Acute Coronary Syndrome

A presentatation on Acute coronary syndrome made while in Emergency Department. If you are making a presentation on ACS, you may want to add more on TIMI score as it is important. Some problems with display of pictures/diagrams due to ?conversion problems. Based on AHA Guidelines 2010 and from Harrison's 18th Ed.. Made using OpenOffice.

1. By Dr. Ahmed Azhad
ACS
(Acute Coronary Syndrome)

2. ACS
(Acute Coronary Syndrome)
C A D
( s t a b l e a n g i n a )
S T E M I U A / N S T E M I
A C S
I H D

3. Coronary Arteries

4. UA/NSTEMI - Definition
UA diagnosis is mainly clinical:
Chest pain or discomfort:
1.Occurring at rest or minimal exertion (>10 minutes)
2.Severe and of new onset (within past 4-6 weeks)
3.Crescendo pattern
4.
NSTEMI:
C/F of UA + Evidence of myocardial necrosis (elevated
biomarkers)

5. UA/NSTEMI - Pathophysiology
Reduction in oxygen supply OR
Increase in myocardial oxygen demand
superimposed on an atherosclerotic plague with
varying degrees of obstruction

Contributors to the above are:
1.Plague rupture or erosion with superimposed non-
occlusive thrombus (most common cause)

6. UA/NSTEMI – Pathophysiology
(continued)
2.Dynamic obstruction (coronary spasm)
3.Progressive mechanical obstruction (rapidly
advancing coronary atherosclerosis or
restenosis following PCI)
4.Secondary UA related to increased myocardial
oxygen demand or decreased supply
(anemia/tachcardia)

7. UA/NSTEMI – Clinical features
History and Examination:
Chest pain – in substernal region or epigastrium, radiating
to neck, left shoulder, and left arm
Diaphoresis
Pale cool skin
Sinus tachycardia
3
rd
and 4
th
heart sounds on auscultation
Basilar rales
Hypotension

8. UA/NSTEMI – Investigations
ECG:
UA : ST-segment depression , transient ST-elevation and/or
T-wave inversion (30-50%)
C/F + new ST-segment deviation of 0.05mV is an important
predictor of adverse outcome
T-wave changes are sensitive for ischaemia but less specific
(exception: new, deep T-wave inversions ≥ 0.3 mV

9. UA/NSTEMI – ECG

10. UA/NSTEMI – Investigations (2)
Cardiac Biomarkers:
CK-MB, Troponin-T
Direct relationship between degree of Troponin-T and
mortality (not available in IGMH)
Patients without clinical history of ischemia: minor troponin
elevations can be caused by:
Congestive heart failure
Myocarditis
Pulmonary embolism
False-positive readings
Unclear history + small troponin elevations = not diagnostic
of ACS

11. UA/NSTEMI – Enzyme assays

12. UA/NSTEMI – Diagnosis
AHA 2010 Algorithm
High-likelihood of ACS:
H/o typical ischemic discomfort
Established CAD by angiography
Prior MI
Congestive heart failure
New ECG changes
Elevated cardiac biomarkers


13. UA/NSTEMI – Diagnosis (2)
Intermediate-likelihood of ACS:
Age > 70 years
Male gender
Diabetes Mellitus
Peripheral arterial disease / Cerebrovascular disease
Old ECG abnormalities

14. UA/NSTEMI – Treatment
Bed Rest with continuous ECG monitoring for ST-
deviation and cardiac rhythm
Ambulation allowed when no recurrence of ischemia
and non-elevation of biomarkers 12-24 hours
Rx: anti-ischemic + anti-thrombotic therapy

15. UA/NSTEMI – Rx anti-ischemic
Nitrates (upto 3 doses, 5 minutes apart; then IV
nitroglycerin 5-10 µg/min with non-absorbing tubing, can
be increased 10 µg/min every 3-5 minutes
Until symptoms relieved OR
Systolic BP < 100 mm Hg
Contraindications: 1) Hypotension 2) Sildenafil use within
past 24 hours
β – blockers
ACE inhibitors
Statins
Morphine if pain not responding to nitroglycerin and β-
blockers

