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If human coronary artery is comparable to live wire , attempting  bifurcation (BFL) stenting is akin to tame a live snake .True BFL  (with Medina 1, 1, 1)  being the most complex of all .The fact is ,we have atleast a dozen strategies for BFL with varying loads of metal abutting the ostia ,side branch and carina.This  would essentially Imply we are still struggling with these lesions .

While current science tends to vouch PCI* for most  BFLs . . . wisdom  might whisper CABG !

Who should do complex PCI ?

Obviously,  not every interventional cardiologist can. Confidence is one thing , but , falling short of minimum standard of care is rampant in India. Newer Imaging tools, techniques are promising , unfortunately  still the gap between, knowledge , science and  reality continue to widen.

* Its true ,some expert Interventionists do a good job !

What is the simplest approach for Bifurcation lesions ?

Final message 

We have come a  long way in BFL. Still , some of the lesions can sting  like a snake ! I am sure, everyone of us would have lost sleep after a complex BFL PCI !( Praying the humble  heparin and DAPT to do the rescue act ! )

bifurcation lesions medina stenting srategies 002

How to escape this double headed threat ?

A meticulous assessment of  patient  &  lesion , mindfulness in choosing the hardware & Imaging , diligent usage of anticoagulants & DAPT and  . . . finally  willingness to listen to your own conscience ,  will ensure a gratifying result that includes abandoning the procedure !

Reference 

For everything in Bifurcation Intervention

The ultimate source : Visit the in this link  European Bifurcation  Club

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

  • Almost unheard in our population.
  • The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
  • Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
  • A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .

http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstract

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Conquering  left main disease is considered as crowning glory for the Interventional cardiologists. For over three decades , CABG has remained the undisputed modality which is being challenged  today. Fortunately, the Incidence of true isolated  left main disease is  low .(If Medina bifurcation subset is excluded)

 

left main

With growing expertise , advanced hardware and Imaging ( like a 360 degree OCT fly through view ) one can virtually sit inside the left main and complete a PCI .

Still , coronary care is much . . . much  . . . more than a technology in transit !

Most importantly, these complex PCIs require rigorous maintenance protocol  with meticulous platelet knockout drugs , patient compliance and the genetic fate of drug efficacy . (Clopidogrel has since entered the final laps of inefficiency while Ticagrelor has some more time I guess !)

What is the current thinking  about  unprotected left main PCI ? Let us know it from real life experts !

For those answered , yes to  the above question please leave this page , as the following question might  trouble you much !

While competent surgeons are waiting to tackle left main by surgical means ,there are many centers which are Inclined towards  PCI though we lack long-term outcome (At least 10 years like CABG )

Why do you think this is happening ? Are you ready for another crooked poll ?!  

What exactly is left main disease ?

Some of  us also suffer from a knowledge gap and tend to think  Bifurcation lesions  and left main disease are two distinct entities .The fact of the matter is , significant subset of bifurcation lesions are Indeed either left main equivalents or true left mains ( Medina 1,1,1 would constitute > 50 % all  bifurc lesions )  If you include Invisible left main lesions in Medina ( 0,1,1 or 0,0,1 ) detected by IVUS/OCT  it might reach easily cross 90% (Scientific guess !)  Does that mean we have to think CABG even for all complex bifurcation lesions ? and reserve left main disease for isolated discrete mid shaft or ostial left main ?

Final message 

My observation (Sincere to my limited conscience !) at least in this part of the world is : Left main Interventions are  “perceived as pride” and its more related to “show of expertise” and is little to do with patient outcome.Unfortunately , cardiologists should not be blamed for it in isolation as the studies they follow are conflicted.

Forget SYNTAX/PRECOMBAT trials, the two famous studies EXCEL (Favor PCI) and NOBLE were published in 2016 made our life tough .One suggested PCI is acceptable /on par with CABG, while the  other one put CABG superior , ensuring clarity  replaced with confusion ! When we have a dispute , logic would suggest we should fall back on the status quo ie “CABG is superior” unless proved convincingly. Many sections of cardiology society failed to appreciate this.

