management of acute mi, role of streptokinase ,nicvd

7/27/2019 Management of Acute MI, Role of Streptokinase ,nicvd

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Management o f Acu te ST-Segment

Elevat ion Myocard ial In farc t ion (STEMI)

Role of Streptokinase

Presenter

Dr. Md. Azizul KarimMD 3rd part student


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Introduction

The management of STEMI patients is complex,

multidisciplinary, and involves the following three differentstages of care

(1)emergency department,

(2)cardaiac catheterization, and

(3)coronary care unit.


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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
http://en.wikipedia.org/wiki/Creatine_kinasehttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Troponinhttp://en.wikipedia.org/wiki/Creatine_kinasehttp://en.wikipedia.org/wiki/Creatine_kinasehttp://en.wikipedia.org/wiki/Creatine_kinase


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Management

A MI is a medical emergency which demands bothimmediate 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.


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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 andpreferred at experienced centers capable of performing

procedure rapidly, especially when diagnosis is in doubt,

cardiogenic shock, bleeding risk.


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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.


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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 foracute stroke within 3 hours).

Suspected aortic dissectionActive bleeding or bleeding diathesis


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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.

Contraindicatons of thrombolytic therapy


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List of Thrombolytics:

Non specific : Streptokinase (SK)

Clot specific: Alteplase(t-PA)

Mutant plasminogen actisvator:

Tenecteplase, Reteplase

Plasminogen

activators

plasminogen plasmin

fibrinFibrin degradation

product (FDP)

Plasminogen activator-inhibitor

2 -antiplasmin


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Comparison of different fibrinlytic agents

Characteristic Streptokinase Alteplase Reteplase Tenecteplase

Dose 1.5106 in 30 to

60 min

Upto 100mg in

90 min

2x10u bolus 0.5mg/kg bolus

Antigenicity ++ - - -

Fibrin specificity

-++ + +++

90 min patency ++ (50%) +++ (75%) ++++ (75%) +++/++++

(75%)

Mortality

reduction+ ++ ++ ++

Hge stroke + ++ ++ ++

Cost + +++ +++ +++

TIMI grade 3

flow(%)

32 54 60 60


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What is Streptokinase?

Stabilized pure streptokinase derived from the culture filtrate ofbeta-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 ofdegrades fibrinand hence

dissolves the thrombus.


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Streptokinase- the drug of choice for thrombolytic therapy

The choice of a thrombolytic agent during therapy is dictated by anumber 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.


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Clinical Study


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Streptokinase


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Streptokinase

Combination of Streptokinse with ASA Results

in a Further Reduction of Mortality Rate


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Trial and Thrombolytic

Agent

Death

(%)

Total

Stroke

(%)

Cerebral

Hemorr

hage

(%)

GISSI-2

(n=20,891)

SK 9.2 0.94 0.2

t-PA 9.6 1.33 0.42

ISIS-3

(n=41,229)

SK 10.6 1.04 0.24

t-PA 10.3 1.39 0.66

APSAC 10.5 1.26 0.55

GUSTO-1

(n=41,021)

SK+ SC

heparin

7.2 1.22 0.49

t-PA+IV

heparin

6.3 1.55 0.72

SK+ IV

heparin

7.4 1.4 0.54

t-PA+SK+IVheparin

7.0 1.64 0.94

Streptokinase


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Streptokinase


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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.


19/22

A Local brand of

Streptokinase

Just Introduced

First Time in Bangladesh


20/22


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Thank You

management of acute mi, role of streptokinase ,nicvd

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