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The therapeutics of coronary stenosis has become a technogical wonder, interwoven with statistical wordplay in the last few decades. PCI is sitting pretty at its peak glory.The term OMT or GDMT is a popular terminology, but realistically exist only in guidelines.

It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. Meanwhile, we haven’t seen any papers from cardiology forums that classify PCI according to its quality. How many of use a term like optimal PCI or guideline-directed PCI (O-PCI, GDPCI). Every PCI, by default, is perceived as good by our flawed coronary intellect.

A single patient experience

Let me share a patient consult from a remote town of north India. He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. His CAG showed a significant looking, yet non-flow limiting LAD lesion without any troubling symptoms. I came to know he had consulted two institutions and was apparently not happy with their approach (In his own words, “They seem to be primarily interested in caging my LAD than listening to me”).

Somebody has suggested my name. He called me over the phone for a consult. I asked him remain there to follow his doctor’s advice. But, he flew some 2000 km to meet me. He was so knowledgeable and was aware of everything I wanted to tell. Like, viability, scars, futility, and benefits of revascularization, imaging-assisted PCI, impact of PCI on exercise capacity, importance of risk factor management, etc.

I told him, “In my opinion, you have technically a single vessel disease that can be managed well with drugs. But if PCI is to be done, it should be done in a proficient manner, as the lesion looked hard and was close to the LAD ostium, trespassing LCX as well.” I stressed the importance of a professionally done procedure with enough expertise and follow-up maintenance care.

He was not entirely satisfied with my response. He wanted a clear yes or no! . I told him, “If you have full trust, continue with the drugs at full intensity and do a stress test after 3 months. otherwise, if you keep getting even the slightest doubt and anxiety over the hidden blocks, go for a stent immediately at a good Institution. (My conscience said the latter half of my advice was unwarranted, but I had to; after all, me too need a protective mechanism)

He left my clinic profusley thanking me. I am not sure , how my consult was useful for him and what he is going to decide.

Academic lessons from this patient.

1.Patient fear factor over coronary blocks may be the ultimate game changer. Cardiologists should try to mitigate this fear and at the least should not be an amplifier to this emotion.

2.Leaving tricky profesionaly complex decisions to the patient, is an easy escape route for us, however it comes very close to professional incompetence. (Of course, we do this on a routine basis, approved by the modern medical guidelines, ethics, and legal system, in the name of patient empowerment)

3.Finally, we can grow a potential research hypothesis. A sub-optimal PCI is non-superior to OMT.It is curious there is no study available to compare sub-optimal PCI to OMT. We must also realize there is nothing called standalone PCI. Without concomitant OMT, PCI is a dud. Every young cardiology fellow need to etch this fact in their cortical cardiac memory. OMT often turns out to be the savior of stents, but the latter ruthlessly steals the credit.

Postamble

I could find one study analyzing suboptimal stenting (Ref 1), but it didn’t compare it with OMT. Suddenly, as I finish writing this, a big fact struck me hard, i.e., even a well-done PCI in sophisticated core labs with meticulous care struggled to beat OMT in a barrage of landmark trials (like COURAGE, ISCHEMIA, ORBITA). What is the big deal to analyze suboptimal PCI vs OMT?

Prati F, Romagnoli E, Gatto L, La Manna A, . Clinical Impact of Suboptimal Stenting and Residual Intrastent Plaque/Thrombus Protrusion in Patients With Acute Coronary Syndrome: The CLI-OPCI ACS Substudy Circ Cardiovasc Interv. 2016 Dec;9(12):e003726. .

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Anyone who is flushed with millions can become a member of “The Hurlinghamin” London or the “Yacht” in Monaco, or any other glamorous clubs in the world. But, EBC* is different. Only cardiologists are privileged to enter. EBC is obviously unique. It is the only club addressing exclusively a subset CAD, ie bifurcation coronary lesions. Apart from immense pride and academic entertainment, it teaches us some deep technical points. (By the way, BFL* is a minuscule spoke in the gigantic wheels of global atherosclerosis)

Approach to BFL

90% of BFL still require only drugs or humble single stent or a provisional second stent strategy. However, as per basic rules of human intellect, lesser problems continue to bother us and consume our precise time. This continues, even after realisng , there are 6 complex two stent strategies that doubles up complications.

