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Acute Coronary


Rich Derby, Lt Col, USAF

MGMC Family Practice Program
• Define & delineate acute coronary syndrome

• Review Management Guidelines

– Unstable Angina / NSTEMI

• Review secondary prevention initiatives

Scope of Problem
(2004 stats)
• CHD single leading cause of
death in United States
– 452,327 deaths in the U.S. in

• 1,200,000 new & recurrent

coronary attacks per year

• 38% of those who with

coronary attack die within a
year of having it

• Annual cost > $300 billion

Expanding Risk Factors
• Smoking  Age-- > 45 for
• Hypertension male/55 for female
• Diabetes Mellitus  Chronic Kidney
• Dyslipidemia Disease
– Low HDL < 40
 Lack of regular
– Elevated LDL / TG
physical activity
• Family History—event
 Obesity
in first degree relative  Lack of Etoh intake
>55 male/65 female  Lack of diet rich in
fruit, veggies, fiber
Acute Coronary Syndromes
• Unstable Angina
Similar pathophysiology

• Non-ST-Segment Similar presentation and

Elevation MI early management rules
STEMI requires evaluation
for acute reperfusion
• ST-Segment
Elevation MI
Diagnosis of Acute MI

• At least 2 of the
• Ischemic
• Diagnostic ECG
• Serum cardiac
marker elevations
Diagnosis of Angina
• Typical angina—All three of the
• Substernal chest discomfort
• Onset with exertion or emotional stress
• Relief with rest or nitroglycerin

• Atypical angina
• 2 of the above criteria

• Noncardiac chest pain

• 1 of the above
Diagnosis of Unstable
• Patients with typical angina - An episode of angina
• Increased in severity or duration
• Has onset at rest or at a low level of exertion
• Unrelieved by the amount of nitroglycerin or rest that
had previously relieved the pain

• Patients not known to have typical angina

• First episode with usual activity or at rest within the
previous two weeks
• Prolonged pain at rest
Non sufficient to cause Complete thrombus
occlusive tissue damage & occlusion
thrombus mild
myocardial ST elevations on
Non specific necrosis ECG or new LBBB
ST depression +/- Elevated cardiac
Normal T wave inversion enzymes
cardiac on
enzymes ECG More severe
Elevated cardiac
Acute Management

• Initial evaluation
& stabilization

• Efficient risk

• Focused cardiac
• Efficient & direct history Occurs
• Initiate stabilization simultaneou

Plan for moving rapidly to

indicated cardiac care
Directed Therapies
Time Sensitive!
Chest pain suggestive of ischemia

Immediate assessment within 10

Initial Minutes
Emergent History &
care Physical
and tests
– 12 lead ECG  IV access  Establish

– Obtain initial  Cardiac diagnosis

cardiac enzymes
monitoring  Read ECG
– electrolytes, cbc
 Oxygen  Identify
lipids, bun/cr,
glucose, coags  Aspirin complicati
– CXR  Nitrates ons
 Assess for
Focused History
• Aid in diagnosis and • Reperfusion
rule out other causes questions
– Palliative/Provocative
factors – Timing of
– Quality of discomfort presentation
– Radiation
– Symptoms associated
with discomfort – Contraindication to
– Cardiac risk factors fibrinolysis
– Past medical history – Degree of STEMI
-especially cardiac risk
Targeted Physical
• Examination • Recognize factors
– Vitals that increase risk
– Cardiovascular • Hypotension
system • Tachycardia
– Respiratory • Pulmonary rales, JVD,
system pulmonary edema,
– Abdomen • New murmurs/heart
– Neurological
• Diminished peripheral
status pulses
• Signs of stroke
ECG assessment

ST Elevation or new LBBB


ST Depression or dynamic
T wave inversions

Non-specific ECG
Unstable Angina
Normal or non-diagnostic
ST Depression or Dynamic T wave
ST-Segment Elevation MI

QRS > 0.12 sec

L Axis deviation
Prominent R wave V1-V3
Prominent S wave 1, aVL, V5-V6

with t-wave inversion

Cardiac markers
• Troponin ( T, I) • CK-MB isoenzyme
– Very specific and more
sensitive than CK – Rises 4-6 hours after
– Rises 4-8 hours after injury injury and peaks at 24
– May remain elevated for up hours
to two weeks
– Remains elevated 36-
– Can provide prognostic 48 hours
– Troponin T may be elevated – Positive if CK/MB > 5%
with renal dz, of total CK and 2 times
poly/dermatomyositis normal
– Elevation can be
predictive of mortality
– False positives with
exercise, trauma,
muscle dz, DM, PE
Prognosis with Troponin
8 7,5 %
6 %
Mortality at 42 Days

4 3,4 3,7
3 %
1,7 %
0 %
0 to <0.4 %
0.4 to <1.01.0 to <2.02.0 to <5.05.0 to <9.0 9,0
Cardiac troponin I (ng/ml)
831 174 148 134 50 67

Risk Stratification
Based on initial
Evaluation, ECG, and
Cardiac markers

- Assess for UA or NSTEMI

- Evaluate for
- Select & Invasive vs.
implement conservative
reperfusion treatment
therapy - Directed medical
- Directed medical therapy
Cardiac Care Goals

• Decrease amount of myocardial

• Preserve LV function
• Prevent major adverse cardiac
• Treat life threatening
STEMI cardiac care
• STEP 1: Assessment
– Time since onset of symptoms
– 90 min for PCI / 12 hours for fibrinolysis

– Is this high risk STEMI?

