Management of Coronary Artery Disease:

1
Management of Coronary Artery Disease

• Saravanan Kuppuswamy MD
• Division of Cardiology
• Department of Internal Medicine
• University of Missouri Hospital

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Coronary blood supply
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Micro circulation
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Temporal Trends in CAD

• CHD is the leading cause of death in adults in US
  (1/3 of all deaths in subjects over age 35)
• Mortality rates for cardiovascular death has
  fallen in most developed countries 24-28 since
  1975
• Estimated that 45 percent of mortality reduction
  in CHD is due to improvement of medical therapy
  and 55 is due to risk factor modification

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Etiology

• Congenital
• Acquired
• Infection
• Inflammation
• Neoplastic

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Management of CAD

• Acute
• Chronic

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ACS The Tip of the Atherothrombotic Iceberg
Acute Plaque Rupture (UA/NSTEMI/STEMI)
Clinical
Subclinical
Presence of Multiple Coronary Plaques
Persistent Hyperreactive Platelets
Vascular Inflammation
ACSacute coronary syndrome. UAunstable
angina. Bhatt DL. J Invasive Cardiol.
2003153B-9B.
NSTEMInon-ST-segment elevation myocardial
infarction. STEMIST-segment elevation myocardial
infarction.
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Chronic stable angina

• Levines sign
• Exercise capacity may vary
• Relieved by nitrates

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CCS classification
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Applying Classification of Recommendations and
Level of Evidence
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Components of Secondary Prevention
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ABCDE Of Management
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A
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• Antiplatelet Agents / Anticoagulation
  Recommendations

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Aspirin Recommendations
Start and continue indefinitely aspirin 75 to
162 mg/d in all patients unless contraindicated
For patients undergoing CABG, aspirin (100 to
325 mg/d) should be started within 48 hours after
surgery to reduce saphenous vein graft closure
Post-PCI-stented patients should receive 325 mg
per day of aspirin for 1 month for bare metal
stent, 3 months for sirolimus-eluting stent and 6
months for paclitaxel-eluting stent
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Aspirin Evidence Secondary Prevention
Effect of antiplatelet therapy on vascular
events
Aspirin was the predominant antiplatelet agent
studied Vascular events include MI, stroke, or
death
Antithrombotic Trialist Collaboration. BMJ
20023247186.
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Aspirin Evidence Dose and Efficacy
Indirect Comparisons of Aspirin Doses on Vascular
Events in High-Risk Patients
Antithrombotic Trialists Collaboration. BMJ.
200232471-86
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Mechanism of action of nitrates
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B
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• b-blocker Recommendations

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b-blocker Recommendations
Start and continue indefinitely in all post MI,
ACS, LV dysfunction with or without HF symptoms,
unless contraindicated. Consider chronic
therapy for all other patients with coronary or
other vascular disease or diabetes unless
contraindicated.
Precautions but still indicated include mild to
moderate asthma or chronic obstructive pulmonary
disease, insulin dependent diabetes mellitus,
severe peripheral arterial disease, and a PR
interval gt0.24 seconds.
MIMyocardial infarction, HFHeart Failure
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b-blocker Evidence
Summary of Secondary Prevention Trials of
b-blocker Therapy
Total Patients
Phase of Treatment
RR (95 CI)
28,970
0.87 (0.77-0.98)
Acute treatment
24,298
0.77 (0.70-0.84)
Secondary prevention
53,268
0.81 (0.75-0.87)
Overall
0.5
1.0
2.0
RR of death
b-blocker better
Placebo better
CIConfidence interval, RRRelative risk
Antman E, Braunwald E. Acute Myocardial
Infarction. In Braunwald E, Zipes DP, Libby P,
eds. Heart Disease A textbook of Cardiovascular
Medicine, 6th ed., Philadelphia, PA W.B.
Sanders, 2001, 1168.
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b-blocker Evidence Post MI with Left Ventricular
Dysfunction
Carvedilol Post-Infarct Survival Control in LV
Dysfunction (CAPRICORN)
6,644 patients with LVEF lt0.40 after a MI with or
without HF randomized to carvedilol or placebo
for 24 months
The CAPRICORN Investigators. Lancet.
200135713851390.
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b-blocker Evidence Benefit in HF and LVSD
Not an approved indication Not a planned end
point. Not approved for severe HF or mortality
reduction alone
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Blood Pressure Control Recommendations
Goal lt140/90 mm Hg or lt130/80 if diabetes or
chronic kidney disease
Blood pressure 120/80 mm Hg or greater
Initiate or maintain lifestyle modification
weight control, increased physical activity,
alcohol moderation, sodium reduction, and
increased consumption of fresh fruits vegetables
and low fat dairy products

