This was another didactics during our rotation in Internal Medicine--Out-patient Department. Source: Harrison's Textbook of Internal Medicine 18th ed.

1. Acute Coronary
Syndrome
Unstable Angina
Non ST Segment Elevation
Myocardial Infarction
Jackie Lou C. Acha
Clinical Clerk
Department of Internal Medicine

2. Objectives
• Definition of terms
• Pathophysiology
• Clinical Presentation
• Physical Examination findings
• Diagnosis
• Management

3. Definition of Terms
• Ischemic Heart Disease
– Inadequate supply of blood and oxygen to a
portion of the Myocardium
=> IMBALANCE between Myocardial Oxygen
Supply and Demand

4. Definition of Terms
• Patients with IHD fall into Two Large Groups
1. Patients with CAD
-commonly present with STABLE ANGINA
2. Patients with Acute Coronary Syndromes
- Unstable Angina and Non-ST-Segment Elevation MI
(NSTEMI)
- Acute Myocardial Infarction (MI) with ST-Elevation
(STEMI)

5. • Stable Angina
– Episodic clinical syndrome
– Due to transient Myocardial Ischemia
– Angina usually crescendo-decrescendo in nature
– Caused by exertion or emotion, relieved by rest
– Typically lasts 2-5 mins
– Can radiate to either shoulder and both arms
Definition of Terms

6. Definition of Terms
• Unstable Angina
– myocardial ischemia with no evidence of heart
muscle death (myocardial necrosis)
– angina pectoris or equivalent ischemic discomfort
with at least one of three features:
(1) it occurs at rest (or with minimal exertion), usually
lasting >10 minutes;
(2) it is severe and of new onset (i.e., within the prior
4–6 weeks); and/or
(3) it occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than
previously)

7. Stable Angina Unstable Angina
Episodic Severe and of New onset
Crescendo - Decrescendo Crescendo pattern
Occurs on exertion, relieved by rest Occurs at rest
Lasts 2-5 mins Lasts > 10 min
Stable vs. Unstable Angina

8. Definition of Terms
• NSTEMI
– Clinical features of Unstable Angina + evidence of
Myocardial Necrosis as reflected by Elevated
Cardiac Enzymes

10. Pathophysiology
• Reduction in oxygen supply and/or an increase in
myocardial oxygen demand
• Four Pathophysiologic Processes
1. Plaque Rupture or Erosion with Superimposed
Nonocclusive Thrombus (most common)
2. Dynamic Obstruction (Coronary Spasm as in Prinzmetal’s
Variant Angina)
3. Progressive Mechanical Obstruction
4. Secondary UA related to Increased Myocardial O2
demand and/or Decreased Supply ( e.g. Tachycardia,
Anemia)

11. Pathophysiology
More than 90% of patients with IHD
have atherosclerosis of one or more
of the epicardial coronary arteries
progressive narrowing of the lumen
leading to stenosis (“fixed”
obstructions) or to acute plaque
disruption with thrombosis, both of
which compromise blood flow
A fixed lesion obstructing 75% or
greater of the lumen is generally
required to cause symptomatic
ischemia precipitated by exercise
(most often manifested as chest pain,
known as angina)
Obstruction of 90% of the lumen can
lead to inadequate coronary blood
flow even at rest

12. Pathophysiology of MI
Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel
Vasospasm (platelet aggregation and mediator release)
Other mediators activate the extrinsic pathway of coagulation
Release potent secondary aggregators(thromboxane A2, adenosine diphosphate, and serotonin)
Platelets adhere, aggregate, become activated
A sudden disruption of an atheromatous plaque

14. Commonly affected
Coronary Arteries in MI
- left anterior descending
artery
- left circumflex artery
- right coronary artery
5% have stenosis of the left
main coronary artery
15% have three-vessel CAD
30% have two-vessel disease
40% have single-vessel
disease

15. Clinical Presentation
• Clinical Hallmark:
CHEST PAIN- substernal region or
sometimes epigastrium, radiates to neck, left
shoulder, and left arm; severe enough to be
considered painful
Anginal equivalents: Dyspnea, Epigastric
Discomfort

16. Physical Examination
– Unremarkable
– If there is large area of MI or Large NSTEMI,
• Diaphoresis
• Pale cool skin
• Sinus tachycardia
• 3rd and 4th heart sound
• Basilar rales
• hypotension

17. DIAGNOSIS
• Four major diagnostic tools used in the
Diagnosis of UA/NSTEMI in ED
1. History
2. ECG
3. Cardiac markers
4. Stress Testing

18. DIAGNOSIS
• ECG
– ST Segment Depression
– Transient ST-segment Elevation
– T-wave Inversion
• Cardiac Biomarkers
– CK-MB
– Troponin

19. Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.
Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
Timing of Release of Various Biomarkers After Acute
Myocardial Infarction

20. Killip Classification
Killip Class Description Mortality Rate
Class I no signs of pulmonary or venous
congestion
0–5%
Class II moderate heart failure as evidenced by
rales at the lung bases, S3 gallop,
tachypnea, or signs of failure of the right
side of the heart, including venous and
hepatic congestion
10–20%
Class III severe heart failure, pulmonary edema 35–45%
Class IV shock with systolic pressure <90 mmHg
and evidence of peripheral
vasoconstriction, peripheral cyanosis,
mental confusion, and oliguria
85–95%

