1. Acute coronary syndrome (ACS) encompasses unstable angina and myocardial infarction, and is caused by reduced blood flow in the coronary arteries, often due to atherosclerosis. 2. Clinical features of ACS include chest pain and discomfort, but it can also be "silent" in some high-risk groups. Diagnosis involves ECG, cardiac troponin levels, and coronary angiography. 3. Treatment depends on whether the ACS is STEMI (ST elevation on ECG) or NSTEMI/unstable angina. For STEMI, primary percutaneous coronary intervention is the treatment of choice if readily available to restore blood flow, along with dual antiplatelet therapy and antico

1. Acute coronary cyndrome
Done by : Hasan Allawi
Tabark fadhel

2. Objectives
1. Definition.
2. Etiology.
3. pathophysiology.
4. Clinical features.
5. Investigation.
6. Management.
7. Complication.
8. Prognosis.

3. INTRODUCTION
Acute coronary syndrome: Encompasses both unstable angina and
myocardial infarction (MI)(STEMI)(NSTEMI(
Unstable angina: Characterized by new-onset or rapidly worsening
angina (crescendo angina), angina on minimal exertion or angina at
rest in the absence of myocardial damage.
MI: Symptoms occur at rest and there is evidence of myocardial
necrosis, as demonstrated by an elevation in cardiac troponin or
CK- MB isoenzyme.

5. 1. Atherosclerosis.
2. Arteritis.
3. CoronaryArtery diseases: dissection.
4. Embolism.
5. Coronary mural thickening.
6. Causes of coronary luminal narrowing.
7. Congenital coronaryArtery disease
Etiology

6. Pathophysiology

7. Risk factor
■ Modifiable risk factors:
• High cholesterol
• Hypertension
• Smoking
• Diabetes
• Obesity
■ Non-modifiable risk factors:
• Age
• Family history(MI in 1st degree relative <55yrs(
• Male sex
• Premature menopause

8. Clinical features of ACS:

9. Clinical features of ACS:
ACS without chest pain is called ‘silent mostly seen in
• Elderly
• Diabetic patients
• Patient under anesthesia
• Patient with cardiac transplantation
Silent MIs may present with: syncope, pulmonary edema, epigasthis pain
and vomiting ( be aware of this!(

10. HowTomanage ACS?
Time is myocardium
We must give initial therapy to the patient then make ECG and
cardiac biomarkers to differentiate between types of ACS and
then giving suitable treatment.

11. Howdifferntiatebetween typesofACS?
ECG

12. Investigation:
1. ECG
• Classically , hyperacute (tall) T waves, ST elevation or new LBBB occur
within hours of transmural infarction . Twave inversion and development of
pathological Qwaves follow over hours to day
• In subendocardial infraction( Unstable angina &NSTEMI( : ST depression, T
wave inversion, no pathological Q wave , or normal.
• In 20% of MI, the ECG may be normal initially.

14. Anterolateral STEMI

17. Investigation
1) Cardiac troponin levels (Tand I) are the most sensitive ( -Ve after 6 hours
from pain can rule out MI ) and specific ( + Ve can rule in ) markers of
myocardial necrosis . Serum levels raise within 3–12h from the onset of
chest pain, peak at 24–48h, and decline to baseline over 5–14 days.CK_MB
enzyme also elevated in myocardial infarction
2) CXR: Look for cardiomegaly, pulmonary oedema .
3) Blood tests : FBC , U&E , glucose , lipids , base line PTT , PT

18. Treatment Of Unstable Angina/NSTEMI
1. Call For Help + Admission In Coronary Care Unit ( CCU ) + Bed Rest Full
Monitoring ( ECG , Blood Pressure , Heart Rate , Respiratory Rate(
2. A.B.C :
A = Air Way → Oxygen Poly Mask High Concentration .
B= Breathing Asses Breathing By Counting the Respiratory Rate .
C=Circulation → Insert Two Large IV Canula and Take Blood For Investigations
)Cardiac Enzyme , Blood Sugar , CBC For Base Line Hemoglobin &
Leukocytosis(
3) Give the Patient Nitrate ( Sub - Lingual GTN ) as First Aid .
4Do Serial ECG Every Half Hour

19. anti3 Give
A – Anti Pain : ( Analgesia )
I.V Morphin5-10mg .
Give Anti - Emetic ( Metoclopramide 10mg ); Because MorphinCauseVomiting .
Note : Don'tGive Morphin I. M Because ItLead to HeamatureaIf Given I . M
B –) Dual antiplatelettherapy) also called DAPT
Aspirin 300mg ...Crushed TabletOrally & Clopidogrel .
Decrease Mortality in 25 % of Patients. Better in First 12 Hours .
Note : IV GlycoproteinIIb / IIIa Antagonist ( Abcximab ) Given to :
1. High Risk PatientsAccording to GRACE Score .
2. If We Will Do PCI.
3 . RecurrentSymptoms
Cont...

