What is the difference between NSTEMI (non STEMI) and STEMI?
Why are fibrinolytics like Streptokinase not used in NSTEMI?
What is the difference between NSTEMI (non STEMI) and STEMI?
Why are fibrinolytics like Streptokinase not used in NSTEMI?
Acute coronary syndromes (ACS) are divided into:
1. STEMI - ST Elevation MI - the classical MI
2. NSTEMI - Non-ST Elevation MI.\
3. UA - Unstable Angina
STEMI is when there is a transmural infartion of the myocardium - which just means that the entire thickness of the myocardium has undergone necrosis - resulting in ST elevation. Usually due to a complete block of a coronary artery (occlusive thrombus). This requires the use of thrombolytics like Streptokinase to lyse the thrombus. Evidence has proven that it is very effective and not as risky (Benefits > Risk)
UA or NSTEMI is when there is a partial dynamic block to coronary arteries (non-occlusive thrombus). There will be no ST elevation or Q waves on ECG, as transmural infarction is not seen. The main difference between NSTEMI and unstable angina is that in NSTEMI the severity of ischemia is sufficient to cause cardiac enzyme elevation.
Why is streptokinase not used in treating UA/ NSTEMI?
In patients with UA/NSTEMI, plaque stabilization to prevent progression of the disease is required. While fibrinolytics like Streptokinase benefit patients with STEMI, they may increase risk of bleeding complications for those with NSTEMI. This is also based on evidence - no benefit, more risk.
Summary/Keywords
1. STEMI - occlusive thrombus - ST elevation (and Q waves) - Cardiac Enzyme elevation - Fibrinolytics beneficial
2. NSTEMI - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation present - Fibrinolytics not beneficial
3. UA - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation absent - Fibrinolytics not beneficial
Hope this is clear.
Ask further if you need any details...
Thanks for this clear answer, but I did not understand the answer to the question "Why is streptokinase not used in treating UA/ NSTEMI?" very well. Can you please explain?
Let me explain.
As you know, unstable angina and NSTEMI (along with STEMI) are part of the spectrum of acute coronary syndrome (ACS). So, it is fair to consider why we cannot use fibrinolytics in in them but only in STEMI. Afterall, all these conditions are due to thrombus in coronary arteries.
You have heard of "Primum non nocere" - first, do no harm. This principle is used in explaining the reason for the above answer.
In STEMI, there is a clear and present danger of mortality. Usage of thrombolyics poses some risks including fatal/morbid bleeding. In the situation of STEMI, the benefits of fibrinolytic usage outweighs the risks it poses for the patient. It saves lives.
However, in unstable angina and NSTEMI, it is not so. The mortality rates of these conditions are much less and there is no impending myocardial cell necrosis. Hence, the risk of bleeding due to fibrinolytics is more than the benefit offered by them. Moreover, usage of anticoagulants (LMWHeparin - enoxaparine) and antiplatelets (aspirin/clopidogrel) is known to significantly reduce the complications.
These are the reasons why I made the statement in the first post - "While fibrinolytics like Streptokinase benefit patients with STEMI, they may increase risk of bleeding complications for those with NSTEMI. This is also based on evidence - no benefit, more risk."
References:
- Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia. http://www.ncbi.nlm.nih.gov/pubmed/8149520
- Revisiting the culprit lesion in non-Q-wave myocardial infarction. Results from the VANQWISH trial angiographic core laboratory. http://www.ncbi.nlm.nih.gov/pubmed/11985907
- Differential sensitivity of erythrocyte-rich and platelet-rich arterial thrombi to lysis with recombinant tissue-type plasminogen activator. A possible explanation for resistance to coronary thrombolysis. http://www.ncbi.nlm.nih.gov/pubmed/2494006
STEMI is ST elevation myocardial infarction and NSTEMI non ST elevation myocardial infarction. Since STEMI is due to sudden thrombotic occlusion (formation of a blood clot) of a coronary artery, the mainstay of treatment is thrombolytic therapy (treatment to dissolve the clot). NSTEMI is due to an unstable plaque with aggregation of platelets. Hence the mainstay of treatment is anti platelet drugs and anticoagulants. Aspirin, clopidogrel, beta blockers and statins are given to both types of infarction. Primary angioplasty is another option for STEMI, if the facility is locally available. Primary angioplasty is considered justified if the difference between the time required to arrange primary angioplasty is not more than 1 hour more than the time for arranging thrombolysis.