Post PCI thoughts

*It may not be that hard to do a complex PCI . But, it’s never easier to understand current cardiology literature that is supposed to raise our intellect , which has a direct relevance to patient welfare. Note, many crucial , high stake studies  tend to play academic deceit games  with  linguistic and statistical hyperboles like Non Inferior , likely superiority , Never inferior , near equipoise , regression of hazards, virtual follow-up in  real vs trial world etc , etc !

I can only hope for a better scientific world !

Reference 

  1. Which is the best option for left main disease PCI or CABG ?  Journal of Individual wisdom and evidence based conscience : Volume 1 Chapter 1- Coronary Intellect : Pages 0 to ∞ Jan 2018.

Answer 

Though PTMC in the presence of LA clot is an option in low risk clots , my strategy would be the last one ,whenever feasible. Intensive, monitored Heparin /Oral anticoagulants ( Heparin 5000 units tds or qid  or Low molecular weight heparin Enoxaparin  40-60mg twice a day , Tablet Warfarin /Acitrom with an INR of 3 ) will dissolve  LA clot in  30-50% of times.(Our experience).

The percutaneous clot retrieval system is not available as on 2018.Aortic filters are FDA approved during TAVR. (Why not use the same in PTMC ?)  LA Catheter based regional lysis through PFO is can be an option if patient agrees to the risk.

How long to wait for clot dissolution with Heparin /OAC?

Most small clots or intermediate sized clots ((Up to 2 CM ?)  have been dissolved by 3  months. Even large clots gets dissolved at least in few Instances.Please note, this strategy is applicable only with valves that is fit for PTMC. All others are referred for surgery.

How does heparin lyse a clot  ?

Its a miracle to see it happen, though heparin / OAC are  never considered as thrombolytic agents .It happens because  both heparin and OAC tilts the local   endogenous fibrinolytic forces and thrombus melts , dissolves or disappear altogether. (I am waiting for the day , the scientific community to re-label heparin as a thrombolytic agent, Indirectly though !)

Is there a risk of dislodgement of LA clot during heparin /OAC therapy ?

This question shall be addressed to  God ! It all happens if bad luck strikes you and your patient.

Be wise  . . .  and call your surgeon Immediately when you encounter something like this !

Even if the valve is perfectly eligible for PTMC , high risk  mobile clots, history of  embolic episodes , probing and hyper-googling patients , its better to refer for surgery Immediately. Wait and watch game has a definite risk of stroke and it is especially bound to happen if your patient or their family is anxious !

Reference

Ventricular pressure volume loop is an Important ( often feared !) concept to learn for cardiology fellows . . . I would say , It is not that hard to understand !

These loops tell us the secret  hemodynamic story of a 300 gram “mass of muscle” called the heart  and how It handles about 100 ml of blood every beat and successfully ejects around 70 ml into Aorta and Pulmonary artery *

108356heart_beating

While doing this life sustaining job , It would seem the heart muscle  conducts a perfect, non stop, hemodynamic orchestra with 4 electro-mechanically coupled phases which is depicted as classical ventricular pressure volume  loop. Mind you, this loop is plotted pressure volume data from a single heart beat and it can’t be time correlated with heart sounds or ECG as the two parameters loop around in same time cycle.

Watch this animation , carefully and read the appearing annotation that come along with each phase.That should suffice to understand the basic. (For Audio version go the video link in the reference )

Modified from a clipping from Giphy.com.Original source of this Image is not located. Whoever has done this thanks and it’s a great attempt.(I have tried a fusion Image of doppler mitral Inflow in diastole and Aortic pressure curve during ssytole to bring PV loop an anatomical perspective.)

*Note: When we say PV loop it means about by LV by default . We do have seperate RV ,LA (even RA?) PV loops.

Is there clinical application for  PV loops ?

It may not have any direct use , but understanding  how a ventricle works in normal conditions or at distress especially during acute decompensations or after surgery  is vital. With modern gadgets like LV assist devices,  Impella used widely and to assess hemodynamic efficiency of transplanted (Very soon total artificial hearts) , PV loop analysis of both RV/LV will be critical.

