Management of Acute ST-Segment Elevation Myocardial Infarction (STEMI)

Role of Streptokinase
Dr. Md. Azizul Karim

Presenter

MD 3rd part student

Introduction
The management of STEMI patients is complex, multidisciplinary, and involves the following three different stages of care (1)emergency department,

(2)cardaiac catheterization, and

(3)coronary care unit.

Diagnosis of Acute MI

A patient is diagnosed with myocardial infarction if 2 (probable) or 3 (definite) of the following criteria are satisfied: 1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes 2. Changes in serial ECG tracings 3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin-i

Management
A MI is a medical emergency which demands both immediate attention and activation of the emergency medical services. As time passes, the risk of damage to the heart muscle increases; hence the phrase that in myocardial infarction,

"time is muscle," and time wasted is muscle lost.

Oxygen, aspirin, clopidogrel, nitroglycerin, analgesia, beta blocker, and heparin are usually administered as soon as possible.

Reperfusion Strategies
The main goal of STEMI management is rapid reperfusion to establish coronary blood flow ischemic myocardium. Currently, there are three main reperfusion strategies: Thrombolytic therapy, Primary PCI, and Thrombolytic- facilited primary PCI Primary PCI is generally more effective than fibrinolysis and preferred at experienced centers capable of performing procedure rapidly, especially when diagnosis is in doubt, cardiogenic shock, bleeding risk.

Thrombolytic Therapy

Thrombolytic therapy is indicated for the treatment of STEMI

If the drug can be administered within 12 hours of the onset of symptoms , Elevation of ST segment in 2 or more contiguous leads(1 mm or more in limb leads and 2mm or more in chest leads), new onset LBBB and Primary PCI is not immediately available.

Contraindicatons of thrombolytic therapy

Absolute contraindications

Any prior intracranial hemorrhage Known structural cerebral vascular lesion Known intracranial neoplasm Ischemic stroke within the past 3 months (except for acute stroke within 3 hours). Suspected aortic dissection Active bleeding or bleeding diathesis

Contraindicatons of thrombolytic therapy Relative contraindications

History of chronic, severe, poorly controlled HTN SBP> 180mmhg or DBP >110mmhg Active peptic ulcer History ischemic stroke 3 months Recent internal bleeding Pregnancy Noncompressible vascular puncture.

List of Thrombolytics:
Non specific : Streptokinase (SK)
Plasminogen activators

Clot specific: Alteplase(t-PA) Mutant plasminogen actisvator: Tenecteplase, Reteplase

Plasminogen activator-inhibitor

plasminogen

plasmin

2 -antiplasmin
fibrin Fibrin degradation product (FDP)

Comparison of different fibrinlytic agents

Characteristic Streptokinase Alteplase Reteplase Tenecteplase

Dose
Antigenicity Fibrin specificity 90 min patency

1.5106 in 30 to 60 min

Upto 100mg in 90 min

2x10u bolus

0.5mg/kg bolus

++

++ +++ (75%)

+ ++++ (75%)

+++ +++/++++ (75%)

++ (50%)

Mortality reduction
Hge stroke Cost TIMI grade 3 flow(%)

+
+ + 32

++
++ +++ 54

++
++ +++ 60

++
++ +++ 60

What is Streptokinase?
Stabilized pure streptokinase derived from the culture filtrate of beta-haemolytic streptococci of Lancefield group C.

How Streptokinae works?

Streptokinase acts with plasminogen to produce an activator complex that converts residual plasminogen into the proteolytic enzyme, plasmin. Plasmin is capable of degrades fibrin and hence

dissolves the thrombus.

Streptokinase- the drug of choice for thrombolytic therapy

The choice of a thrombolytic agent during therapy is dictated by a number of factors, which depends essentially upon the relative merits and demerits of individual PG activators. These include: Cost of the drug Side-effects and their severity In-vivo stability Specificity towards fibrin clots Immunological reactivity The TPA, despite being a relatively immunologically inert when compared to SK, they possess significantly lower in vivo half-lives and significant excess of hge stroke. On the other hand, TPA considerably more expensive than SK. Therefore, SK is the drug of choice in thrombolytic treatment in developing nation.

Clinical Study

Streptokinase

Streptokinase
Combination of Streptokinse with ASA Results in a Further Reduction of Mortality Rate

Streptokinase

Trial and Thrombolytic Agent

Death (%)

Total Stroke (%)

0.94 1.33

Cerebral Hemorr hage (%)

0.2 0.42

GISSI-2 (n=20,891)

SK t-PA

9.2 9.6

ISIS-3 (n=41,229)

SK
t-PA APSAC SK+ SC heparin t-PA+IV heparin SK+ IV heparin

10.6
10.3 10.5 7.2 6.3 7.4

1.04
1.39 1.26 1.22 1.55 1.4

0.24
0.66 0.55 0.49 0.72 0.54

GUSTO-1 (n=41,021)

t-PA+SK+IV heparin

7.0

1.64

0.94

Streptokinase

Conclusion

Although t-PA has become a more popular thrombolytic agent in developed nations like the United States, Streptokinase continues to be widely used in developing nations like Bangladesh. Because the cost of t-PA is nearly 10 fold more than that streptokinase, streptokinase continues to be the available fibrinolytic agent for millions who sustain AMIs in developing countries.

A Local brand of
Streptokinase

Just Introduced
First Time in Bangladesh

Thank You