Posts Tagged ‘coronary thrombosis’

First and foremost is

Avoid the procedure if  not really indicated.A lesion which  has more thrombus load  than a plaque and it is ,  subcritical and not limiting the flow  , PCI may be inappropriate  especially if the ACS is stabilised.

  • Adequate anticoagulation  along with  2b 3a blockers should be used
  • Predilatation should be minimally used or to avoided.Direct stenting preferred.
  • In primary PCI suction devices (Export etc may be useful)
  • Distal protective devices  are  “hyped up devices” rarely useful in an occasional patient with good distal vessel diameter.
  • Pseudo stent approximati(fig 1) may occur. A Layer of thrombus may get plastered between stent and the vessel wall.In the post PCI  phase , with intense anticoagulation and antiplatelet regimen this layer may get dissolved and stent  may lose it’s grip and may dislodge or migrate.Another possibility is the dead space  beneath the stent  becomes a potential site for future  thrombus and ACS.


Fig 1

  • To prevent this complication , high pressure inflations and Post procedure IVUS (Intra vascualr ultraound may be done to ascertain lack of thromus between stent/vessel wal  interface)
  • Drug eluting stent evoked a special concern , when used in thrombotic milleu.This , has now been  proven to be  safe

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Intraluminal filling defect is often  observed during coronary angiogram .Thrombosis  has become the default diagnosis in most situations.This has resulted in over diagnosis of thrombosis .In fact a strategically located plaque stained by the dye is an equally common cause for intraluminal filling defect.

In fact there are many recognised caused of filling defect

  1. Thrombus
  2. Dissection
  3. An eccentric plaque
  4. Dye trapped within  plaque fissures
  5. Calcification projecting into lumen
  6. Plaque prolapse from stent struts
  7. Artifacts-End on view of  side branches
  8. Static myocardial bridges
  9. Trapped air bubble(Transient filling defect)
  10. Streaming  effect  dye may mimic a filling defect


It is  not advicable  to make a  default dignosis of coronary thrombosis in all cases of intraluminal filling defects

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              Intra coronary thrombosis is the sine qua non of acute coronary syndrome ( Both STEMI and NSTEMI.) But thrombolysis is the specific therapy in STEMI and is contraindicated in NSTEMI/UA.

Why is this apparent paradox ? What is basic differnce between UA and AMI ?

In STEMI there is a sudden & total occlusion of a coronary artery usually by a thrombus with or without a plaque .The immediate aim is to open up the blood vessel . Every minute is important as myocardium undergoes  a continuous process ischemic necrosis. So thrombolysis (or more specifically fibrinolysis should be attempted immediately) .The other option is primary angioplasty,  which will not be discussed here.

The thrombus in STEMI  is RBC &  fibrin rich and often called a red clot. Number of fibrinolytic agents like streptokinase, Tissue palsminogen activator,(TPA) Reteplace, Tenekteplace etc have been tested and  form the cornerstone of STEMI management.The untoward effect of stroke  during  thrombolysis  is well recognised , but usully the risk benefit ratio favors thrombolyis in most situations except in very elderly and previous history of stroke or bleeding disorder.

Unstable angina is a  close companion of STEMI . Many times it precedes STEMI often called preinfarction angina. During this phase blood flow in the coronary artery  becomes sluggish gradually,and patients develop  angina at rest .But unlike STEMI there is never a total occlusion and myocardium  is viable but ischemic,  and emergency salvaging of myocardium is not a therapeutic aim but prevention of MI becomes an aim. It is a paradox of sorts ,  even though thrombus is present in  UA ,  It has been learnt by experience thrombolytic agents are not useful in preventing an MI .


Why  thrombolysis is not useful in UA ?

1.In unstable angina  mechanical obstruction in the form of plaque fissure/rupture is more common than completely occluding thrombus. So lysis becomes less important.

2. Even if the thrombus is present , it is often intra plaque  or intra lesional and the  luminal  projection of thrombus is reduced  and hence thromolytic agents have limited area to act.

3.Further in UA/NSTEMI since it is a slow and gradual occlusion (Unlike sudden & total occlusion in STEMI) the platelets  get marginalised and trapped within the plaque .Hence in UA  thrombus is predominantly  white  . Often, a central platelet core  is  seen over which fibrin clot may also be  formed.

4.All available  thrombolytic agents act basically as a fibrinolytic agents,  and   so it finds   difficult to lyse the platelet rich clot.There is also a small risk of these agents lysing the fibrin cap and exposing underlying platelet  core and trigger a fresh thrombus.This has been documented in many trials( TIMI 3b to be specific) So if we thrombolyse in UA , there could be a risk of recurrent ACS episodes in the post thrombolytic phase.

5. UA is a semi emergency where  there is no race against time to salvage myocardium .Administering a  stroke prone thrombolytic agent tilts the risk benefit ratio against it.

6. Among UA, there is a significant group of secondary /perioperative UA   due to increased demand situations. Here there is absolutely no role for any thromolytic agents,  the  simple reason is , there is  no thrombus to get lysed. 

7.Many of the UA patient have multivessel CAD and might require surgical revascualarisation directly .


So fibrinolytic  agents are contraindicated in UA so what is the next step ?

The emergence of  intensive and aggressive platelet-lytic agents.

A combination of aspirin, clopidogrel, heparin, glycoprotien 2b 3a antagonist formed the major therapeutic protocol in these patients.Even though these are called antiplalet agents some of them  like 2b/3a antagonist eptifibatide, tirofiban, and many times even heparin has a potential to dissolve a thrombus. So technically one can call these agents  as thrombolytic agents.

What are the unresolved issues

                                       Even though clinical trials have convincingly shown thrombolytic agents  have no use in UA .There is a nagging belief  THAT  there could  be group of patients  with UA , still might benefit from thrombolysis as total occlusions have been documented  in some cases with UA.This is  especially true in peri-infarction unstable angina (Pre & post) as there is a fluctuation  between total and subtotal occlusions ) .But bed side recognition of this population is very difficult.

Many would consider this issue as redundant now,  since  most of  these patients  are taken up for emergency revascularisations

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