Essential Cath lab philosophy !

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How do you tackle this man’s RCA ?

This is an  RCA of   a  patient who had chronic stable angina  , class 2  with moderate anti anginal medication.

What shall we do ?

1. The RCA needs  multiple stenting
2. Multiple plain balloon angioplasty
3. CABG to PDA
4. No intervention ?
5. It depends upon status of LAD  and LCX

The correct response would be 5

Without knowing  the status LAD and LCX . . .  RCA should not be touched . Further,  the concept of tackling  the  coronary artery  by itself  is   fundamentally wrong !  We are supposed to tackle patient’s symptom ,   reduce future risk of  events and   not merely  their coronary artey !

His LAD and LCX was near normal. In the weekly  cath   meet   PCI to mid RCA  covering  the critical segment was  strongly debated but  lost a close race .

The final decision was to allow the patient to continue   intensified   medical management (Statin 80mg /Metoprolol 100mg ) . He is comfortable with that .

Medical management  in a tight  single vessel disease  can never be digested by  any   Interventional cardiologist  whatever   may be  the guidelines !

Final  message

Do not decide PCI on the basis of   how ugly a coronary artery looks , rather spend some time on true  symptomatology ,  optimise baseline therapy  and re assess risk profile

One learned dictum is ,  do not  meddle a RCA ,  however severe the lesion may be   if  LAD and LCX are fine.*

*This  rule is not applicable in ACS

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Is there an entity called borderline positive exercise stress test ?

In this politically and scientifically  uncertain world nothing is  in black and white. How can you  expect  EST to behave differently ?

Even as  we  are fully  aware of the  limitations  of EST  ,  it  does not make sense   to categorize  EST result into either positive or negative .

In fact , our  estimate suggests  a significant bulk of the patient would fall in the grey zone  .

It is referred  in various terms by  the reporters of EST .

• Borderline positive
• Mildly positive
• Equivocal
• Inconclusive

What does all these terms mean to the patient ?

It mans only one thing . . .

Physician  who reports  the  EST    is unable to  conclude whether  his patient has  significant  CAD  or not . It is a dignified way of  expressing  the  limitations .

Many factors may play a role. (See the illustration above )

• Patient factors : Poor exercise stress levels and conditioning
• Lesion factors:  Collateralised CAD, treated CAD  can result in partial or mild  changes.
• Machine factors :Caliberation errors.
• Interpreter : (Physician ) factors

Error in measurement of ST segment . What is borderline  for  one doctor may indeed be true positive  for the other and vice versa .

How will be the  EST in  a  revascularised  or  medically treated CAD ?

If revascularization is a complete success ,  stress test  would  revert back to normal or it can be a borderline as we have just mentioned.

To our  surprise ,  it may  remain  positive in spite of apparently successful procedure.(Residual wall motion defects , scar mediated  ?)

How to proceed  after this borderline EST/TMT ?

Few options are available for the physician/patient

Talk  with the patient again  , assess the  baseline risk  of CAD   if it is low ignore the TMT result and reassure.

• Repeat  stress test after  a month.
• Stress thallium
• Doubutamine  stress
• CT angiogram
• Regular Cath  angiogram* (May be the best , of course it also carries a  risk of labeling  the condition as  mild  CAD / non critical CAD etc )

For the  patient  the  easiest  option  may be ,   self  referral to a different cardiologist .   (Also called second opinion )

Final message

There is indeed an entity called   borderline  EST  . Do not dare to  ignore it  or else  face the consequences .

Read  related articles in this site .

1.Can medical management convert EST positive to negative ?

2. Should every one with positive EST should undergo CAG ?

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

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

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

Is it a right way of practicing cardiology ?

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

Can we do this without doing coronary angiogram ?

Yes ,  we can .

Step by step  Ask these questions

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

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

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

give the above certificate  “with a frame”  now .

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

Echo : The forgotten tool  for screening left main lesion.

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

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

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

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

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

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

Counter point ?

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

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

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

Final message

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

 

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

It is not the way cardiology is to be practiced !

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

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

Reference:

Please refer your own Brain.

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A defiant LAD refuses to die even after hanging !

Thousands of  coronary angiograms are done every day. Cardiologist no longer get excited to see exotic coronary lesions .Still , some images can be striking and dramatic. Here is an angiogram from a middle aged man  with stable angina  , who was  one among the routine early morning diagnostic studies  in our cath lab.

Who chopped the neck of this LAD ?

How this man was able to fill up the distal LAD almost completely? (With a complete cut off  right in the neck of LAD )

Are you sure there is antegrade flow ?

Do you get any clue ?

• Can a trickle of  ante grade flow  sustain  a  TIMI 3 FLOW  ?
• Or is it a  very efficient  instant collaterals  from LCX ?

Yes . The first one is right . An almost invisible antegrade channel  doing a exemplary job !

How is it possible ?

Realize an important fact . The distal flow beyond an obstruction  is not primarily dependent on degree of obstruction but the status of the distal vascular  bed .  If it is normal  even a hair-line patency  can  profusely perfuse the distal myocardial segment. This is what is happening to this man with a stable angina and perfectly normal micro vascular bed.

Lessens  from this Image.

Do not get fooled by the lay man’s logic. Realise there is  no simple relation  between  the degree of obstruction and degree of  blood flow impediment.It can be linear , curvilinear , or even inverse depending upon   the evolution and timing of obstruction  ,  number of lesions , presence or absence of collateral support , finally and  most importantly  the integrity of microvascular bed .