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What would be a suitable alternative to Streptokinase e.g. if patient had a peptic ulcer or recurrent bleeding? I was thinking heparin but since this only prevents clot-formation and not clot-destruction is this wrong?
And thank you for the original explanation, I was unsure about this topic and it is now much clearer.
There are many contraindications for streptokinase. These can be classified as absolute and relative:
Absolute contraindications:
- Past history of intracranial bleeding
- Stroke in the preceding 12 months
- Any active bleeding
- Uncontrolled high blood pressure
- Malignant cerebral neoplasm
- Recent previous treatment with or known allergy to streptokinas
Relative contraidications
- Current anticoagulant use
- Surgical procedure in the preceding 2 weeks
- Prolonged cardiopulmonary resuscitation (CPR >10 minutes)
- Known bleeding diathesis
- Pregnancy
- Proliferative diabetic retinopathy
- Active peptic ulcer
- Controlled severe hypertension
As you see, active peptic ulcer (if not bleeding) is a relative contraindication and a bleeding ulcer is an absolute contraindication.
Now, to answer your specific question, the alternative in this situation is to use non-pharmacological means of revascularization like PTCA (percutaneous transluminal coronary angioplasty).
I was recently involved in the resuscitation of a STEMI patient who became unstable and required CPR. In addition to the standard CPR drugs (Adrenaline, lignocaine, amiodarone), the team leader used Alteplase for thrombolysis. The patient went on to survive (yay!)
Given that streptokinase causes hypotension, is its use in unstable patients appropriate (assuming there are no other contraindications)? Is it reasonable to initiate streptokinase during CPR if alteplase is not available?
Last edited by keno; March 29th, 2010 at 06:58 AM.
Congratulations for being on the team that saved that patient. How long was the CPR performed?I was recently involved in the resuscitation of a STEMI patient who became unstable and required CPR. In addition to the standard CPR drugs (Adrenaline, lignocaine, amiodarone), the team leader used Alteplase for thrombolysis. The patient went on to survive (yay!)
This issue of the use of streptokinase during CPR is controversial. It is not routinely recommended, but there are some reports pointing in both ways:Given that streptokinase causes hypotension, is its use in unstable patients appropriate (assuming there are no other contraindications)? Is it reasonable to initiate streptokinase during CPR if alteplase is not available?
FOR - http://www.ncbi.nlm.nih.gov/pubmed/16261290
NEUTRAL - http://www.ncbi.nlm.nih.gov/pubmed/18409362Thrombolysis with streptokinase during cardiopulmonary resuscitation: a single center experience and review of the literature.
OBJECTIVE: To report our experience with use of thrombolysis with streptokinase during cardiopulmonary resuscitation of patients with cardiac arrest due to myocardial infarction. DESIGN: A case series. METHODS: Thrombolytic therapy (streptokinase) was administered during cardiopulmonary resuscitation of 4 patients with suspected myocardial infarction as the cause of cardiac arrest. RESULTS: 3 of the 4 patients survived and were discharged from the hospital without any major complications or neurological sequela. CONCLUSION: Thrombolysis with streptokinase during cardiopulmonary resuscitation of patients with suspected acute myocardial infarction is associated with reduced mortality and favorable neurological outcome.
Given the ambiguous nature of the available evidence, it is wiser to use thrombolytics only if it is used as a last life-saving option when everything else seems to be failing. If alteplase is not available, streptokinase may also be considered, but bleeding complications are likely to be more.Thrombolysis during cardiopulmonary resuscitation--own clinical observations--case report
Thrombolytic therapy is contraindicated in the course of cardiopulmonary resuscitation (CPR). If the primary cause of cardiac arrest is myocardial infarction or massive pulmonary embolism, fibrynolysis may be life-saving. We present a case report of a woman admitted to the Intensive Care Unit with cardiac arrest with symptoms suggesting myocardial infarction or pulmonary embolism. After unsuccessful conservative CPR a single dose of 500000 IU streptase was administered. Heart action returned 10 minutes later, nevertheless the patient needed mechanical ventilation and circulatory system stabilization therapy (catecholamines) in doses dependent on haemodynamic parameters. During hospitalization she regained consciousness. She presented no neurological defects and after 5 days was discharged to the Cardiology Department. Electrocardiography and echocardiography done after successful resuscitation was specific to infero-lateral myocardial infarction. Although safety and efficacy of thrombolytic therapy at resuscitation was extensively studied, this procedure is still controversial. Till now, there is no data concerning thrombolytic treatment in such clinical situations, which are based on clinical trials, and such treatment is introduced in dramatic situations, as a last, lifesaving option.