(*EBC -European Bifurcation club .BFL-Bifurcation lesion)

We will address one unique issue in BFL. May not be a major clinical issue .Still, it’s worth it. It is about the side branch crossing after the intentional jailing of the side branch.

Let us answer this query first

Pure science: Observations from Bench test (Text from Ref 1)

In contrast to provisional stenting in which re-crossing through a distal strut is desirable, initial re-crossing the crushed SB stent in the DK crush technique should be done through a proximal stent strut to minimise the risk of SB stent deformation. A theoretical exception could include bifurcations with a particularly narrow angle for which proximal re-crossing may shift more struts towards the MV, leading to a less desirable, longer neocarina. The 2nd recrossing should be done through a distal strut.

Bench testing is clear. Still , Why this confusion ?

We are all talking about theory in bench testing in stable non-hemodynamic conditions that lacks a biological carina and the dynamics of plaques. We are aware that there are at least 5 virtual ostia in every bifurcation arena (or trifurcation) . The qunatum and direction of plaque sharing occurs with a random effect. We also know the final kissing either cements these plaques perfectly or unsettles in a most bizarre way. So, these strut crossing stuff, are more of an imaginary bio-engineering principles. Whichever strut you cross, do it slowly, gently dilate it to the maximum within the polygonal confluence and good approximation. Don’t get too much carried away , even live online OCT guidance do not guarantee a perfect crossing.

Final message

The answer to the title question seems to be (me), one need not hair-split much on the site of crossing at the side branch. Fortunately, in whatever way, we weave the metallic mesh*, at the epicenter of the coronary highway, it is the natural secretagogues like TPa, Nitric oxide, PGI-2, along with DAPT decides the patient’s genomic fate.

*An appeal to all EBC club members.Before embarking upon a compex PCI on a stable patient , please think for one last time , whether your patient might do well, only with medicines.

Referecne

1.Hall AB, Chavez I, Garcia S, Gössl M, Poulose A, Sorajja P, Wang Y, Louvard Y, Chatzizisis YS, Banerjee S, Xenogiannis I, Burke MN, Brilakis ES; Collaborators. Double kissing crush bifurcation stenting: step-by-step troubleshooting. EuroIntervention. 2021 Jul 20;17(4):e317-e325. doi: 10.4244/EIJ-D-19-00721. PMID: 32310131; PMCID: PMC8919516.

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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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Fundamental principle  of  human biological system is to live in harmony with nature and environment.Each cell  has a unique reaction  when it comes into contact with  external  material. This reaction can be acute or chronic  ,   local or systemic. The most severe form of allergy is called anaphylaxis  that can result in instantaneous loss of life. There  is a whole gamut of disorders  that  resulted  in a  separate  speciality called allergic medicine .

Further ,the transplantation  science have   taught us  an  organ or cell can be rejected at any point of time after implantation (Hyperacute -chronic) .With advancement of science we have started implanting a variety of devices  with complex metallurgy ,inside human body, metal clips, prosthesis, valves, wires, etc .How the body handles them .The consequences can be a mild reaction to major ones occasionally.

Consider ,a local allergy due to a orthopedic prosthesis  in one of the leg bones  is far less serious than a metal within a coronary artery  irritating the intima .

Remember hypersensitivity reactions can be severe . This lady reacted  like this to a sandal slipper -A  fiery red  infiltration

contact dermatits stent allergy pci coronary

Imagine  if a stented coronary artery react like this what would be the possible consequence ?

In susceptible  individuals  , can a metal cause

  • Intimal hyperemia
  • Intimal induration
  • Intimo-medial edema  following stent deployment

pci stent coronary angiogram thrombosis des

Why drug eluting stents are more prone for hypersensitivity ?

The answer is simple , while metal allergy is a comparatively rare phenomenon, the drugs we  coat and the polymers used are  many fold likely to result in hypersensitivity reaction.

