perhaps saved my legs and feet.
I also have heart disease, and had a fairly minor heart attack in 1999. No stents were placed nor angioplasty performed at that time. I recently had an arteriogram and cardiac stress MRI which showed that two of the three coronary arteries are now 100% occluded (apparently I had another cardiac event and did not know it). The cardiologist says that the LAD is in extremely good condition and has numerous collaterals branching from it. I have no symptoms whatever from all of this, except that my LVEF is low (about 35%). I walk at a very brisk pace six miles per day, five days per week, and I monitor my pulse rate with a pulse monitor when I walk. I keep my pulse between 115 and 120 which I calculate to be 80% of maximum for my age. I believe this cardio exercise / walking has also helped with the collateral formation, and I am hoping to bring the LVEF back up to a reasonable number with this exercise regimen.
My cardiologist has recommended an ICD, but I have decided against that since I have never had VT or VF or any other type of cardiac arrythmia (except for non-symptomatic PVC’s which I was born with).
I believe that I am the lucky recipient of good genetics to begin with, but also I am highly motivated now to take better care of myself, and know as much as I can about the conditions that I have. I plan to have an echocardiogram in six months to see if the LVEF numbers have improved, and I fully expect that they will have. I give credit to the smoking history for the vascular problems that I have including the cardiac problems. I am a lucky person I think, and suspect that not everyone has the fortunate ability to heal themselves the way I have.
I have asked for copies of my arteriogram and stress MRI records. If you are interested in looking at these I would be happy to share them with you.

The letter ends .

Dear Mr Weigel

Yours is an extremely interesting story  told in a most scientific manner.Thank you .

It gives me great insight  ,  how a  human vascular system  can  transform when confronted with  natural disasters like multiple blocks on its way .A flowing river will definitely reach its destination  however bizarre the path it takes . Human biology is vested with vast reserves of genetic building blocks put on sleep  mode. While billions of dollars are being pumped into do research in human angiogenesis we have tuned a  blind eye to the vast net work of natural collaterals.

Our clinical experiences also tell the same thing . In chronic total occlusion  majority of patients would develop good collaterals if only we do not  tamper  the  main vessel  .None of scientific studied available has proven opening CTOs (Chronic total occlusions) has improved the clinical outcome .

Regarding  the guidelines  for revascualrisation ,  I am yet to come across a standard scientific guidelines that includes the extent of collateral circulation  as one of the determinant for need for revascularisation !

I will definitely use your case study for the benefit of so many patients !  I always feel , a properly interpreted experience  , even from a  single patient   can make a tremendous impact in the growth of science .

Thanks again for sharing your personal health issues !

Dr Venkatesan
Chennai .India .

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