Acute Coronary Syndrome
and Coronary Artery Disease
Garrett Preston Clark, D.O.
What is ACS?
Includes clinical presentations that cover the following
range of diagnoses:
1.
2.
3.
Unstable angina
Non–ST-elevation myocardial infarction
(NSTEMI)
ST-elevation myocardial infarction
(STEMI)
http://www.emedicine.com/emerg/topic31.htm
What is ACS?
1.
2.
Unstable angina & NSTEMI  unstable
plaques w/ nonocclusive thrombosis
STEMI  thrombotic occlusion of
epicardial coronary artery
http://www.emedicine.com/emerg/topic31.htm
ACS / CAD
Spontaneous and cocaine-related coronary
artery dissection are unusual causes of
ACS
 Still, should be included in your differential
especially when a younger female or
cocaine user is being evaluated.

Other considerations for ACS:
Marfan syndrome
 Kawasaki disease
 Takayasu arteritis
 Cystic medial necrosis with aortic root
dilatation
 Aneurysm formation
 Dissection into the coronary artery

ACS / CAD
Higher incidence in males in all patients
<70 y/o
 Incidence of angina occurs equally 15
years postmenopause
 Women more likely to have coronary
events without typical symptoms

ACS Risk Factors:
Male gender
2. Diabetes mellitus (DM)
3. Smoking history
4. Hypertension
5. Increased age
6. Hypercholesterolemia
7. Hyperlipidemia
8. Prior CVA
9. Inherited metabolic disorders
10. Methamphetamine use
11. Occupational stress
12. Connective tissue disease
1.
ACS  Whats In Your Diff ?
Anxiety
Aortic Stenosis
Asthma
Cardiomyopathy, Dilated
Esophagitis
Gastroenteritis
Hypertensive Emergencies
Myocardial Infarction
Myocarditis
Pericarditis and Cardiac Tamponade
Pneumothorax, Iatrogenic, Spontaneous and
Pneumomediastinum
Pulmonary Embolism
Alternative diagnoses to
cardiac ischemia for patients
with chest pain
Non-ischemic
cardiovascular
Aortic dissection*
Myocarditis
Pericarditis
Chest wall
Cervical disc disease
Pulmonary
Pleuritis
Pneumonia
Pulmonary embolus*
Tension pneumothorax*
Psychiatric
Gastrointestinal
Biliary
Cholangitis
Cholecystitis
Choledocholithiasis
Colic
Esophageal
Costochondritis
Affective disorders (eg,
depression)
Fibrositis
Anxiety disorders
Spasm
Herpes zoster (before the rash)
Hyperventilation
Reflux
Panic disorder
Neuropathic pain
Primary anxiety
Rib fracture
Somatiform disorders
Sternoclavicular arthritis
Thought disorders (eg, fixed
delusions)
Esophagitis
Rupture*
Pancreatitis
Peptic ulcer disease
Nonperforating
Perforating*
WHAT’S HAPPENING?
Disease process includes:
1.
2.
3.
4.
5.
A chronic phase of atherosclerosis 
modification of the blood vessel wall
Development of an atherosclerotic plaque
Thin fibrous cap of extracellular matrix proteins
is formed over a lipid core (rich in foam cells &
comprised of cholesteryl esters & tissue factor)
Thickened intima.
Rupture of the fibrous cap  thrombosis &
partial or total occlusion of the vessel
http://www.uspharmacist.com/index.asp?page=ce/2686/default.htm
Whoop, THERE IT IS:
OUCH !
www.univie.ac.at/.../BE513/EKG/normalEKG.GIF
ACS  The Meat & Potatoes Part I:
Unstable Angina
The ACC/AHA guidelines state that UA
and NSTEMI differ primarily in
whether the ischemia is severe
enough to cause sufficient
myocardial damage to release
detectable quantities of a marker of
myocardial injury.
http://www.utdol.com/utd/content/topic.do?topicKey=chd/10116&type=A&selectedTitle=1~72
ACS  The Meat & Potatoes Part I:
Unstable Angina
Unstable angina is considered in
patients with ischemic symptoms
suggestive of an ACS and no
elevation in troponins or CK-MB,
with or without ECG changes
indicative of ischemia.
http://www.utdol.com/utd/content/topic.do?topicKey=chd/10116&type=A&selectedTitle=1~72
ACS  The Meat & Potatoes Part I:
CLASSIFICATIONS OF UNSTABLE ANGINA
1.
2.
3.
4.
5.
6.
New onset exertional angina
Rest angina
Early post-MI angina
Postrevascularization angina
Periprocedural
Late
New onset angina:
CLASSIFICATIONS OF UNSTABLE ANGINA
If occurring only after heavy physical
exertion, patients have a prognosis
similar to patients with chronic stable
angina
 New angina occurring after minimal
exercise or at rest, has a poorer
prognosis.