While  the world is worried  more  about penicillin , sulpha allergy which occurs in 1 in 100000 ,  we tend to ignore the metal and drug  reactions within  the tender coronary arteries.

stent des rejection virmani  pci

What is  the clinical expression of  stent hypersensitivity ?

It is  often a coronary event in the acute phase and restenosis in chronic phase.

How much of acute stent thrombosis is related to stent allergy mediated reaction ?

The exact incidence  will  never be known. It could be high. Whenever a sudden unexpected early stent occlusion can be a suspect .

Is stent allergy a local reaction or systemic reaction ?

It is most often local .The drugs the stent elute can elicit a systemic reaction occasionally.

So what can be done to prevent this complication ?

Drug companies in it’s  package regularly  include the warning  message ! What does it imply to have a caution  on the covers ? .This warning simply represent about our ignorance in this issue. We presume it is a minor problem.

pci stent thrombosis stent allergy metal

Questions unanswered

  1. How does a cardiac patient knows whether he is hypersensitive to stainless steel or nickel ?
  2. Is it practical to have a stent allergic test in every patient before PCI ?
  3. Is routine administration of corticosteroids for few days after PCI an answer ?

Reference

R.Virmani , circulation 2004

http://circ.ahajournals.org/cgi/content/full/109/6/701?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=stent+%27allergy%22+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

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Annual workshops for interventional cardiologists has been  hugely popular events.They have  become the forum for all technological breakthroughs. Some of the popular ones are

Japanese have gained a unique place in  complex cardiovascular  therapeutics interventions especially in chronic occlusions.

Landmark article for CTO crossing

cto chronic total occlusion  Katoh coronary angiogram

www.cct.gr.jp/2003/wirehand/index.html

www.cct.gr.jp  cto japan

How to reach Japan ?

Click below

CCT2010

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Total coronary artery occlusion is a common finding in CAD  especially in chronic stable angina. Normal coronary blood flow is 5 % of cardiac output  that amounts to 250-300ml/mt.At an average  heart rate of  70/mt  , each  beat  injects  about 5cc blood into the coronary circulation.This is shared between two coronary arteries.  This means , only few CC (2-3cc) of blood enters  each coronary artery with each cardiac cycle .

When one of coronary artery is totally occluded what happens to the coronary

blood flow ?

A.Total coronary blood flow  can be be  maintained   normal  at rest  as it  forms  only about 5% of cardiac output  (or it is only  slightly reduced )

B. It is believed , the unobstructed coronary artery  could receive the blood meant for the contralateral coronary artery. This  possibly explains the increased coronary artery diameter in the non obstructed artery.

C. It’s nature’s wish ,  that the  contralateral  coronary artery  shall share  50% of  it’s  blood through  collaterals if available.

D.If collaterals are not formed it , the unobstructed coronary  artery  may be over perfused with double the amount  of blood flow.

E. Some times , the collaterals steal  much more than what  the  obstructed coronary artery  deserves and make the feeding coronary artery ischemic. This is many times observed in  total RCA occlusion with well formed  collaterals  from LAD/LCX.

F.The collateral flow  in CTO also depend on whether flow is directed from LAD system to RCA or from RCA -LAD system. The LAD is better placed to assist RCA than vice versa.This is for two reasons.1.LAD blood flow is higher than RCA so it can share it.2.The driving pressure is more  from LAD -RCA , as RCA can receive  blood flow even during diastole .

F.During exertion , the coronary hemodynamics become further complex.The collateral’s are traditionally thought to be less than adequate during times of exercise.But it is more of a perception than solid scientific data.This rule  may be applicable in only certain group of patients. We know CTO patients with very good exercise tolerance who have documented collateral’s.

G.Collaterals can be either  visible or invisible by CAG. The strength of collateral circulation is not in it’s visibility but it’s capacity to dilate and  respond to neuro humoral mediators at times of  demand.  Currently  , there is lot to be desired  regarding  our knowledge about  the physiology  of visible collaterals , no need to  mention about invisible collaterals !

Final message

The above statements  are based  on logics and observations .

Is it not a  irony  in cardiac literature ,  where  thousands of articles  are coming out every month  to tackle  totally occluded coronary artery(CTOs) ,  there is  very little data   regarding the coronary hemodynamics in chronic total occlusion .   How  does a patient with CTO can manage a active life with only one functioning  coronary artery ?

