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Posts Tagged ‘plain balloon angioplasty’

Inferior STEMI, and see the first shot in RCA below. The patient was pain-free and hemodynamically stable at the time of the angiogram. (Don’t wonder how this is possible, defying the fundamental rules learned from  animal experiments after acute ligation of the coronary artery)

                

What needs to be done ?
  • Go ahead and do a primary PCI as we do in any other  IRA.
  • Be watchful, just pass on the wire, feel the lesion, and decide thereupon. Consider intracoronary lysis.
  • How about a long stent from proximal to distal RCA?
  • Kissing the lesion with DEB in the tightest segment (Not a funny option )

 

 

What was done? How is the patient?

Nothing was done & nothing happened to the patient as well. Just guidewire was crossed and few minutes of balloon touch-up work. Did the patient improve? Can’t say anything because he was fine even with this total occlusion. 

Lessons to be learned 

  • The art of leaving a lesion left unattended (rather unstented) in IRA without guilt.
  • TIMI zero flow in IRA need not be a death sentence for the distal myocardium, even in STEMI. 
  • Sometimes, a simple guidewire crossing can do the same job as a complex angioplasty in an IRA.(For acute salvage TIMI 2 or even TIMI 1 is good enough) Most IRA accidents happen when trying improve upon this in an ectatic vessel.
  • Risks of stenting in ectatic /Thrombotic segment is real
  • There can be a useful role for  STENTYS self-expanding stents in localized ectasia (Ref 1)
  • Long-term OAC (Soon NOACs) is a perfect remedy for protecting this type of coronary. 

* By the way, who are all bothered to know LAD anatomy in this patient.  Is it surprising the  RCA is sending collaterals to the left side in its hour of crisis? Yes. LAD had chronic sub-total lesion as well.

Reference

1.The Role of Self-expanding Stents in Patients with Atypical Coronary Anatomy | ICR Journal https://www.icrjournal.com/articles/role-self-expanding-stents-patients-atypical-coronary-anatomy

 

2.

 

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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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