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Posts Tagged ‘pci’

Reporting a coronary  angiogram  may look like child’s play  for most cardiologists. Many do it in less than a minute. (It goes something like this  90 % LAD , 30 % ostial OM1, 50 % mid RCA etc etc ) The famous and meticulous  classification of Ellis and Ambrose proposed  two  decades ago appear largely redundant.

In this review we shall  briefly  debate an eccentric plaque or lesion .

Pathological definition

Pathologically  an eccentric lesion  will have a disease free arc  within an  atherosclerotic lesion.If we apply this criteria most of the plaques appear to be eccentric.

Angiographic definition

In simple terms  eccentricity is  said to be present when the plaque  volume is three times more on one side when compared  to opposite side .

The incidence of eccentric lesion is largely under estimated.  It can be up to 40 % of all lesions.

It has histological  as well as  hemodynamic  significance.

How to measure eccentricity index ?

Ratio between maximum plaque thickness and minimum plaque thickness (Including the media )

Image courtesy modified from Circulation. 1996;93:924-931

In the above figure : The eccentricity index is measured  as the ratio of the maximum  to minimum plaque plus media thicknesses. In the eccentric lesion  the maximum wall thickness measures 2.6 mm, minimum wall thickness measures 0.2 mm, and eccentricity index is calculated to be 5.2.  In the  concentric lesion  the maximum wall thickness measures 2.2 mm, minimum wall thickness measures 1.6 mm, and eccentricity index is calculated to be 1.4.

What are the associations of eccentric plaque ?

Calcification and hard plaques are more common in eccentrically placed plaques.The  most vulnerable point for plaque  rupture or disruption is  the shoulder region between normal and plaque segment.

A long eccentric lesion with over hanging plaque

 

Clinical implications

  • Acute recoil
  • Coronary spasm
  • Mechanical effects : Asymmetric expansion of stent
  • Drug eluting stents

An arc of normal plaque circumference predispose to acute recoil and spasm.this is logical as the normal  arc will have a fully functional  medial smooth muscle  which are prone for spasm.

Does stenting reverse  the eccentricity of plaque ?

It may not .  The drag effect of major plaque mass may either result in plaque prolapse or  asymmetric stent approximation  or even stent crushing effect.

How does the  the stents  elute in an eccentric lesion ?

Stents are not intelligent enough to  differentiate  the plaque surface and normal surface. We  also know these drugs are  toxic to  normal endothelium  and hence  are not welcome in the normal arcs of an eccentric lesion.

Since the drug secretion   is uniform throughout the circumference   it makes the   DES a perfect misfit in eccentric lesions  As  we  realise most of the lesions are pathologically eccentric one can guess the long term  consequences .

Final message

The more we think we know . . . the less  is understood .

The images we see daily in cath labs are too simplistic to make vital decisions .There are  constant innovations coming up but none seems succeed in  imparting  common sense to  majority  us.(Namely  direct plaque intervention can never succeed over a diffuse medical  disease called atherosclerosis  )

A good reference article

http://circ.ahajournals.org/cgi/content/full/93/5/924

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  • It is a complex PCI procedure meant for  high risk  bifurcation /Trifurcation lesions
  • Two stents are simultaneously  deployed.
  • It aims to prevent sudden acute occlusion of one of the major  branches .
  • It is not an easy procedure , and be used only in rare circumstances .
  • Distal left main and ostio proximal LAD/LCX  is a  classical  example.
  • Navigation can be difficult , only well experienced operators should attempt it.

*Is there a ready made two lumen stent available ?

The image is meant for concept purpose only !

 

It is one of the techniques available to stent unprotected left main

An excellent review  in  ACC intervention journal for unprotected left main .

Click on the Image to reach the article

 


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Coronary angiogram is probably the commonest invasive cardiac investigation done  world wide. It should run into millions every year. The procedure once thought dangerous  is now performed in few minutes in day care centers . While doing a  coronary angiogram  has become a minuscule task to most cardiologists, interpreting  it correctly remains a huge task !

