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Posts Tagged ‘timi 3 flow’

A defiant LAD refuses to die even after hanging !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology innovation, cardiology- coronary care, Cardiology-Coronary artery disese, Hemodynamics, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , on May 15, 2011| Leave a Comment »

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 !

Posted in Cardiology -Interventional -PCI, tagged , , , , , , , on March 25, 2011| Leave a Comment »

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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The enigma of TIMI 3 flow !

Posted in Uncategorized, tagged on June 3, 2009| 2 Comments »

Coronary arterial obstruction  is  considered,  dangerous because it obstructs the coronary blood flow . Is it possible ,  for an  obstruction  to have  little  impact  on the blood flow  ? Fortunately ,”yes” , the physics of   fluid dynamics  is patient  friendly .It is  well known , coronary blood flow goes on smoothly, uninterrupted until very late stages of obstruction .*This  has created the concept of flow limiting lesions and non flow limiting lesion .

The most popular form of reporting coronary blood flow across a stenosis is TIMI grading. Originally used   following thrombolysis , now universally used for all angiogram (Is it appropriate ?)

TIMI Grading

Grade 0 (No perfusion): There is no antegrade flow beyond the point of occlusion.

Grade 1 (Penetration without perfusion): The contrast material passes beyond the area of obstruction but “hangs up” and fails to opacify the entire coronary bed distal to the obstruction.

Grade 2 (Partial perfusion): The contrast material passes across the obstruction and opacifies the coronary bed distal to the obstruction. However, the rate of entry of contrast material into the vessel distal to the obstruction or its rate of clearance from the distal bed (or both) is perceptibly slow.

Grade 3 (Complete perfusion): Antegrade flow and clearance  of the dye   distal to the obstruction occurs as promptly as antegrade flow .

When does a coronary blood  flow gets impeded  following obstruction ?

Contrary to the  popular belief , the distal blood flow in a coronary artery  is  less dependent on the degree obstruction than the status of the  distal microvasculature.Classical teaching tells us if a coronary artery narrows >70% diameter stenosis (90%area) the blood flow gets impeded on exertion . For resting blood flow to get blocked it needs still further narrowing .

These rules are written in the era  before we knew the concept of coronary vascular  reserve . We , have since understood  ( or confused !)  more about coronary microcirculation.The major misconception could be what we interpret as epicardial blood flow is actually reflect the status of coronary micro vascular integrity.

How else you explain a patient with a same degree of coronary obstruction has vastly different distal blood flow profile ! There are innumerable examples of patients with 50% obstruction having  TIMI one flow and a 99% obstruction with TIMI 3 flow  !

Have a look at this angiogram ,  / Click  here  to view the video

LCX TIMI 3 FLOW CORONARY ANGIOGRAM

What are the factors  other than the  degree obstruction that determine  the  distal  flow?

  • Acuteness of obstruction.
  • Status of   coronary microvascular bed
  • Interstitial  (Myocardial)  edema
  • Coronary microvascular  reactivity
  • Recruitment of collaterals
  • Coronary perfusion pressure (Aortic diastolic pressure – RVEDP/Coronary sinus pressure)

Final  message

The most important determinant of  blood flow distal to obstruction is the vascular reactivity , tone  and the integrity microvascular reserve .This rule  applies  both in  in acute  and chronic coronary syndrome  . In  CTOs  it may  not apply as distal flow is near zero.  Here  also  the  inherent  intraluminal resistance   of collapsed distal vessel  will determine the  distal flow.

Note :TIMI 3  flow  ,does not represent  a homogeneous class of coronary blood flow .They can have variable myocarial blush and frame counts.It may need further analysis.

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What is no reflow ? What is the mechanism of no reflow ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , , , , , , on September 24, 2008| Leave a Comment »

No reflow is the terminology used primarily in cath labs where, even  after a successful opening and stenting  of a coronary artery the coronary blood flow is not  restored to myocardium . The point to be emphazised here is blood do cross  successfully the site of  the obstruction but fails to enter the muscle segment  to which the coronary artery is supplying. So the paradoxical situation of artery  being open but the  myocardium is closed to receive  blood flow  happens . This is termed as no -reflow.  Actually it is a  misnomer , and  ideally it should be called “no flow” because  normal distal flow  does not  occur (After PCI)  in the first instance  to get interrupted  later on  and be labeled as  no re-flow.  .The only positive effect of PCI in these situation is blood flow would have improved by few centimeters ie till it reaches  but falls short of myocardium . In fact no reflow , can be termed as  glorified and concealed  terminology  for  PCI failure . It needs urgent action . No reflow is also called as myocardial epicardial dissociation.

Mechanism of no reflow.

Curious case of open coronary artery and closed myocardium !

Coronary  microvascular plugging  is mainly  due to thrombus and atheromatous debri , myocardial  edema , microvascular spasm may also contribute.

Where can it occur ?

  • First described in cath lab, especially following primary angioplasty.
  • It can very  well happen following thrombolysis in STEMI.

  • Can occur in venous grafts.

How do you recognise no reflow?

In cath lab it will be self evident from the check angiogram. Some times it is less obvious and may  require, myocardial  blush score, TIMI frame  count, contrast echocardiography, PET scan etc. In post MI a very simple method to recognise this entity could be the observation of persistent ST elevation in ECG .

Treatment.

Extremely difficult. Almost every coronary vasodilator has been tried.(Nitrates, nicorandil, calcium blockers, etc).Success is less than 30%.  High pressure flushing with saline inside the coronary artery is advocated by some.Others believe it’s dangerous to do it. So prevention is the key. Avoid doing PCI in complex, thrombotic lesions. Use thrombus suction device like export catheter(Medtronic). Distal protective devices are double edged devices , useful only in experienced hands.

Unanswered question

What is the size of the particle (thrombotic and atheromatous  debri)  the   coronary microcirculation safely handle and push it into the coronary venous circulation and the coronary sinus for disposal ?

If we can lyse the thrombus into micro particles by some mechanism and make it traverse the coronary circulation this complication of microvascular  plugging can be treated and prevented .

What is the final message ?

  • No reflow is relatively common condition during emergency PCI done for ACS patients
  • More common in complex thrombotic lesions.
  • Can also  occur in STEMI
  • Treatment is often vexing . In fact the treatment of this condition is so difficult , it can be termed  almost synonymously with “Failed PCI” if flow is not restored.
  • Successful treatment of no- reflow  means not momentry restoration of  myocardial flow  by mechanical and pharmacological modalities ,but to maintain sustained myocardial   perfusion. This we realise, as patients who have had a no reflow during  a PCI, do not perform as well in the follow up  .
  • So prevention is the key.

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