• Blood pressure 140/90 mm Hg or greater (or 130/80
  or greater for chronic kidney disease or
  diabetes)
• As tolerated, add blood pressure medication,
  treating initially with beta blockers and/or ACE
  inhibitors with addition of other drugs such as
  thiazides as needed to achieve goal blood
  pressure

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Blood Pressure Lower is Better
Ischemic Heart Disease Mortality
Age at Risk (Y)
Age at Risk (Y)
80-89
80-89
70-79
70-79
60-69
60-69
50-59
50-59
Ischemic Heart Disease Mortality
Ischemic Heart Disease Mortality
40-49
40-49
Usual Diastolic BP (mm Hg)
Usual Systolic BP (mm Hg)
BPBlood pressure
Prospective Studies Collaboration. Lancet.
20023601903-1913
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Blood Pressure Risk of CHD with Active Treatment
0.79 (0.69 to 0.90)
0
2.0
0.5
1.0
1.5
CHDCoronary heart disease
Better than placebo
Worse than placebo
He J et al. Am Heart J 1999 138211-219
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JNC VII Guidelines for Management and Treatment
Initial drug therapy
Lifestyle modification
DBP mmHg
SBP mmHg
BP classification
With compelling indications
Encourage
lt80
lt120
Normal
Drug(s) for compelling indications.
Yes
8089
120139
Pre- hypertension
Yes
9099
140159
Stage 1 Hypertension
Drug(s) for the compelling indications. Other
antihypertensive drugs (diuretics, ACEI, ARB, BB,
CCB) as needed.
Yes
gt100
gt160
Stage 2 Hypertension
ACEIAngiotensin converting enzyme inhibitor,
ARBAngiotensin receptor blocker, BBb-blocker,
BPBlood pressure, CCBCalcium channel blocker,
DBPDiastolic blood pressure, SBPSystolic blood
pressure
Treatment determined by highest blood pressure
category. Initial combined therapy should be
used cautiously in those at risk for orthostatic
hypotension. Treat patients with chronic kidney
disease or diabetes mellitus to blood pressure
goal of lt130/80 mmHg.
Chobanian AV et al. JAMA. 20032892560-2572
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JNC VII Lifestyle Modifications for BP Control
BMIBody mass index, SBPSystolic blood pressure
Chobanian AV et al. JAMA. 20032892560-2572
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JNC VII Compelling Indications for Drug Classes
Clinical-Trial Basis
Compelling Indication
Initial Therapy Options
MERIT-HF, COPERNICUS, CIBIS, SOLVD, AIRE, TRACE,
Val-HeFT, RALES
Diuretic, BB, ACEI,ARB, Aldo Ant
Heart Failure
ACC/AHA Post-MI Guideline, BHAT, SAVE, Capricorn,
EPHESUS
Post-MI
BB, ACEI, Aldo Ant
ALLHAT, HOPE, ANBP2,LIFE, CONVINCE
High CAD Risk
Diuretic, BB, ACEI, CCB
NKF-ADA Guideline,UKPDS, ALLHAT
Diuretic, BB, ACEI,ARB, CCB
Diabetes Mellitus

