Thrombolysis is not used in unstable angina/NSTEMI because the pathophysiology is different from STEMI. In UA/NSTEMI, the occlusion tends to be gradual rather than sudden and complete, and the thrombus is often located intraplaque rather than completely occluding the lumen. Additionally, the thrombus in UA tends to be platelet-rich rather than fibrin-rich, and thrombolytic agents are less effective at lysing platelet-rich clots. Finally, UA is not generally a medical emergency in the same way STEMI is, so the risks of thrombolytic therapy outweigh the benefits.

1. Why NO THROMBOLYSIS IN
UNSTABLE ANGINA/ NSTEMI?
KESHAB RAJ NEUPANE

2. UA/NSTEMI
 the presence of ischemic chest pain (or an equivalent),
the notable absence of ST segment elevation on electrocardiography,
and
the presence of either ST segment depression or T-wave inversion on
electrocardiography and/or
abnormal cardiac biomarkers.
• The difference  based on the presence of myocardial necrosis or
infarction on serum tests such as creatine kinase-myocardial band,
troponin I, or troponin T in NSTEMI.

3. Pathophysiology of UA/NSTEMI
• six possible etiologies:
1) thrombus arising from a disrupted or eroded plaque,
2) thromboembolism from an erosive plaque,
3) dynamic obstruction (such as coronary spasm),
4) progressive mechanical obstruction,
5) inflammation, or
6) coronary artery dissection.
Most patients with UA/NSTEMI have thrombus formation or progressive arterial
narrowing that leads to subtotal occlusion of an epicardial coronary artery.
1.Braunwald E. Unstable angina: an etiologic approach to management. Circulation 1998;98(21):2219-22.
PMID: 9826306.

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

5. Why is this apparent paradox ?
What is basic difference between UA and STEMI ?

6. • 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.

7. • 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 usually the risk benefit ratio favors thrombolyis in
most situations except in very elderly and previous history of stroke
or bleeding disorder.

8. On the other hand,
• 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.

9. 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.

10. Why thrombolysis is not useful in UA ?
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.

11. 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.

12. 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 .