Is there any simple Lab modality that can draw this Loop curve instantaneously ?

echocardiography lab methods for ventricular pressure volume loop

 

Very few companies make it . AdInstruments that make power lab monitors, enable us to visualise PV loops invasively .

 

Can we get PV loops non invasively by Echocardiography ?

Echocardiography  provide us both volume  and pressure data.With improving accuracy of data it should be possible to plot the loop manually with some effort. (Still , we can’t get pressure in all points of cardiac cycle )

I guess, sooner 3D volumetric machines with automated online doppler pressure data across the valves  can help us draw the ultimate LV functional  curve live on real time.If that happens cardiologists will be further enriched and hemodynamically enlightened !

Final message

The shape , size , timing and the slopes of this loop  givs us vital info about the functional aspects of ventricle. First one should understand the normal loop , then , we can dwell on the effects of acute and chronic lesions like regurgitations, cardiomyopathy ,cardiogenic shock etc.

Reference 

An excellent knwoledge base on the topic with a  video 

Dr. Richard E. Klabunde, PhD

In the modern era of cardiology,  PCI has become the single therapeutic modality  that determines the survival of both cardiologists and possibly their patients! The procedure is all about launching  a metal coil inside the coronary artery of a live beating heart.

Post dilatation vs pre dilatation

Millions of diseased and (not much) diseased coronary arteries are serviced (either re/deconstructed ) world-wide on a day-to-day basis.The benefits of the modality is  directly related to the wisdom of treating cardiologist and patient’s luck than the original severity of the disease. However, with greatly improved coronary  metallurgy , well assisted by drug coating technology and antiplatelet Industry , cardiac physicians believe they have reached the zenith of this procedure.

But the truth is , PCI still has many lingering issues regarding safety , efficacy and cost effectiveness.Early hazard in the form of acute stent thrombosis and sudden death is  a  reality. Blaming it on patients and their lesions ( condition of blood , gene included) , metal behavior is easy , but, wrong selection (Ignoring the option of CABG) and technical inadequacy of the procedure in the setting of complex  vessel wall disease (Hard calcium , deep tunnels , fissures , dead spaces ) is a major cause for concern.

Some personal thoughts about Post dilatation 

Lesion preparation , pre/per-dilatation /POTS , etc by itself  a big topic (which is not discussed here) Post dilatation after direct stenting is much more vital concept that determines not only the immediate but also the , Intermediate and long-term outcome.

Is routine post dilatation harmful ? or beneficial ?

This is the most tough question to answer . The answer is both Yes and No !  While it was thought useful and mandatory by some , the oppositeis also being adviced few  (CCL 2003 POSTIT trial)

What balloon pressure one should post dilate ? At what compliance ?  What is the Inflation time ? 

It’s akin to asking a musician  how to play a piano with fingers or guitar with various strings !

The effect of balloon pressures in the long term outcome. note both low and high pressure dilatation ( blue and orange worms ) hike the risk of restenosis. Too gentle is as dangerous as too harsh making post dilatation a secret and unique art.

 

Physics of post-dilatation  . . . again more questions !

  • Is there a role for compliant balloons ?
  • Does the compliance of balloon gets altered with hard lesions?
  • Is regional compliance matters ?
  • Can balloon exert same radial pressure all 360 degrees ?

It’s very likely, the moment balloon encounters an area of resistance it tends to avoid that area and would love to drag on to the area of least resistance and this is often diagonally opposite  zone of hard lesions ( if that segment  is free from hardness).Then , it  will face more stress and likely to bear the brunt of the force risking endothelial disruption . In other words , concentric hard lesions are more amenable for dilatation than patchy hard segments. While the physical forces vary in a stented vs non stented segment , the principle of dynamic forces on static tissue masses  with Intervening metal is too complex. (Mind you , we are not discussing  entirely different  issue , ie  thrombus laded ACS lesion , where displacement and pinching of of inter-strut thrombus into distal circualtion would cause no reflow!)