Rest angina:
CLASSIFICATIONS OF UNSTABLE ANGINA
Patients at increased risk if:
1.
2.
Prolonged
Associated with transient ST
segment changes >0.05 mV
Early post-MI angina:
CLASSIFICATIONS OF UNSTABLE ANGINA



Chest pain occurring within 48 hours
after an acute MI
Associated with high risk without
immediate intervention
GUSTO (Global Use of Strategies to Open Occluded
Coronary Arteries) IIb trial 

Refractory ischemia was associated with an
approximate doubling of mortality among
patients with ST-segment elevation and a
near tripling risk among those without ST
elevation.
Circulation 1998 Nov 3;98(18):1860-8.
GUSTO IIb TRIAL:
Global Use of Strategies to Open
Occluded Coronary Arteries
Occurrence of refractory ischemia
was associated with a higher 30
day mortality compared to
responsive ischemia or no
ischemia.
Postrevascularization &
Periprocedural angina:
CLASSIFICATIONS OF UNSTABLE ANGINA
Postrevascularization  Angina
occurring after PCI or CABG
 Periprocedural  Ischemic chest pain
within 48 hours after stenting.

LATE:
CLASSIFICATIONS OF UNSTABLE ANGINA
Delayed onset of angina
 May reflect restenosis after PCI, graft
stenosis after CABG, or progression
of native disease
 Patients usually progress to return of
effort angina

ACS  The Meat & Potatoes Part II:
Non–ST-elevation myocardial
infarction (NSTEMI)
UA & NSTEMI often indistinguishable at
time of initial evaluation
 Most patients present with chest pain and
ST segment depression
 ST seg depression is an unfavorable
predictor
 Increased incidence of left main or three
vessel disease compared to those without
ST segment depression

ACS  The Meat & Potatoes Part II:
Non–ST-elevation myocardial
infarction (NSTEMI)
http://www.postgradmed.com/issues/2004/06_04/tak1.gif
ACS  The Meat & Potatoes Part II:
Non–ST-elevation myocardial
infarction (NSTEMI)
Absence of Q waves suggests a high rate
of spontaneous reperfusion
 May occur after percutaneous
coronary intervention (PCI) or CABG

Braunwald classification
Classification of UA which included patients
with NSTEMI since troponins were not
measured:
Class I — New onset, severe, or accelerated
 Class II — Angina at rest and subacute (no
anginal episodes within the preceding 48 hours)
 Class III — Angina at rest and acute (angina
within the preceding 48 hours)

Braunwald classification
Clinical circumstances:
Class A — Secondary UA (in the setting of
anemia, infection, fever, etc)
 Class B — Primary UA
 Class C — Post

Braunwald classification
Intensity of treatment:
No or minimal treatment
 Symptoms occurring in the setting of
standard medical therapy
 Symptoms occurring despite maximally
tolerated doses of beta blockers, nitrates,
and calcium channel

Goldman risk score for chest pain:
ACS Risk Factors Reinforcement:
Male gender
2. Diabetes mellitus (DM)
3. Smoking history
4. Hypertension
5. Increased age
6. Hypercholesterolemia
7. Hyperlipidemia
8. Prior CVA
9. Inherited metabolic disorders
10. Methamphetamine use
11. Occupational stress
12. Connective tissue disease
1.
ACS  The Meat & Potatoes Part III:
ST-elevation (Q-wave)
myocardial infarction (STEMI)
Enough Said?
ACS  The Meat & Potatoes Part III:
ST-elevation (Q-wave) myocardial
infarction (STEMI)
In 2000, the European Society of
Cardiology (ESC) with the
American College of Cardiology
(ACC) set out to define an acute,
evolving, or recent MI.
ESC / ACC Definitions:
Rise and gradual fall in troponin or more rapid
rise and fall of biochemical markers of
myocardial necrosis with at least one of the
following:

a. Ischemic symptoms
b. Development of pathologic Q waves
c. ECG changes indicative of ischemia (ST
segment elevation or depression)
d. Coronary artery intervention (eg,
angioplasty)


Pathologic findings of an acute MI
SO, WHAT’S A Q-WAVE ? ? ?
Q = 1st deflection of the QRS which is
negative
 When QRS complex consists soley of a Q
wave, it’s called a “QS” complex
 Normal Q = less than 0.03 seconds and
can be common in most leads (except
aVR, V1-V3)

“Is It Evil ???”
Dr_Evil.jpg848 x 440 pixels - 49.0kB diary.ru/~green-filin
THE EVIL Q-WAVE ! ! !

Any Q-Wave in leads V1-V3 is an Evil Q
Q’s in leads I, II, aVL, aVF, & V4-6 are
considered evil if they are greater than or
equal to 0.03 seconds
 Evil Q’s must be greater than or equal to
1mm in depth in @ least 2 contiguous
leads to be considered for Q-wave MI and
thereby, making them very evil !