21. Risk Stratification
TIMI Risk Score for UA/NSTEMI

22. Algorithm for risk stratification and treatment of patients with suspected coronary
artery disease

23. Management
A. Medical Treatment
- Bed rest with continuous ECG monitoring
for ST-Segment Deviation and Cardiac rhythm
- ambulation is permitted if patient shows no
recurrence of ischemia and does not develop
a biomarker necrosis for 12-24 hours

24. Medical Therapy
Drug Category
Clinical
Condition
When to Avoida Dosage
Nitrates Administer
sublingually,
and, if
symptoms
persist,
intravenously
Hypotension
Patient receiving
sildenafil or other
PDE-5 inhibitor
Topical, oral, or buccal nitrates
are acceptable alternatives for
patients without ongoing or
refractory symptoms
5–10 g/min by continuous
infusion titrated up to 75–100
g/min until relief of symptoms
or limiting side effects
(headache or hypotension with
a systolic blood pressure <90
mmHg or more than 30% below
starting mean arterial pressure
levels if significant hypertension
is present)

25. Medical Therapy
Drug Category Clinical Condition When to Avoida Dosage
Beta blockersb Unstable angina PR interval (ECG)
>0.24 s
2° or 3°
atrioventricular block
Heart rate <60
beats/min
Systolic pressure <90
mmHg
Shock
Left ventricular
failure
Severe reactive
airway disease
Metoprolol 25–50
mg by mouth every 6
h
If needed, and no
heart failure, 5-mg
increments by slow
(over 1–2 min)
IV administration

26. Drug Category Clinical Condition When to Avoida Dosage
Calcium channel
blockers
Patients whose
symptoms are not
relieved by adequate
doses of nitrates and
beta blockers, or in
patients unable to
tolerate adequate
doses of one or both
of these agents, or in
patients with variant
angina
Pulmonary edema
Evidence of left
ventricular
dysfunction (for
diltiazem or
verapamil)
Dependent on
specific agent
Morphine sulfate Patients whose
symptoms are not
relieved after three
serial sublingual
nitroglycerin tablets
or whose symptoms
recur with adequate
anti-ischemic
therapy
Hypotension
Respiratory
depression
Confusion
Obtundation
2–5 mg IV dose May
be repeated every 5–
30 min as needed to
relieve symptoms
and maintain patient
comfort

27. • Anti-Ischemic Treatment
– Bed rest
– Nitrates
– Beta Blockers
• Anti-Thrombotic Therapy
– Aspirin
– Clopidogrel
• Anticoagulation Therapy
– Unfractionated Heparin
– LMWH Enoxaparin

28. Oral Antiplatelet Therapy
Aspirin Initial dose of 162–325 mg nonenteric formulation followed by 75–162
mg/d of an enteric or a nonenteric formulation
Clopidogrel Loading dose of 300-600 mg followed by 75 mg/d
Prasugrel Pre-PCI: Loading dose 60 mg followed by 10 mg/d
Intravenous Antiplatelet Therapy
Abciximab 0.25 mg/kg bolus followed by infusion of 0.125
g/kg per min (maximum 10 g/min) for 12 to 24 h
Eptifibatide 180 g/kg bolus followed by infusion of 2.0 g/kg
per min for 72 to 96 h
Tirofiban 0.4 g/kg per min for 30 min followed by infusion
of 0.1 g/kg per min for 48 to 96 h

29. Heparins*
Unfractionated Heparin (UFH) Bolus 60–70 U/kg (maximum 5000 U) IV followed
by infusion of 12–15 U/kg per h (initial maximum
1000 U/h) titrated to a PTT 50–70 s
Enoxaparin 1 mg/kg SC every 12 h; the first dose may be
preceded by a 30-mg IV bolus; renal adjustment
to 1 mg/kg once daily if creatine Cl < 30 cc/min
Fondaparinux 2.5 mg SC qd
Bivalirudin Initial bolus intravenous bolus of 0.1 mg/kg and
an infusion of 0.25 mg/kg per hour. Before PCI,
an additional intravenous bolus of 0.5 mg/kg was
administered, and the infusion was increased to
1.75 mg/kg per hour.

30. Invasive Strategy
• Class I recommendations for Use of an Early Invasive
Strategy
– Recurrent angina at rest/ low level activity despite
medications
– Elevated TnT or TnI
– New ST-segment Depression
– Recurrent angina/ Ischemia with CHF symptoms, rales, MR
– Positive Stress Test
– EF <0.40
– Decreased BP
– Sustained VT
– PCI <6 moths, prior CABG

31. Long Term Management
• Risk factor modification
• Long Term Treatment
– Beta blockers (anti-ischemic; reduce triggers for
MI)
– Statins (long term plaque stabilization)
– ACE Inhibitors (long term plaque stabilization)
– Anti platelet therapy (Aspirin + Clopidogrel for at
least 9-12 months)

32. THANK YOU!