Impact of newer hardware

*Ablation catheters either rotational or Orbital can help , but must be done prior to stenting .Unfortunately , the hardness of a lesion is often realised  only after stenting

Is selective high pressure inflations over a particular struts possible ?

As of now , it would be challenging ,( if not outright impossible) .

Let us realise with all our intellect, complex PCI as a whole is taking an uncalculated risk  and leave the rest to GOD and DAPT !

Reference article 

In an elegant study of more than 90000 PCIs from Sweden and  Holland (Ref : Fröbert O, PLoS ONE. 2013 ) found routine post-dilatation pushes the harm curve little more than benefit.  The was more with both low and very high pressures .

The outcome of post-dilatation  in 900,00 PCIs 

 

Estimated cumulative event rates of stent thrombosis (Panel A) Restenosis (Panel B ) Cumulative death (Panel C) in relation to post-dilatation .Note the height of coronary Irony, Post dilatation Increase stent thrombosis and restenosis but saves life too !

 

The stunning truth revealed in this study was , early deaths were more common if  post dilatation was not done ! (Panel C in above figure) 

Role of Imaging in the decision-making prior to  Post dilatation

IVUS, OCT has been extensively used in recent times to diagnose suboptimal deployment and to asses lesion morphology.Though they are expected to improve the quality of angioplasty and hence the  outcome , the real world scenario is not really confirming our expectations.

This is because , eagle-eyed HD  imaging throws  more questions than answers in many and it converts coronary artery into a confused Pandora’s box . In fact these Imaging modalities has created fresh confusions , definitions and guidelines for malapposition under and over expansion , strut fracture, plaque prolapse, internal elastic laminar stress.( Still , I am not able eo understand  whats malapposition  vs  under deployed stent from a practical , pateint point of view !)

Is the Self expanding  stent is the answer ?

The conundrum of post dilatation might be cracked if the built-in radial force of self expanding stents is optimally utilised .This could be useful in some  tricky lesions when the vessel goes for progressive Glagovian  remodeling post PCI. The self expanding stent because of the stored potential energy keep hugging the vessel wall as it expands centrifugally.

Final Message

Post dilatation is neither a mandatory nor a sacred  protocol in cath lab. However , it would seem bulk of PCI’s still will require it . Its done judiciously with reference to   clinical setting, (ACS vs CCS) , type and location of lesion , stent characteristics etc .Most Importantly , the experience of the cardiologists counts ,and he or she will decide when, where, how much of post dilatation is required (or not required) .

Please remember , PCI as a whole (more so the Pre/ Post dilatation !)  is an art by itself. It’s never learnt in text books or even  watching  live work shops. Every young Cardiologists are enouraged to master the art of PCI ,  with a huge caveat . Always ensure  patient’s  Interest are placed first in every step forward. If you are not clear in comphrehending  “What is meant by true  patient’s Interest ? never Indulge in the procedure or call your mentor , if you have one !

Reference

1.Brodie BR1, Cooper C, Jones MCatheter Cardiovasc Interv. 2003 Jun;59(2):184-92. Is adjunctive balloon postdilatation necessary after coronary stent deployment? Final results from the POSTIT trial. Postdilatation Clinical Compartative Study (POSTIT) Investigators.

2.Fröbert O, Sarno G, James SK, Saleh N, Lagerqvist B. Effect of Stent Inflation Pressure and Post-Dilatation on the Outcome of Coronary Artery Intervention. A Report of More than 90 000 Stent Implantations. Agostoni P, ed. PLoS ONE. 2013;8(2):e56348. doi:10.1371/journal.pone.005634

3.Zhang Z-J, Marroquin OC, Stone RA, et al. Differential effects of post-dilation after stent deployment in patients presenting with and without acute myocardial infarction. American heart journal. 2010;160(5):979-986.e1. doi:10.1016/j.ahj.2010.07.007.