– KILLIP classification
– If higher risk may manage with more invasive rx

– Determine if fibrinolysis candidate

– Meets criteria with no contraindications

– Determine if PCI candidate

– Based on availability and time to balloon rx
Fibrinolysis indications

• ST segment elevation >1mm in two

contiguous leads
• New LBBB
• Symptoms consistent with ischemia
• Symptom onset less than 12 hrs
prior to presentation
Absolute contraindications for fibrinolysis
therapy in patients with acute STEMI

• Any prior ICH

• Known structural cerebral vascular lesion (e.g., AVM)
• Known malignant intracranial neoplasm
(primary or metastatic)
• Ischemic stroke within 3 months EXCEPT acute ischemic
stroke within 3 hours
• Suspected aortic dissection
• Active bleeding or bleeding diathesis (excluding menses)
• Significant closed-head or facial trauma within 3 months
Relative contraindications for fibrinolysis
therapy in patients with acute STEMI
• History of chronic, severe, poorly controlled
• Severe uncontrolled hypertension on presentation
(SBP greater than 180 mm Hg or DBP greater than
110 mmHg)
• History of prior ischemic stroke greater than 3
months, dementia, or known intracranial pathology
not covered in contraindications
• Traumatic or prolonged (greater than 10 minutes)
CPR or major surgery (less than 3 weeks)
• Recent (within 2-4 weeks) internal bleeding
• Noncompressible vascular punctures
• For streptokinase/anistreplase: prior exposure (more
than 5 days ago) or prior allergic reaction to these
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the INR, the
higher the risk of bleeding
STEMI cardiac care
• STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred PCI preferred if:

if:  PCI available
 <3 hours from onset  Door to balloon <
 PCI not 90min
available/delayed  Door to balloon
 door to balloon > minus door to needle
90min < 1hr
 door to balloon  Fibrinolysis
minus door to contraindications
needle > 1hr  Late Presentation >
 Door to needle goal 3 hr
<30min  High risk STEMI
 No contraindications  Killup 3 or higher
Comparing outcomes
Comparing outcomes
Medical Therapy
• Morphine (class I, level C)
• Analgesia
• Reduce pain/anxiety—decrease sympathetic tone,
systemic vascular resistance and oxygen demand
• Careful with hypotension, hypovolemia, respiratory

• Oxygen (2-4 liters/minute) (class I, level C)

• Up to 70% of ACS patient demonstrate hypoxemia
• May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation
• Nitroglycerin (class I, level B)
• Analgesia—titrate infusion to keep patient pain free
• Dilates coronary vessels—increase blood flow
• Reduces systemic vascular resistance and preload
• Careful with recent ED meds, hypotension,
bradycardia, tachycardia, RV infarction

• Aspirin (160-325mg chewed & swallowed) (class I,

level A)
• Irreversible inhibition of platelet aggregation
• Stabilize plaque and arrest thrombus
• Reduce mortality in patients with STEMI
• Careful with active PUD, hypersensitivity, bleeding
• Beta-Blockers (class I, level A)
• 14% reduction in mortality risk at 7 days at 23%
long term mortality reduction in STEMI
• Approximate 13% reduction in risk of progression to
MI in patients with threatening or evolving MI
• Be aware of contraindications (CHF, Heart block,
• Reassess for therapy as contraindications resolve

• ACE-Inhibitors / ARB (class I, level A)

• Start in patients with anterior MI, pulmonary
congestion, LVEF < 40% in absence of
• Start in first 24 hours
• ARB as substitute for patients unable to use ACE-I
• Heparin (class I, level C to class IIa, level C)
– LMWH or UFH (max 4000u bolus, 1000u/hr)
• Indirect inhibitor of thrombin
• less supporting evidence of benefit in era of reperfusion
• Adjunct to surgical revascularization and thrombolytic / PCI
• 24-48 hours of treatment
• Coordinate with PCI team (UFH preferred)
• Used in combo with aspirin and/or other platelet inhibitors
• Changing from one to the other not recommended
Additional medication therapy
• Clopidodrel (class I, level B)
• Irreversible inhibition of platelet aggregation
• Used in support of cath / PCI intervention or if
unable to take aspirin
• 3 to 12 month duration depending on scenario

• Glycoprotein IIb/IIIa inhibitors

(class IIa, level B)
• Inhibition of platelet aggregation at final
common pathway
• In support of PCI intervention as early as
possible prior to PCI
Additional medication therapy

• Aldosterone blockers (class I, level A)

– Post-STEMI patients
• no significant renal failure (cr < 2.5 men or
2.0 for women)
• No hyperkalemis > 5.0
• LVEF < 40%
• Symptomatic CHF or DM
• Monitor for complications:
• recurrent ischemia, cardiogenic shock, ICH,