Many  of the young cardiologists  get fascinated in   doing a coronary  angiogram and hardly spend enough time and mind in interpreting it.

Most of  us  succumb to the popular occulo  coronary reflex and describe a coronary  artery  lesions as though it is a  number game . It is very rarely we use the quantitative angiography tools available  in the machine. We need to meticulously  analyse   the length , morphology , distal flow, thrombus  , collaterals  etc . (FFR a new avatar tries to do some justice )

Calling   atherosclerois   by numbers alone,   such as  50 %  LAD  and 70 %  diagonal    20 % left main  is a huge  insult    to the deadly  & diffuse  disease process of atherosclerosis .We are paying the penalty for it .This is  the fundamental  flaw in our  reporting , that  makes every coronary intervention redundant.We must first  remember  we are looking at the lumen not the wall of coronary  artery.

Coronary  interventions is not about removing obstructions but  regression of  atherosclerosis  load within the coronary artery , prevent progression of it and ultimately reduced cardiac events and improve  survival. It  is obvious, it can not be achieved by wires and catheters alone . At best they can be adjuncts.One can  easily understand  why medical therapy  scores over wires  as it can take care of the overall disease process.

But still  ,  most* of  the  learned cardiology community  considers medical therapy   to be an adjunct to coronary intervention  , which  is  a  gross ignorance at it’s best !

* This is my perception. If  I am proven wrong ,  I am happy our patients  will be benefited !


Final message

Do not reduce  the importance of coronary angiogram   to a  farce  number game !

Do not get excited  by visualizing your patient’s  coronary artery. It may make you richer by few thousands. Realise , what you are seeing in a CAG is a fraction of coronary  circulation.

It is estimated coronary  circulation we visualize  daily in cath lab as epicardial coronary arteries  is less than  2  % of entire cross section of coronary  circulation.

This means we are 98 % blind ! ( or  2 % wise  !) .Spend  adequate  time and  mind to interpret it correctly  , so that logical and useful  ( non ) interventions can  be done .This only can make you a  true cardiac professional and your patients will respect you.


//

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Life cycle of PTCA : Let us hope it do not become extinct !

Does PTCA  , a great Innovation for mankind,  is facing a threat of  extinction ?

It seems so . . . the stents  are losing its shine  in most situations. A simple evidence  . . . for that . . . can  be found in answering the following question

What drives the extensive research in biodegradable stents now ?

The simple answer is , we are fed up with the metals inside the coronary  artery. We want to get rid of it !

Too much of knowledge , often blunts our senses . Our track record clearly  reveals this fact. We needed a major study INTERHEART to tell the world   that  ,exercise is good and tobacco is bad for heart  !  Now ,we forgot a  simplest solution for  getting rid of  metal inside the coronary artery ,  which  is  “not to implant  the stent”  at all ! (Instead we do billion dollar research for making  bio – absorbable stents ,  which in the first place may not be required in the majority !

Read the related article . Does POBA has a role now ? in my site

The only situation  , where PCI   may  withstand the test of time could be in ACS (Both in STEMI and high risk NSTEMI !) PCI is cosmetic in most of the chronic coronary syndromes .

Final message

Our fight against human atherosclerosis will have to be , by medical means .PCI at best will  provide  a supportive role in selected patient group. It requires lots of common sense  and   scientific ignorance to achieve this.   Risk reduction ,  prevention , optimal   medical therapy  will have to play a dominant role in the next few decades .  This is something similar to the environmental issues we face in protecting our planet .No amount of green industry  will protect  the earth . It requires better social and  behavioral  ethics  from  mankind   and their  rulers !

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Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make  a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.

                                                Some articles , which are very important  may not get the due  attention . Journal editorial boards often  have a scorecard called impact factor .That is ,   how  a  journal  is  impacting the practice habits of  medical professionals . Ideally we need to have to grade individual   articles with impact factor .Many articles may not have any significant  impact  however good the impact factor of the journal.

Here is an article,  which excellently depicts the principles of management of ACS.  It was published in 2003 JACC,  by Steven Nissen  from Cleveland,  Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.