Bernoulli principle states  that , when a high pressure jet (Air, Water, blood etc ) moves over a conduit,  the pressure exerted by the jet on its sides (Lateral wall) reduces . The velocity gain is equal to pressure drop .This is why we take velocity as a rough guide to pressure gradient and the sacred formula in doppler echocardiography 4V2 came in to vogue . (Incidentally, Bernoulli principle shares the same principle when aircrafts  lifts from runway at its peak speed as the pressure above the wings   drops to zero or negative  and the plane lifts up.)

Please note , the pressure should drop both above and below the aircraft by Bernoulli principle .But, the engine and wings are arranged in such a way , the air speed below the aircraft is slower and hence the pressure is high below and low above and the lift occurs promptly at take of velocity. Imagine , how the valve leaflets in heart is subjected to lift and drag forces every time the blood gushes with high velocity flows.This is also the reason for the Pulsus bisferiens, SAM in HOCM, Coanda effect in supra valvular stenosis, and any post stenotic dilatation.

 

In Echocardiography the Bernoulli equation is modified.

In clinical doppler echocardiography, we have liberally simplified the original Bernoulli equation by ignoring the the proximal sub valvular velocity V1 . Further , two more components in the equation is also amputated  for our convenience ! (Flow acceleration and the viscous friction) .This is the reason we tend to err many times  especially in outflow tract gradients and prosthetic valve gradients .

Pressure recovery phenomenon.

This  is another  hemodynamic lacunae in clinical echocardiography. We know, thepeak velocity of blood is attained  just distal to site of  obstruction. As the distal velocity beyond the obstruction begins to fall, the pressure tends to recover corresponding to the loss of velocity. This happens to certain distance beyond the obstruction. Since continuous wave doppler measures the pressure in its entire axis of alignment , it  is likely to pick more pressure samples  from the recovered areas and net result is, it measures more than the true difference in gradient across the valve.The phenomenon is most relevant in assessment of Aortic stenosis and results in over estimation of severity of stenosis.

How much can be the overestimation ?

It can be up to 30 % or even more.Especially in prosthetic Aortic valves.

How to recognise it and overcome it ?

  1. First of all,  recognise such a hemodynamic phenomenon  exists and the sacred 4v square can be a myth !
  2. Never go with gradient alone in diagnosing valve stenosis. Look for 2D features also.This is more vital when you suspect acute valve obstruction.
  3. Always add the proximal sub valvular velocity (V1 ) in your Bernoulli equation .It need to be subtracted.
  4. The effect of heart rate on pressure recovery has not been properly studied.(The impact of which  could be vital and hence too many false prosthetic emergencies could be avoided, as cardiologists tend to rely mostly on gradient than anatomical diagnosis of valve obstruction like visualising thrombus or struck leaflet by TEE or fluro.

Does this phenomenon happen with cath gradient ?(Generally it’s more pronounced in doppler echo )

Yes, It does happen in cath lab also , as its related to physics of flow. It can be minimised if we can use two simultaneous catheters ,one in LV  and the other Aortic catheter placed very close to the leaflets.

pressure recovery in aortic stenosis animation

Click below for an Animated version

pressure recovery phenomenon in aortic stenosis 005

Note the pressure recovers from P 2 to P3

Reference

Pressure recovery phenomenon in doppler echocardiography

pressure recovery phenomenon doppler echocardiography

Pre-op cardiac evaluation prior to non cardiac surgery is an important area for cardiology consultation . Unlike other clinical consults this one primarily involves in the delicate and tricky job of  predicting  future events  !

acc aha guidelines for perioperative evaluation noncardiac surgery riskPeri-operative  cardiac evaluation  is done for what ?

1.To evaluate and assess established CAD or other heart disease and get a proper pre-operative work up , drug adjustment and risk reduction for a possible peri-operative event.

2.To screen for any significant CAD or other heart diseases which is hiding and asymptomatic.

3.To   treat those conditions that are detected prior to surgery .(Or simply assess & mark the risk and send them for surgery)

4.Finally and most importantly it is  often done as a routine “legal point of view”  or ” perceived  anxiety “as litigation for missed cardiac condition  looms large on the surgeon !