20. C- Anti Coagulant : Heparin .. Advantages :
1. Decrease Thombo- Embolic Complications ( DVT )
2. Prevent FormationofNew Thrombus .
3. PreventThrombus to Increase in Size.
4. Continue Giving Heparin° Until DischargeOR For 8 Days
Cont...

21. Coronary angiography
• Coronary angiography should be considered with a view to revascularisation
in all patients at moderate or high risk , including :
1. Those who fail to settle on medical therapy
2. Those with extensive ECG changes
3. Those with an elevated plasma troponin
4. Those with severe pre - existing stable angina .
This often reveals disease that is amenable to PCI ; However, if the lesions are
not suitable for PCI the patient should be considered for urgent CABG.

22. Management of Acute mi (STEMI(
Immediate management

23. PrimaryPer- CutaneousCoronaryIntervention
- R - Perfusion : To Restore Coronary Patency , Improve
Survival & Decrease Mortality ( 25 % - 50%(
It's the Treatment of Choice If Readily Available.
The routine use of GP Ilb / Illa inhibitors is no longer
recommended.
Decrease Risk of Death More Than Thrombolytic By 50 % .
If 1ry PCI Can't Achieved within 2 Hours of Diagnosis : Then
Give Thrombolytic .

24. Dual
Antiplatelet
Dual
Antiplatelet

25. • Antiplatelet options that use with pci
aspirin and an ADP - receptor blocker ( prasugrel or ticagrelor ) .
Anticoagulant options include unfractionated heparin , enoxaparin or
bivalirudin
• Antiplatelet options that use with thromblytic therapy
Aspirin and clopidogrel are recommended in patients undergoing
thrombolysis .
Anticoagulation options include unfractionated heparin , enoxaparin or
fondaparinux .
N
ote
:

26. Thrombolytic therapy
Absolute Contra-indications
1. Previous intracranial haemorrhage.
2. Ischaemic stroke <6months.
3. Cerebral malignancy or AVM.
4. Recent major trauma/surgery/ head injury (<3wks).
5. GI bleeding (<1 month).
6. Known bleeding disorder.
7. Aortic dissection.
8. Non-compressible punctures <24h, eg liver
biopsy, lumbar puncture.

27. Relative CI :
1.
7. Active peptic ulcer ( not blee
Thrombolytic therapy
Relative CI :
1. TIA <6 months.
2. Anticoagulant therapy.
3. Pregnancy/<1wk post partum.
4. Refractory hyperten
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(>180mmHg/110mm
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5. Advanced liver diseas5e..Advancedliv
6. Infective endocarditis.
6. Infective endoc
7. Active peptic ulce8r.(
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8. Prolonged/traumatic resuscitation

28. Thrombolytics therapy
Thrombolytic Therapy ( Fibrinolysis ) : They Increase Activity of
Fibrinlytic System .
1 - Streptokinase :
It is a Foreign Protein ( Bacterial EnzymeStreptococcus ) :
So May Induce Allergic reaction & Hypotension.Given IV Infusion .
Side Effect :
1. Bleeding & Reperfusion Arrhythmi
2. Allergic Reaction Antibody Production
. Note : Streptokinase If Given Once →Antibody Formation ; So You Can't
Give It More

29. Other Drug
2 - Alteplase ( Tissue Plasminogen Activator )
It is Human Tissue Plasminogen Activator But is a Recombinant
Protein : So Not Allergic. Given I.V Infusion
Side Effect :
1. High Risk of Cerebral Heamorrhage .
2. Bleeding & Reperfusion Arrhythmia .
Note : Ateplase Has Better Survival Rate than Streptokinase .

30. Late management
1. Risk stratification and further
investigation.
2. Lifestyle modification:
- Stop smoking.
- Regular exercise.
- Diet(weight control,lipid-lowering).
3. Secondary prevention drug therapy:
- Antiplatelet therapy (aspirin and/or
clopidogrel).
- β-blocker.
- ACEinhibitor.
- Statin.
-Additional therapy for control of
diabetes and hypertension.
4. Rehabilitation.

31. Complications
Early complications
Arrhythmia
AcuteHeart failure
• Rupture of free wall of left ventricle
•ventricular septal defect
•acute mitral regurgitation
Late complications
Post Mi angina
Post Mi syndrome °Dressler’s syndrome°
Anurysm
Embolism
Frozen shoulder

32. Prognosis
• ¼ cases, death within few minutes without medical care
• ½ death within 24 hours of onset
• 40% affected patients die within first month
• Reach hospital & receive medication; 28-day survival >85%
• Worse prognosis with anterior and inferior infarction
• Who survive acute attack;
>80% live a further year
75% for 5 years
50% for 10 years
25% for 20 years