The  distal vascular bed drops its resistance drastically  once it senses  the problem in  proximal segment . This is based on Bernoulli principle and  is akin to how a  garden hose pipe  can simply increase  the velocity  by tightening the nozzle.*

* The garden hose analogy is a gross simplification of   complex factors that determine coronary blood flow.But it effectively clarifies a point ie  coronary blood flow is least dependent on coronary  stenosis (until  very late stages)

**Note further : This  hemodynamic  principle may not apply in acute occlusion as in STEMI  , where   acute  obstruction  often has a linear relationship with the quantum of blood flow.

By the way what happened to the above patient ?

Since he had significant angina there were no debates regarding management.  He  is posted for elective PCI this week-end .(We  can’t  get a stent just like that unless it is a real emergency  .Ours is a  Govt hospital !)

What is your take . Is it a going to be tough cross ?

I feel so , but my colleague Dr Gnanavelu   strongly  differs !

Let me post  our experience during PCI shortly.

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The mystery called post stenotic dilatation !

Newtons third law of motion  says for every  action  there is  an equal and opposite  reaction .

In vascular hemodynamics  whenever there is a an obstruction , there tend to be a dilatation of   the same blood vessel  somewhere distally.

It may not be linked to newtons law but it is  observed in many .It is more common in large vessels than small ones.

Here is a patient with a tight LAD lesion with a significantly  dilated segment located immediately beyond the  obstruction.This can be considered as a post stenotic dilatation. Coronary ectasia is  also a  possibility but since it is related to site of obstruction the former is likely .

What determines the post stenotic dilatation ?

The exact mechanism is not clear. There is  a definite ,sudden  pressure drop distal to  the  obstruction. This  pressure drop  recovers beyond a certain distance . At this point ,  the rate of increment in  velocity of   peaks .This somehow has an effect on the  distending  pressure  and the adjacent vessel wall gets radially stressed and begins to dilate. (Opposite of what is expected in Bernoulli effect ?)

Is there a anatomical defect in  post stenotic dilatation ?

Not every  one goes for post stenotic dilatation.There is a possibility it occurs only in genetically susceptible individuals .

Significance in  interventional cardiology

The post stenotic segment has a potential to misbehave in the period following  PCI . If the distal instent stenosis  occur (even if it is minor ! ) it can induce a cycle of post stenotic eversion of normal segment and risk of edge effect or stent thrombosis is more.

Read also Glagovian phenomenon – A form of  intra stenotic coronary artery dilatation

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Syntax calculator for reporting coronary angiogram

This is one of the wonderful corporate initiatives to assess the coronary angiogram and reporting . This calculator and teaching material was created by Boston scientific and Syntax study team . This  was used primarily during the  SYNTAX study.  This scoring system ,  though  appear  elaborate,  is a very  useful ,  objective way to assess coronary angiogram.

http://www.syntaxscore.com/calc/start.htm

Final message

It is encouraged to use this scoring system liberally . This will help us  to take more scientific decisions .

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Why doing a coronary angiogram is much easier than interpreting it !

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, interpenetrating 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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Rare coronary angiograms : Split left main coronary artery

Is it not ,  boring to  see  normal coronary arteries every day  ! There need to be surprises  in cath lab to make our time lively  and keep our brain alert .  Have a look at this angiogram in  RAO caudal view.One of our junior cardiology fellows thought it was  a split left main artery .

How can an artery split . . .of course the image indeed looks like that !

It was indeed an absent left main.  Also called as separate origin of LAD and RCA.

Note : There can be three  types of absent  left main.

• LAD and LCX from same ostia on the left coronary sinus*
• LAD and LCX separate  ostia but both from same sinus**
• LAD from left coronary sinus, LCX from right sided sinus (Probably the  common type )

* Some books mention about a left main of 0 -5mm .

** Very difficult to delineate and is rare

Zero  mm  left main is nothing but  single  ostial origin of both LAD and LCX. A very short left main , say 1 0r 2 mm will practically mimic an absent left main.

Here is the  the dynamic angio image. It is  surprising how a catheter in left sinus is able to visualise the LCX from right sinus so well !

Note the separate origin of LAD and LCX.The LCX was originating near the right sinus.It is intriguing to note even though they originate in different sinuses , the main stem of LAD and LCX wants to maintain a close parallel relation.

 

 

Advantages of having  absent left main .

• It requires no great brains  ,  to predict  the above patient is  immune  to  develop  Left main  or true bifurcation disease
• Sudden death is  presumed to be less common in this population.

Implications for interventional cardiologists

Guiding catheter selection and positioning could be difficult.

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Is septal branches of left anterior descending coronary artery immune to atherosclerosis ?

                                         Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of  cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA  and its branches .

Septal branches , even though divide very early  from the LAD , it  is  uncommon  to get affected by coronary atherosclerosis.  Even for an experienced   interventional cardiologist  , it  would be very rare to have  performed a  PCI for septal disease.

Why septal branches of LAD is rare to suffer from atherosclerosis ?

We don’t know the answer yet.

But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation  point , the atherosclerosis tend to occur ,  if the angle is more acute , and is  less common in abtuse angles .It is  almost rare  ,  if branching happens at   exact  90 degree angle or so !

The other reason for septal branches being immune to atherosclerosis is  , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also)  makes it difficult for the  process of atherosclerosis to sustain and grow .

Can you still get a  septal CAD ?

Yes,  usually as  a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and  atherosclerosis involves  both ostia.

What is  the implication for the  cardiologist to perform  a PCI with stenting in a septal branch of LAD  ?

PCI and stenting in the septal branches are more prone for crushing and fracture   as it is constantly exposed to the mechanical effects of muscle contraction.

Any other significance for septal branches of LAD ?

• Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
• Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol)  in patients  with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !

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