Risk stratifying established heart disease is relatively easy task as we know what we are talking about .The term “cardiac fitness” is used in some institution which should  probably be discouraged .No patient’s  cardiovascular system is deemed to be fit or unfit at any point of time.It all goes with the nature  and  aim of surgery .An apparently  fit person can develop more complications than a potential unfit  person as cardiac events are dynamic and directly influenced by the stress of surgery .

It’s about the probability of occurring possible events , and of course one should add to this , all those  invincible  random or remote events of Heisenberg .

How do you rule out CAD ?

A  middle aged man or women with diabetes with a T wave inversion and non specific ST segment is being planned for ca-prostate or breast  surgery .Both of them couldn’t do stress test due to associated OA knee.

If coronary atherosclerosis is defined as CAD , there is no way you can rule out CAD.In fact near 100% of elderly population will have evidence for CAD ( at least some degree)  in the walls of the coronary .All that is required is  just few minutes  of  heightened adrenergic drive or prolonged fall in blood pressure to trigger  acute coronary syndrome in any person who may have shown even a  normal coronary angiogram. How does it happen ?  We have sufficient technological jargons to use in such situations endothelial dysfunction, plaque erosion  erosion ,micro or macro vascular spasm  coronary auto circulation failure etc ..

Is exercise stress test , Doubtamine stress , or CAG must for all persons suspected to harbor CAD ?

This could be the key question that makes most  cardiologist tentative in their office .suspicion is relative and subjective term .So we have the guidelines .Guidelines are simply guidelines. It may give you comfort if you follow that either academically or legally .

Iam not convinced .Iam new gen cardiologist. Iam unable to rule out CAD without CAG , my cardiology training over a decade has never taught me to r/o CAD clinically

I will go ahead with a screening coronary angiogram in all persons in whom I suspect CAD strongly  .If the patient is not willing for CAG I will do a doubtamine stress echo.

What if  you detect a positive Doubtamine  test or a significant multi-vessel CAD in an other asymptomatic person ?

Now you are stuck again !

  • Are you going to postpone the surgery pending further evaluation possible revascularization
  • Are you going to clear the patient with added risk frightening every one from surgeon to anesthetist, pateitn and their  family.

How guilty are we ?  If we fail to predict a cardiac event during non cardiac surgery ?

We need not feel guilty at all as long as you have done the basic tests and given your learnt opinion.I would think no court of law can plead guilty for that. (But your local reputation may be at stake !)

Final message

It is very important to realise , pre-op screening should not be a “hunting ground for CAD”.What we refer to as cardiac fitness is actually is  a  logical guess  considering all risk factors and comorbid conditions and make a learnt decision depending upon the  aim of surgery and the urgency of surgery .(Read at least once the meticulously prepared ACC guidelines of 2014)

Forbidden thoughts

In real world , it  appears the task of  risk stratification and pre-op evaluation is mainly driven by the fear of litigation rather than true concern about  the impact of surgery on the ultimate outcome.In this  gentle world of noble professionals  one can’t question the true Indication of a surgery however dubious it may appear  as it considered serious violation of Hippocrates oath* (Not respecting or suspecting  your colleagues’s  credentials !) But , I earnestly believe a genuine review of decision about surgery or procedure is to me made.

In my humble opinion , if surgery can be postponed or( if could be altogether avoided in few !)  till complete cardiac stability is achieved is the  most desirable option in high risk patients .

* Am I misquoting Hippocrates ?

Consider this true story . Recently a elderly women  came for cardiac clearance for  laproscopic  Cholecystectomy . As I was doing echocardiogram the patient  asked me  with real concern , “Is the surgery really necessary doctor ? my doctor says its urgent “ . I casually told her since its a incidentally detected small gall stone , if its not troubling  you surgery may be not be urgent , rather may be avoided. Few days went past. I don’t know whatever happened to that women , she opted out of the  scheduled surgery .