16. UA/NSTEMI – Rx anti-thrombotic
Aspirin 162 – 325 mg loading, then 75 – 162 mg/d
Clopidogrel – 300mg loading, then 75mg/day
IV antiplatelet therapy: Abciximab, Eptifibatide, Tirofiban
Heparins: UFH 60-70 U/kg (max: 5000 U), then 12-15
U/kg/hr (init. Max: 1000 U/hr – titrated to a PTT 50-70s)
Enoxaparin 1mg/kg s.c. Q12h, first dose preceded by 30mg
iv-bolus. (If CC < 30 cc/min, 1mg/kg OD)
Fondiparinux, Bivalirudin

17. UA/NSTEMI – Rx Additional
High-risk patients (multiple risk factors, ST-segment
deviation and/or postive biomarkers)
Coronary ateriography within 48 hours of admission
followed by coronary revascularisation (PCI or CABG)
Low-risk patients: Watchful waiting; arteriography
if:
Rest pain
ST –segment changes
Evidence of ischemia on stress test

18. UA/NSTEMI – Prognosis
Wide spectrum:
30 day risk of Death: 1-10%
30 day risk of new or recurrent infarct: 3-10%
TIMI Trials:
7 independent risk factors
CRP and BNP (marker of increased myocardial wall
tension) correlate independently with increased
mortality

19. UA/NSTEMI – Discharge
Teachable moment
Risk-factor modification: smoking cessation, optimal
weight, daily exercise, diet, BP control, control of
hyperglycemia, lipid management
Drugs: beta blockers, statins, ACE inhibitors, aspirin
+ clopidogrel 9-12 months, then aspirin alone
thereafter

20. STEMI
Occurs when there is thrombotic occlusion of a
coronary artery.
Thrombus develops rapidly.
Cardiac biomarkers can be used to distinguish UA
from NSTEMI and to assess the magnitude of
STEMI.

21. STEMI - Pathophysiology
Thrombotic occlusion of a coronary artery previously
affected by atherosclerosis.
Occurs due to rapid development of a thrombus at
the site of vascular injury.
Facilitating factors:
Cigarette smoking
Hypertension
Lipid accumulation

22. STEMI - Pathophysiology

23. STEMI – Pathophysiology (2)
Occurs when the surface of an atherosclerotic plaque
becomes disrupted and conditions favour
thrombogenesis
Coronary artery gets occluded by a thrombus
Rarely by coronary emboli, congenital abnormalities,
coronary spasm, inflammatory diseases

24. STEMI – Clinical Features
Half of the cases have a precipitating factor:
Vigourous physical exercise
Emotional stress
Medical or Surgical illness
Usually in the morning / within a few hours of
waking up – but can occur anytime
C/o:
Pain – deep, “heavy”, “squeezing”, “crushing”, stabbing or
burning

25. STEMI – Clinical Features (2)
Similar to angina pectoris, but is usually more severe and
lasts longer
Central portion of the chest and/or epigastrium
Radiation upto occipital area but not below umblicus
Associated with weakness, sweating, nausea, vomiting,
anxiety and a sense of impending doom
Does not subside with rest

26. STEMI – DD of chest pain
Acute pericarditis (radiation of pain to trapezius)
Pulmonary embolism
Acute aortic dissection
Costochondritis
Gastrointestinal disorders

27. STEMI – Other presentations
STEMI in Diabetes – painless
STEMI in elderly - sudden-onset breathlessness
→
pulmonary edema
Others with or without pain:
Sudden loss of consciousness, sudden profound weakness,
arrhythmia, unexplained drop in arterial pressure

28. STEMI – Physical findings
Anxious, restlessness
Pallor
Pain > 30 minutes + diaphoresis -> STEMI
BP/Pulse: can be normal or increased (sympathetic
hyperactivity); decreased in inferior infarcts
3
rd
and 4
th
heart sounds
Mid-systolic or late systolic murmur

29. STEMI - Investigations
1.ECG – ST elevation, Q waves (ideal time: within 10
minutes)
2.Cardiac biomarkers:
1.Troponin-T (preffered) – lasts till 7-10 days after STEMI
2.CK/CK-MB: Rises within 4-8 hours, returns to normal in 48-
72 hours (can also rise due to cardiac surgery,
myocarditis, electrical cardioversion). CKMB mass:CK ≥
2.5 suggestive of cardiac muscle damage.
Should be noted that recanalisation would cause earlier
and higher peak of enzymes.
3. TLC rise: 12,000 – 15,000/µL. Few hours upto 3-7 days.
4. ESR rise – peaking in 1
st
week, raised for upto 2 weeks.