• Review guidelines for specific

management of complications & other
specific clinical scenarios
• PCI after fibrinolysis, emergent CABG, etc…

• Decision making for risk stratification at

hospital discharge and/or need for CABG
Unstable angina/NSTEMI cardiac
• Evaluate for conservative vs. invasive
therapy based upon:
• Risk of actual ACS
• TIMI risk score
• ACS risk categories per AHA guidelines

Low High
Risk Stratification to Determine the Likelihood of
Acute Coronary
Syndrome Findings indicating HIGH Findings indicating
Assessment Findings indicating LOW
likelihood of ACS INTERMEDIATE likelihood of ACS in absence
likelihood of ACS in absence of high- or intermediate-
of high-likelihood findings likelihood findings

History Chest or left arm pain or Chest or left arm pain or Probable ischemic symptoms
discomfort as chief symptom discomfort as chief symptom Recent cocaine use
Reproduction of previous Age > 50 years
documented angina
Known history of coronary
artery disease, including
myocardial infarction

Physical examination New transient mitral Extracardiac vascular disease Chest discomfort reproduced by
regurgitation, hypotension, palpation
diaphoresis, pulmonary edema
or rales

ECG New or presumably new Fixed Q waves T-wave flattening or inversion of

transient ST-segment deviation Abnormal ST segments or T T waves in leads with dominant
(> 0.05 mV) or T-wave waves not documented to be R waves
inversion (> 0.2 mV) with new Normal ECG

Serum cardiac markers Elevated cardiac troponin T or Normal Normal

I, or elevated CK-MB
TIMI Risk Score
Predicts risk of death, new/recurrent MI, need for urgent
revascularization within 14 days
ACS risk criteria
Low Risk ACS
Intermediate Risk ACS
No intermediate or high
Moderate to high likelihood
risk factors
of CAD
<10 minutes rest pain
>10 minutes rest pain,
now resolved
Non-diagnositic ECG
T-wave inversion > 2mm
Non-elevated cardiac
Slightly elevated cardiac
Age < 70 years
High Risk ACS
Elevated cardiac markers
New or presumed new ST depression
Recurrent ischemia despite therapy
Recurrent ischemia with heart failure
High risk findings on non-invasive stress test
Depressed systolic left ventricular function
Hemodynamic instability
Sustained Ventricular tachycardia
PCI with 6 months
Prior Bypass surgery
Low Intermediate High
risk risk risk

Chest Pain
Conservati Invasive
ve therapy therapy
Invasive therapy option
• Coronary angiography and
revascularization within 12 to 48 hours
after presentation to ED
• For high risk ACS (class I, level A)
• Clopidogrel
– 20% reduction death/MI/Stroke – CURE trial
– 1 month minimum duration and possibly up to 9
• Glycoprotein IIb/IIIa inhibitors
Conservative Therapy for
• Early revascularization or PCI not
• Clopidogrel
• Glycoprotein IIb/IIIa inhibitors
– Only in certain circumstances (planning PCI,
elevated TnI/T)
• Surveillence in hospital
– Serial ECGs
– Serial Markers
Secondary Prevention
• Disease

• Behavioral
– smoking, diet, physical activity, weight

• Cognitive
– Education, cardiac rehab program
Secondary Prevention
disease management
• Blood Pressure
– Goals < 140/90 or <130/80 in DM /CKD
– Maximize use of beta-blockers & ACE-I

• Lipids
– LDL < 100 (70) ; TG < 200
– Maximize use of statins; consider fibrates/niacin
first line for TG>500; consider omega-3 fatty

• Diabetes
– A1c < 7%
Secondary prevention
behavioral intervention
• Smoking cessation
– Cessation-class, meds, counseling

• Physical Activity
– Goal 30 - 60 minutes daily
– Risk assessment prior to initiation

• Diet
– DASH diet, fiber, omega-3 fatty acids
– <7% total calories from saturated fats
Thinking outside the box…
Or maybe just move….
Secondary prevention
• Patient education
– In-hospital – discharge –outpatient

• Monitor psychosocial impact

– Depression/anxiety assessment &
– Social support system
Medication Checklist
after ACS
• Antiplatelet agent
– Aspirin* and/or Clopidorgrel
• Lipid lowering agent
– Statin*
– Fibrate / Niacin / Omega-3
• Antihypertensive agent
– Beta blocker*
– Aldactone (as appropriate)
Prevention news…
From 1994 to 2004 the death
rate from coronary heart
disease declined 33%...
But the actual number of
deaths declined only 18% 
Getting better with
But more patients developing
disease –need for primary
prevention focus
• ACS includes UA, NSTEMI, and STEMI
• Management guideline focus
– Immediate assessment/intervention (MONA+BAH)
– Risk stratification (UA/NSTEMI vs. STEMI)
– RAPID reperfusion for STEMI (PCI vs. Thrombolytics)
– Conservative vs Invasive therapy for UA/NSTEMI
• Aggressive attention to secondary
prevention initiatives for ACS patients
• Beta blocker, ASA, ACE-I, Statin