Next week,  , there was  huge uproar from the surgeon , who  called my associate and censured my behavior.He went on to add , as a cardiologist I have no business to comment about the gall bladder condition. Even if what I uttered could be truth , as a doctor you don’t have  a right to breach  other doctors opinion.

After few days of self deliberation , I agreed with  him and realised in harsh way ,  freedom of expression can never be taken as granted especially in dealing with others patients  !

My colleagues ridiculed my Ignorance  , aren’t you aware every patient is a registered property of some doctor ? An Anesthetist friend of mine working in a corporate hospital, said If I start scrutinising the indication of surgeries I assist, I cant win my bread for my family beyond few days !

I simply couldn’t comprehend .” A patient is a patient “ What is the demarcation between my and your patient. She asked me a question I answered it to my conscience , that’s it. Should I behave like a deaf mute ?after 30 years in to medical practice !

I was still restless over the week .Finally, I decided to  get the answer from Horse’s mouth and  mailed  the query direct to father of medicine,

To  query@hippocrates.heaven

Dear Mr Hippocrates ,

Here  is a story of  “Fit gall bladder and an unfit surgeon” . Did I really err on that day or was my behavior unprofessional in any way as others thought ?

Yours greatly

S.Venkatesan.Physician,Chennai .India

I got a surprisingly shocking reply ,

From query@hippocrates.heaven to drvenkatesans@yahoo.co.in

Dear Dr.Venkatesan

I could feel your inner fight about the things happen in medical profession . However genuine your thoughts are, I am sorry , I say this with pain , you are largely unfit to practice medicine in the planet earth. Please try to change yourself or try changing the planet !

Learn to take things easy in life !

With regards.

Hippocrates. (Digitally signed )

 

We know, The Mysterious Alibaba cave opens  with a voice password . . . legend  tell us it had unlimited hidden treasures. It would appear , CTOs mimic the cave in several ways. What is inside ? Should we open it ?  Can we come out safely ? Do we have any magical password in cath lab to get across the complex tissue boulders ?,   every cardiologist would love to have one !

chronic total occlusion alibaba cave corsair fileder xt pronova guideliner micro catheter asahi cart reverese cart cross boss sting ray

Dear CTO,Open Sesame . . . I have come with all the wires you love !  Please let me in !

Indication

“CTOs are never an emergency  . . .but please realise  we can very easily create one  while resuscitating a dead snake  ! 

Don’t think hard on evidence , then , you may not do a single case of CTO in your life .Forget all those pessimistic trials like OAT,COAT, etc and the recent ones DECISION-CTO. Ignore all guidelines. Ask your patient, and his insurance company , if they are willing , reserve the cath lab and get ready.

Pre-procedure  planning

Spend at least a hour to analyse the CTO Imagery one day prior and create n action plan.

Keep knowledgeable staff for assisting , but never ask for fellow colleagues help because it hurts our ego !  Cardiac surgeon’s back up is a welcome addition even if it’s on paper.

If possible , try to ask the patient genuinely ,what is his symptom at least once !  before starting the procedure. 

Timing of the procedure.

Don’t post a CTO patient  either on a busy Monday morning  or lazy Friday afternoon.

Hardware Inventory

The wires ,catheters, the balloons form the essential tool box .There is more than a  handful of coronary automobile companies manufacture this .It is all about metallurgy , knowledge of wires, catheters , and tip thickness, (Bullet shaped as in Asahi ) , slipping , hydrophophic or philic,  polymer coating , trackability, pushability , memory etc etc.

Guide wire tip morphology is as Important as the  Lesion characteristics !

Analysis of the lesion (Probably most important)

Unlike conventional PCI we have no initial target.We need to poke first and find the target next ! Distal vessel status  is most important ( Careful review of retrograde filling  through collaterals could give more information than CT angiograms .Calcification, diffuse disease can be a real hurdle)

Lesion morphology

Softness of lesion has to be felt (Requires good wire which has sensor (Paccinian corpuscles and Merckle disc ideal ?) I guess the cortical tactile feel is as vital as the  intervention expertise .I know at least one diabetic colleague of mine who finds it difficult  to cross a CTO  and admits he never found it easy to feel  the lesion through the wires . Autonomic dysfunction ?)

