Posts Tagged ‘open artery hypothesis’

“We have a 24/7 cath lab with an open door policy. Our cardiologist arrives at 15 minutes’ notice. Door to balloon time is less than 60-90 minutes”, 

“Great, so, you can always offer a successful treatment for STEMI”

“No, that we can never guarantee.” 

 “Oh, It Is not the answer, I  expected”

“I agree, it sounds disappointing, but. truths are less pleasing. What I am trying to say is, there are a number of factors other than the availability of a grand cath lab and agile and effortless hands, that try to reperfuse the myocardium in distress.  I agree, we do save lives occasionally in a dramatic fashion. Recently we resuscitated an almost dead man with CPR and ECMO-guided PCI. But, most times it turns out to be just a customary ritual that takes us to the legal and therapeutic  endpoint* of STEMI management”

*Both salvage & non-salvage

“I didn’t get you, Can you explain further?

See this curve and try to understand it yourself. (I would say, this is the ultimate curve to understand in the entire field of coronary care)

Can you guess what will be the outcome for C to B, or B to A ?  In the real world, a substantial number of interventions take place at an Invisible point E beyond A  Source: Gersh BJ, Stone GW, White HD, Holmes DR Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA. 2005;293:979–86

Slippery slopes and edgy Interventions

At what point the patient lands up in the curve & at what point the interventional cardiologist intervenes (or does not intervene) matters the most. 

The gaps between benefit and harm can change in a few strokes of time. The reperfusion tamasha can get more curious if we realize both the slope of the curve & its absolute position are dynamic. It can shift to the right or left with reference to the patient’s Initial medications, MVo2 confounders, the quantum of collateral circulation, myocardial hypoxia threshold,  previous ischemic episodes, conditioning, etc. So, basically, we are reacting to events and trying to rush up things. Don’t worry about all this. Cardiologists have every expertise and equipment to tackle untoward events.

STEMI is not always myocardium under fire

Finally, and most importantly STEMI, though a cardiac emergency. all should not be equated with the house(myocardium) on fire analogy. It can also be a spontaneously aborting, settling, or evolving, self-extinguished controlled fire, and the myocardium may take it easy. All that it requires is some deep ischemic slumber. Don’t try to poke it with all our violent hardware at one go in the name of salvaging. What is required is proper CCU care to take care of potential arrhythmia, angina, or failure. One may create more damage if trying to dowse non-existing flames furiously, which expresses in the form of reperfusion Injury and no-reflow to the myocardium. (Which might have reperfused at leisure without experiencing the injury.)

It is worth pondering over this question.

Why does even an apparently well-timed primary PCI of IRA leave behind a significant LV dysfunction or even a  scar? This is a clear case of “successful PCI failed reperfusion syndrome”. It is better cardiology community defines successful primary PCI with reference to predischarge  LV function, not on the IRA patency and mystery endpoint called TIMI 3 flow.

Final message

Cath lab doors that are open 24/7,  with experienced cardiologists may matter little if we are double-blinded against multiple scientific and non-scientific factors that are visible as well as invisible. 


How good is late PCI? Are you not aware benefits of the open artery hypothesis?

You need to learn a lot man, before posting such posts.

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Hot debate in STEMI

Acute total obstruction (ATO) of coronary artery is an emergency .Opening it  by pharmacological or catheter is the  standard ( logical ) protocol.However, time plays a crucial role in this coronary re-perfusion game.It can either be a sure shot of success or end up in total spoilsport. One more issue as important as time is from the overflowing scientific data  fired  by different regulators  in conflicting directions  (Also called knowledge) .

What to do with STEMI coming late ?

  • ATO with cardiogenic shock is an  absolute emergency at any time.
  • Symptomatic ATO  other than CS beyond 24 hrs still  considered  emergency for most.(Symptom should be true angina )
  • Hemodynamic instability is misunderstood term . Stabilizing it medically is not forbidden.

Asymptomatic stable ATO  beyond  24-72 hours can be  semi emergency, true emergency or as cool  as a cucumber depending upon the cardiologist’s wisdom , experience or inexperience  and the  Institutional Integrity !

*Please be reminded ,LV dysfunction is not an absolute indication for urgent intervention unless it is due to ischemic dysfunction attributable  to a critical non IRA lesion

When does a ATO become safe CTO ?

1 month , 3 months, 6 months ?

Why we are  not defining a sub-acute ATO ? or CTO in transition   ?

Is living peacefully with sub acute ATO or CTO a coronary crime ?

We don’t require a debate , whether these  questions are worth answering  or not !

Final message

Though cardiac professional  are committed  to open up occluded arteries to save  lives , reality is repeatedly teaching different stories ! The greatest danger of keeping an artery open( In disputed indications ) is the newly conferred risk of sudden closure and the attendant  unpredictable aftermath !

Or should we conclude : Living with CTO is ok , but don’t intentionally create one by denying PCI in late  post STEMI ATOs


Arguing closed artery is better than an open artery is straw man argument and inability to interpret positive things in science.  However it may still be right  when science suffers  from hostile incursions from non academic forces.

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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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