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Failed thrombolysis is an important clinical  issue  in STEMI   as  successful thrombolysis  occurs  only in  about 50-60%  of pateints . The typical criteria to define failed thrombolysis is  the  regression  of less than 50% of sum total( or maximum)  ST elevation in infarct leads.

So what do you do for these patients with failed thrombolysis ?

It depends upon the patient’s symptom, hemodynamic stability, LV dysfunction .

They  should  get one of the following .

  1. Conservative medical management  with /without CAG
  2. Repeat thrombolysis
  3. Rescue PCI
  4. CABG

Medical management is  thought to be  too inferior a  management,  many of the interventional cardiologists  do  not want to talk about . But  , there is  an important  group of patients (Not often addressed in cardiology literature)  who  technically fulfill the criteria  of failed thrombolysis  , but   still  very  comfortable , asymtomatic  and in  class 1. These patients ,  have  a strong option for continuing the conservative management .

Repeat thrombolysis does not have a consistent effect but can  be  tried in some  stable patients. CABG  can be a genuine option in few

Rescue PCI

This terminology  has become  the  glamorous one since the  catchy word  rescue is tagged in the title  itself. For most of the cardiac physicians ,  this has become the default treatment modality.This is an unfortunate perception . What  one should realise   here is  , we are  tying to rescue  the myocardium and  the patient ,   not the patient’s coronary artery !

Opening up a coronary obstruction is not synonymous with rescue .

For rescue PCI ,  to be effective it should be done within the same time window as that for thrombolysis (ie within 6 or at the most  12 hours) .This timing  is  of vital importance  for the simple reason , there will be nothing to rescue after 12 hours as most of the muscle  would be  dead. Reperfusing a dead myocardium has been shown to be hazardous in some ,  as it converts a simple  infarct into a hemorrhagic  infarct.This softens the core of the infarct and  carry a risk of rupture. Further,   doing a complex emergency  PCI  ,  in  a thrombotic milieu with   presumed  long term  benefit ,  is  a  perfect recipe for a potential  disaster.

While the above statement may be seen as pessimistic view , the optimistic cardiologist would vouch for the“Curious  open artery hypothesis” .This theory simply states , whatever be the status  of the distal myocardium ( dead or alive !)   opening an obstruction in the concerened coronary artery  will benefit the patient !

It is  huge surprise , this concept   continues to  be alive even after  repeatedly shot dead by number of very good clinical trials (TOAT, CTO limb of COURAGE etc ).

The REACT study (2004) concluded undisputed benefit of rescue PCI for failed thrombolysis  , only if the rescue was done  within  5-10 hours after the onset of symptoms.The mean time for  pain-to-rescue PCI was 414 minutes (6.5hours)

Final  message

It is fashionable to talk about time window for thrombolyis but not for PCI  .The time window for rescue PCI is an redundant issue  for many  cardiologists ! . But ,  the fact of the matter is ,  it is not . . .

The concept of time window in rescue PCI  , is as important as ,   that of  thrombolysis. Please , think twice or thrice !  if some body suggest you to do a rescue PCI in a stable patient  ,  12hours after the index event .

Important note : This rule   does not (  or need  not  ) apply for patients in cardiogenic shock  or patient ‘s with ongoing iscemia and angina.

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pci-ptca-ebm-stent

Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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Coronary artery  perforation is a dreaded complication of PCI. Perforations are the Interventional cardiologists ultimate worry   as they need to  manipulate their  hardware for  long periods in many complex lesions.  Especially  it is a  real threat in chronic total occlusions.

Still , an important fact is ,  many of the coronary perforations are not life threatening ?

How is this possible ?  (Type 1 Ellis has zero mortality Read below)

As the guide wire injures and perforates the cor0nary vessel,  it results in  small puffs of dye extravasating  into peri coronary space .

The coronary artery , which is located   within the  atrioventricular groove  (LAD), or AV groove (LCX, RCA) have  two distinct anatomical relationship with reference to epicardium and pericardial space.

50 % 0f circumference of the coronary artery is  hugged  by the myocardium  another 50% or so is related directly to the pericardial aspect.