NKF Guideline, Captopril Trial, RENAAL, IDNT,
REIN, AASK
Chronic Kidney Disease
ACEI, ARB
Recurrent Stroke Prevention
PROGRESS
Diuretic, ACEI
ACEIAngiotensin converting enzyme inhibitor,
Aldo AntAldosterone antagonist, ARBAngiotensin
receptor blocker, BBb-blocker, CADCoronary
artery disease, CCBCalcium channel blocker,
MIMyocardial Infarction
Chobanian AV et al. JAMA. 20032892560-2572
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C
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Cigarette Smoking Recommendations
Goal Complete Cessation and No Exposure to
Environmental Tobacco Smoke

• Ask about tobacco use status at every visit.
• Advise every tobacco user to quit.
• Assess the tobacco users willingness to quit.
• Assist by counseling and developing a plan for
  quitting.
• Arrange follow-up, referral to special programs,
  or pharmacotherapy (including nicotine
  replacement and bupropion.
• Urge avoidance of exposure to environmental
  tobacco smoke at work and home.

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Cigarette Smoking Cessation Risk of Non-fatal MI
RR (95 Cl)
Study
10
0.1
1.0
Ceased smoking
Continued smoking
Includes those with known coronary heart disease
CIConfidence interval, RRRelative risk
Critchley JA et al. JAMA. 200329086-97.
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Lipid Management Goals NCEP
ATPAdult Treatment Panel, CHDCoronary heart
disease, LDL-CLow-density lipoprotein
cholesterol, TLCTherapeutic lifestyle changes
Grundy, S. et al. Circulation 2004110227-39.
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Lipid Management Recommendations
For all patients
Start dietary therapy (lt7 of total calories as
saturated fat and lt200 mg/d cholesterol) Adding
plant stanol/sterols (2 gm/day) and viscous fiber
(gt10 mg/day) will further lower LDL Promote
daily physical activity and weight management.
Encourage increased consumption of omega-3
fatty acids in fish or 1 g/day omega-3 fatty
acids in capsule form for risk reduction.
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Lipid Management Recommendations
Assess fasting lipid profile in all patients, and
within 24 hours of hospitalization for those with
an acute event. For patients hospitalized,
initiate lipid-lowering medication as recommended
below prior to discharge according to the
following schedule
If baseline LDL-C gt 100 mg/dL, initiate
LDL-lowering drug therapy If on-treatment LDL-C gt
100 mg/dL, intensify LDL-lowering drug therapy
(may require LDL lowering drug combination) If
baseline is LDL-C 70 to 100 mg/dL, it is
reasonable to treat to LDL lt 70 mg/dL
When LDL lowering medications are used, obtain at
least a 30-40 reduction in LDL-C levels.
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Lipid Management Recommendations
If TG are 200-499 mg/dL, non-HDL-C should be lt
130 mg/dL Further reduction of non-HDL to lt 100
mg/dL is reasonable Therapeutic options to
reduce non-HDL-C More intense LDL-C lowering
therapy I (B) or Niacin (after LDL-C lowering
therapy) IIa (B) or Fibrate (after LDL-C lowering
therapy) IIa (B) If TG are gt 500 mg/dL,
therapeutic options to prevent pancreatitis are
fibrate or niacin before LDL lowering therapy
and treat LDL-C to goal after TG-lowering
therapy. Achieve non-HDL-C lt 130 mg/dL, if
possible
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HMG-CoA Reductase Inhibitor Secondary Prevention
Heart Protection Study (HPS)
20,536 patients with CAD, other occlusive
arterial disease, or DM randomized to
simvastatin (40 mg) or placebo for 5.5 years
Event Rate Ratio (95 CI)
Statin Better
Statin Worse
0.76 (0.720.81) Plt0.0001
CADCoronary artery disease, CIConfidence
interval, DMDiabetes mellitus,
HPS Collaborative Group. Lancet 20023607-22
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HMG-CoA Reductase Inhibitor Secondary Prevention
Pravastatin or Atorvastatin Evaluation and
Infection Therapy (PROVE-IT)TIMI 22 Study
4,162 patients with an ACS randomized to
atorvastatin (80 mg) or pravastatin (40 mg) for
24 months
ACSAcute coronary syndrome, CVCardiovascular,
MIMyocardial infarction, RRRRelative risk
reduction
Cannon CP et al. NEJM 20043501495-1504
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HMG-CoA Reductase Inhibitor Secondary Prevention
Relationship between LDL Levels and Event Rates
in Secondary Prevention Trials of Patients with
Stable CHD
Statin Placebo
LDL-CLow density lipoprotein cholesterol
TNTTreating to New Targets HPSHeart Protection
Study CARECholesterol and Recurrent Events
Trial LIPIDLong-term Intervention with
Pravastatin in Ischaemic Disease 4SScandinavian
Simvastatin Survival Study.
LaRosa JC et al. NEJM. 20053521425-1435
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Lipid Management Pharmacotherapy
HDL-CHigh-density lipoprotein cholesterol,
LDL-CLow-density lipoprotein cholesterol,
TCTotal cholesterol, TGTriglycerides Daily
dose of 40mg of each drug, excluding rosuvastatin.
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Lipid Management Goal
LDL-C should be less than 100 mg/dL Further
reduction to LDL-C to lt 70 mg/dL is reasonable
If TG gt200 mg/dL, non-HDL-C should be lt 130
mg/dL
Non-HDL-C total cholesterol minus HDL-C
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D
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ATP III Dietary Recommendations
ATPAdult Treatment Panel
Expert Panel on Detection, Evaluation, and
Treatment of High Blood Cholesterol in Adults.
JAMA 20012852486-2497.
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Weight Management Recommendations
Goal BMI 18.5 to 24.9 kg/m2 Waist Circumference
Men lt 40 inches Women lt 35 inches