Operator  expertise

(Note: These are like reading  swimming guidelines , you can’t learn in the shores reading books ! you have to plunge !)

Many techniques are proposed .Sequential approach (Ironically experts are licensed to use  specialized wired wires directly .Beginners  are advised to go with non specialized hardware and escalate step by step) Some centers are blessed with new age weapons like cross Boss and sting ray that confront the lesions in multiple frontiers. (Carpet bombing?)

CTO playground. : Its essentially a coronary contact sport with expert septal surfing , tunnelling, knuckling , kneeling , bending . Of course , It  can end up in a gratifying win in few , still most of us tend to play this game without a goal (post !)

They are basically about poking the head of the lesion and trying to cross an occluded vessel  millimeter  by mm towards the presumed distal vessel in an Imaginary trajectory. Proximal cap, central core ,the blind tunnel , distal capsule and exit points each must be successfully conquered.

CTO crossing is  the ultimate capacity of the operator to realise and feel the position of the wires in true lumen and their confidence levels in their conviction!

Multiple wires up to three are used some times to poke the lesion two of them are used to shut the false tracks and the other one is expected to enter the true lumen (Looks too good on theory !) . These are referred to in as many terms like parallel wire see-saw , CART ,Reverse CART etc .Retrograde techniques do help us but has no magic solutions.The lumen contrast , guide wire tip movement and its  side branch entry  would help.

Tacking complication :Always anticipate , it’s not negative mind set to look for it  !

Keep pericardiocentesis kit , covered stents , micro  snares and other retrieval devices ready in cart. Your support staff should be well versed with what is happening around them. Some of  the dye leaks and stains are safe .They imply minor perforations that form  sealed hematomas  (The plane of perforations also matters. myocardial (ab-pericardial ) leaks are well tolerated .Distal perforations are also safe as long as CTO is not opened ) Online echocardiography should be readily available to monitor  pericardial space leak.

When bleed into pericardial space is life threatening , A comical, but life saving option is to close the artery and restore the CTO  its original state and come out of the lab quietly ! 

Newer Imaging guidance : Can be useful , still may not matter much  when considering the interventional acumen .

CTO PCI : Time as therapeutic end point.

CTO is not an endless game with out time frame .In my opinion it shouldn’t cross 45 minutes each as in a  soccer  game with a brief  strategic time out and of course with liberal use of ,yellow and red cards

Future directions

Japanese are the ones who pioneered  CTO Interventions . We expect more Innovations ! Is it the forward looking IVUS ? It is akin to tunneling for underground metro train with GPS guiding .If you can mark the proximal and distal  points , rest will be be taken care by mortised self tunneling catheters from Robotic arms steered by sophisticated algorithms.

Final  message

CTO PCI remains a real Interventional challenge. We are often double blinded  in both directions (antegrade as well as retrograde ). Needs much effort ,time, hardware and most importantly a non fatigued mind and body. The benefits we get may vary  between  gratifying to outright mediocre .Of course , it surely satisfies operator ego and express pride and courage !

Is crossing and stenting  a CTO  synonymous with true success ?

Yes it is , for the cardiologist and  the hospital  . . . I’m not sure about it for the patient !

In this  sense , CTOs  mimic the mysterious Alibaba cave that tempts us with Imaginary treasures but can trap us with a wrong password !

Post-Ample

* Who should CTO PCI  ?

I have seen  young , enthusiastic cardiologists with Immature support staff attempting CTO in remote sub- urban settings ! Though patience and expertise are essential ingredients, some amount of organised training and hardwares make CTO PCI safe and effective. Enthusiasm and affordability alone can’t be an Indication for this complex set of coronary lesions.

Reference 

 

I still wonder why  this vital paper was never published , it was just presented in the Annual ACC conference March 2017

http://www.eurocto.eu/

 http://www.cct.gr.jp/