ACS  The Meat & Potatoes Part III:
ST-elevation (Q-wave)
myocardial infarction (STEMI)
“Clinically significant ST segment elevation is
considered to be present if it is greater
than 1 mm (0.1 mV) in at least two
anatomically contiguous leads, or 2 mm
(0.2 mV) in two contiguous precordial
leads”.
http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print
ACS / TREATMENT:

1.
2.
3.
4.
5.
6.
7.
8.
In the initial assessment, the following should be
implemented if ACS is suspected:
Airway, breathing, and circulation assessment
12-lead ECG obtained
Crash cart nearby
Cardiac monitor attached
Oxygen given
IV access and blood work obtained (series cardiac)
Aspirin
Nitrates and morphine (unless contraindicated)
http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print
ACS / TREATMENT:
Morphine reduces sympathetic stimulation
caused by pain and anxiety  lowers
cardiac workload
Lower cardiac workload = less O2 demand
= Patients feel better
http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print
ACS / TREATMENT:
Due to the lack of data, the ACC/AHA, &
ACCP guidelines did not address the use
of clopidogrel in patients managed without
reperfusion Tx.
 However, most experts give clopidogrel,
300 mg loading dose then 75 mg daily
based on benefits demonstrated in nonrevascularized patients with non-ST
elevation syndromes.

http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print
Clopidogrel in Unstable angina to
prevent Recurrent ischemic Events
(CURE) TRIAL:
Clopidogrel  platelet ADP receptor
antagonism
 Something to consider if ASA sensitive
 CURE Trial suggests more efficacy with
ASA and Plavix combo therapy, but at a
cost = increased risk of nonintracranial
bleeding complications.

Foreign Cars May Save Your Life !
If It’s Good Enough for Bond…
www.jamesbondlifestyle.com/.../au010.jpg285 x 218 - 18k
http://www.impawards.com/2002/posters/die_another_day_ver1.jpg
Interventions Shown To Decrease
Mortality in CAD
(Die Another Day 007 ):
©
1.
2.
3.
4.

Statins
ASA
ACE Inhibitors
Beta Blockers
“SAAB”
Nitrates shown to minimize angina Sx’s,
but NO conclusive evidence that show
decreased mortality.
DON’T FORGET:
Initial EKG is often NOT diagnostic.
Repeat EKG at 5 to 10 minute intervals if
patient remains symptomatic & high
clinical suspicion for MI
 Ask about phosphodiesterase-5 inhibitors
(Viagra, Levitra, Cialis). Nitrates are
contraindicated if used w/in 24 -36 hours
due to risk of severe hypotension

DON’T FORGET:
In the setting of an inferior wall MI,
remember the possibility of right
ventricular involvement. Patient
dependence on preload to maintain
cardiac output may result in severe
hypotension w/ nitrate use.
ST elevation in the right precordial leads - V4, V5,
and V6 indicates right ventricular involvement
http://www.utdol.com/utd/content/image.do?imageKey=card_pix/right_5.htm&altImageKey=card_pix/normal3.htm
DON”T FORGET:
About ½ the patients with LBBB & acute
MI do NOT have Sx’s of chest pain w/
their ischemia
 = Much less likely to receive ASA, beta
blockers, and reperfusion therapy
 = Not a good idea
 = Beware the LBBB ! ! !

ACS
THERAPY:
Evidence Supports early aggressive
strategy
 ASA
 Beta-Blocker
 ACEIs
 Statin
 LMW Heparin or Unfractionated
 Clopidogrel (PLAVIX)

TEST YOUR SKILL…
TEST YOUR SKILL…
A 67 y/o postmenopausal woman w/ CAD, stable angina,
CHF, and hyperlipidemia comes for her regular 3-month
exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical
exam is WNL. Her LDL is 129, HDL is 45. Which of the
following therapeutic options would you prescribe that
have been shown to decrease mortality:
A)
B)
C)
D)
E)
Atorvastatin
Digoxin
Diltiazem
Estrogen
Isosorbide mononitrate
TEST YOUR SKILL…
A 67 y/o postmenopausal woman w/ CAD, stable angina,
CHF, and hyperlipidemia comes for her regular 3-month
exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical
exam is WNL. Her LDL is 129, HDL is 45. Which of the
following therapeutic options would you prescribe that
have been shown to decrease mortality:
A)
B)
C)
D)
E)
Atorvastatin
Digoxin
Diltiazem
Estrogen
Isosorbide mononitrate
THE END
References:
6.
http://www.kup.at/kup/images/browser/787.jpg
http://services.epnet.com/GetImage.aspx/getImage.aspx?ImageIID=4708
http://www.chd-taskforce.de/ny2001_schober.htm
sfghed.ucsf.edu/.../ClinicImages/MI%20EKG1.1.jpg
http://www.utdol.com/utd/content/image.do?imageKey=card_pix/schema_m.htm
http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print
7.
http://www.utdol.com/utd/content/image.do?imageKey=card_pix/right_5.htm&altImageKey=card_pix/normal3.htm
8.
Circulation 1998 Nov 3;98(18):1860-8.
http://www.postgradmed.com/issues/2004/06_04/tak1.gif
1.
2.
3.
4.
5.
9.