Link to article placed her with courtesey of JACC

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Ever since coronary stents were introduced   metal market is having a  good time within human coronary arteries.The search  for the the elusive , ideal metal is still on   . . .  Nickel , stainless steel  , platinum  etc .

Some body thought , why not gold ?

For long ,  gold is known to be a good bio -compatible metal .

Two Gold stents were tried  .

  • Inflow dynamics  – AG Germany
  • Boston scientific –  NIR stent

Surprisingly , both showed   increased reactivity  with  coronary endothlium . The verdict  was  clear . Gold coated stent  was not good enough.

http://circ.ahajournals.org/cgi/content/abstract/101/21/2478?ijkey=f03f3c40dc4c5b2673d783f91c19f5ea685ed514&keytype2=tf_ipsecsha

Gold allergy

http://onlinelibrary.wiley.com/doi/10.1111/j.0105-1873.2005.00522.x/abstract

Final message

With the advent of DES ,  gold coating of stents lost it’s popularity  .Unless  new innovations happen in gold metallurgy , the  future looks bleak  for this precious metal  , at-least  in  the human coronary arteries.

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Interventional cardiology is a glamorous  specialty. Everything is innovated . New devices come every day to ease the work of cardiologists.

But, the percutaneous vascular  closing devices are used for over a decade. Has it won the battle against the hand and sand ?

Still the judgment is not out regarding it’s utility.

My personal  opinion  is  . . .

And it is some what , ratified by this Meta analysis in

American Heart journal 2010 (.We expect the devices to evolve

and ultimately should prevail over the hands  )

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Bifurcation lesions and ostial lesions  continue to  challenge the expertise of   interventional cardiologists.

Variety of techniques have been described. Geo positioning of a ostial lesions ,  exactly on the rim of ostium  is required  . This is very difficult in  many patients  , as stent migration either into side branch or protrusion into the main branch is common. Both reduce  optimal  PCI outcome  .

Here is a innovative  technique   described  first by  Szab0 in 2005 TCT conference .

Highlights of the technique

  • It is a twin guide  wire technique.
  • The Circumflex guide  wire  is threaded over the most proximal strut  of  balloon mounted  LAD stent .
  • The guidewire makes sure the LAD stent move beyond the LAD ostium .
  • Of course some technical limitation is  there, this seems to be a good option at least in some deserving  LAD ostial or LCX ostial lesions

Technical hitch

The balloon and stent is to be manhandled prior to deployment.  We are little awry to do it

The review article in the journal  Eurointervention

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It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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  1. Do 64slice MDCT  in all patients who has  a coronary event and follow it up with catheter based CAG.
  2. Use liberally the new biochemical marker ,  serum  B-naturetic peptide (BNP) to diagnose cardiac failure in lieu of basal auscultation.
  3. Advice  cardiac resynchronisation therapy in all patients  who are in class 4 cardiac failure with a wide qrs complex .
  4. As it is may be considered a  crime to administer empirical  heparin, do ventilation perfusion scan in all cases with suspected pulmonary embolism.
  5. Do serial CPK MB and troponin levels in all patients with well  established  STEMI .
  6. Open up all occluded coronary arteries irrespective  of symptoms and muscle viability.
  7. Consider  ablation of pulmonary veins as an  initial strategy in  patients with recurrent idiopathic AF. If it is not feasible  atleast occlude their left atrial appendage with watch man  device.
  8. Never tell  your patients   the  truths  about the  diet , exercise &  lifestyle modification (That can  cure most of the early hypertension) . Instead encourage the  use of  newest ARBs  or even  try direct renin antoagonists   to treat all those patients in  stage 1 hypertension.
  9. Avoid regular heparin in acute coronary syndromes   as  it  is a disgrace to use it  in today’s world. Replace all prescription of heparin with  enoxaparine  or  still better ,  fondaparinux  whenever  possible.
  10. Finally never discharge  a  heftily  insured patient   until  he completes all the  cardiology investigations  that are available in your hospital  .

Coming soon :  10 more ways to  increase cost of cardiology care . . .beyond common man’s reach

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