30. STEMI – ECG (1)
1.ST-segment elevation or presumed new LBBB
ST-segment elevation in 2 or more contiguous leads =
STEMI
Threshold values:
Men ≥ 40 yrs : J-point elevation (V2 and V3) - 0.2 mV :
and 0.1mV in all other leads
Men < 40 yrs : J-point elevation (V2 and V3) - 0.25 mV
: and 0.1mV in all other leads
Women: L-point elevation (V2 and V3) – 0.15 mV :
and 0.1mV in all other leads

31. STEMI – ECG (2)
2.Ischemic ST-segment depression > 0.05mV or
dynamic T-wave inversion with pain or
discomfort = UA/NSTEMI
Non-persistent/transient ST-elevation ≥ 0.5mm for < 20
minutes is also included in this category.
Threshold values: J-point depression 0.05mV in leads
V2 and V3, and 0.1mV in all other leads (men and
women)

32. STEMI – ECG (3)
3.Non-diagnostic ECG with non-specific ST-segment
or T-wave changes = non-conclusive for
ischemia
Threshold values:
Normal ECGs
ST-segment deviation < 0.5mm, T-wave inversions ≤
0.2 mm

33. STEMI – Other Investigations
2-D Echo – wall motion abnormalities
Radio-nuclide imaging with 99m-Tc labelled blood
red cells


34. STEMI – Initial Rx
Prehospital care
Management in the Emergency Department
Goals:
Control of cardiac discomfort
Rapid identification of patients for reperfusion
Avoidance of inappropriate discharge of patients with STEMI
Rx:
Aspirin – 160 – 325 mg chewable tablets
O
2
at 2-4L/min for hypoxemic patients

35. STEMI – Initial Rx (2)
Control of discomfort
Sublingual nitroglycerin 0.4mg at 5-min intervals
Abolishes chest pain
Decreases myocardial oxygen demand (by lowering preload)
Increases myocardial oxygen supply (by dilating coronary
vessels)
If chest discomfort returns, consider IV nitroglycerin
Avoid nitrates in patients with systolic BP <90mm Hg or
clinical suspicion of right ventricular infarction, patients
taking sildenafil within preceding 24 hours
Idiosyncratic reaction to nitrates – hypotension – can be
reversed with atropine i.v.

36. STEMI – Initial Rx (3)
Control of discomfort
Morphine 2-4mg i.v. repeated in 5-min intervals as needed
I.v. beta blockers (metoprolol 5mg every 2-5 minutes – total
3 doses;; HR > 60, SBP > 100mm Hg. After this 50mg
Q6H oral x 48 hrs, then 100mg Q12H.

37. STEMI - Rx
Limiting infarct size:
Primary PCI (Door-balloon time – 90 minutes)
Thrombolysis (Door-needle time – 30 minutes)
Tissue plasminogen activator
Streptokinase (1.5 MU over 60 minutes)
Tenecteplase
Reteplase
Contraindications: Active internal bleeding, Recent CVA,
Intraspinal or intracranial surgery, intracranial neoplasm,
severe uncontrolled hypertension
Complications: Hemorrhagic stroke (0.5 – 0.9%)

38. STEMI – Post reperfusion
Pharmacotherapy:
Antiplatelet + Antithrombotic therapy
Aspirin
Clopidogrel
Heparin
Beta blockers
ACE Inhibitors

40. References
Harrison’s Principles of Internal Medicine 17
th

Edition
Circulation (journal of AHA)
http://circ.ahajournals.org/content/122/18_suppl_3/S787

41. Thank You