Guide wires hitting on the myocardial aspects face a stiff resistance than the pericardial aspect. So , generally the risk of perforating pericardial aspect is more than myocardial aspect

Even if , the coronary artery is punctured on myocardial aspect , no great danger occur as there is no potential space for the blood to drain and further,  the  elastic nature of myocardial muscle plane effectively seals the leak. At the most , mild myocardial staining is noted .

coronary-perforation-2

While ,  perforations  into  the pericardial space  , often threaten with a tamponade. The fact that pericardial space has negative pressure and  the mean  coronary arterial pressure around 40mmhg ,  it is  , all the more likely blood is sucked into the pericardial  space. Of course , very minute  perforations  even into the pericardial space ,  could  be self limited and  benign.

coronary-perforation

What is unrecognised coronary perforation?

Many times , the guidewire goes in a false track in the tissue plane.This is  nothing,  but perforation without hemodynamic implication. Most often , these are the instances of guide wire entering the epicardium.They mimic , false lumen entry , dissections, etc. There are occasion , where false lumen of the  coronary artery were  stented.

What are the  factors which increase risk of perforation ?

perforation-6

 How do you classify coronary perforations ?

perforation-3

*Ellis SG, Ajluni S, Arnold AZ,  Increased coronary perforation in the new device era. Incidence, classification, management, and outcomeCirculation. 1994;90:2725–2730

 

How do you manage coronary perforation?

Simple guide wire induced perforations are less trouble some unless we have crossed it with balloon without realising the fact the wire has entered the pericardial space. So, caution is required and always watch for guide wire tip movement which is often funny looking wihtin false lumens or very freely moving within pericardial space. Anticipate the complication especially so when you do CTOs and venous graft PCI.  Keep one cath lab  tamponade crash  bin  in ready mode before embarking upon a complex PCI

  • Neutralise the heparin action with protamine is the first step
  • Most are self limited, no intervention is required  but requires close observation for next 24 hours.
  • Temporary balloon occlusion may be suffice in many cases
  • Tamponade requires immediate tapping. Small collection without fall in BP can be observed.
  • keep doing the echocardiogram liberally to assess the leak and watch for any new collection.
  • PTFE covered stents if prolonged leak.
  • Emergency surgery may required in few.

2018 update 

This is  nearly 10 years old article. Now, we have gained much experience and hardware utilisation have rapidly expanded. While expertise has minimised this complication , more PCIs in complex lesion subset tend to keep the incidence static , if not higher.(Its around .5% )

Tips to use balloon occlusion during perforation

Perforations which are active and flowing should be immediately occluded with a balloon either at the site of leak or just proximal to it. Doing a proximal occlusion is easier in emergency , as often times its technically difficult to reach the site of leak especially in CTOs where the leaky site is not defined clearly or forward looking (Local balloon inflation across the leaky site is not feasible )

 

How long to occlude , Intermittent /complete, proximal ? or at the site of perforation ? These queries are answered in Ref 4

Reference

1.Largest report (1762 cases) of perforation from British Cardiovascular Intervention  Society Database Circ Cardiovasc Interv. 2016;9:e003449.

2.Al-Lamee R, Ielasi A, Latib A,. Incidence, predictors, management, immediate and long-term outcomes following grade III coronary perforation. JACC Cardiovasc Interv. 2011;4:87–95.

3Xiangfei Wang and Junbo Ge Balloon Occlusion Types in the Treatment of Coronary Perforation during Percutaneous Coronary Intervention   Cardiology Research and Practice Volume 2014, Article ID 784018,

4.A very good review comes from Royal Hospital, Muscat, Sultanate of Oman

 

iFAQs in coronary perforations

1.Does the plane of the coronary artery (Sub epicardial within the fat layers)  determine the likely hood of tamponade ?

While myocardial tissue can resist flow we are not sure about sub-epicardial fat on the pericardial aspect.

2.How common is Intra-cavitory perforation ?

Perforations into chamber is invariably associated with septal branches (PCI to septal branch itself is less common )

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Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease


edited by Seung-Jung Park

hbleftmn

//

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