• Assess BMI and/or waist circumference on each
  visit and consistently encourage weight
  maintenance/
• reduction through an appropriate balance of
  physical activity, caloric intake, and formal
  behavioral programs when indicated.
• If waist circumference (measured at the iliac
  crest) gt35 inches in women and gt40 inches in men
  initiate lifestyle changes and consider treatment
  strategies for metabolic syndrome as indicated.
• The initial goal of weight loss therapy should be
  to reduce body weight by approximately 10 percent
  from baseline. With success, further weight loss
  can be attempted if indicated.

BMI is calculated as the weight in kilograms
divided by the body surface area in meters2.
Overweight state is defined by BMI25-30 kg/m2.
Obesity is defined by a BMI gt30 kg/m2.
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CV Risk Increases with Body Mass Index
CVCardiovascular
Body mass index is calculated as the weight in
kilograms divided by the body surface area in
meters2.
Mhurchu N et al. Int J Epidemiol 200433751-758
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Definition of the Metabolic Syndrome
Defined by presence of gt3 risk factors
HDL-CHigh-density lipoprotein cholesterol
Grundy, et al. Diagnosis and management of the
metabolic syndrome an AHA/NHLBI Scientific
Statement. Circulation 20051122735-2752.
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Metabolic Syndrome Risk of Developing DM
Diabetes Prevention Program (DPP)
3,234 patients with elevated fasting and
post-load glucose levels randomized to placebo,
metformin (850 mg twice daily), or lifestyle
modification for 2.8 years Lifestyle
modification reduces the risk of developing DM
Includes 7 weight loss and at least 150 minutes
of physical activity per week
Knowler WC et al. NEJM 2002346393-403
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Diabetes Mellitus Recommendations
Goal Hb A1c lt 7
Lifestyle and pharmacotherapy to achieve near
normal HbA1C (lt7). Vigorous modification of
other risk factors (e.g., physical activity,
weight management, blood pressure control, and
cholesterol management as recommended).
Coordinate diabetic care with patients primary
care physician or endocrinologist. )
HbA1c Glycosylated hemoglobin
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E
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Physical Activity Recommendations
Goal 30 minutes 7 days/week, minimum 5 days/week

• Assess risk with a physical activity history
  and/or an exercise test, to guide prescription
• Encourage 30 to 60 minutes of moderate intensity
  aerobic activity such as brisk walking, on most,
  preferably all, days of the week, supplemented by
  an increase in daily lifestyle activities
• Advise medically supervised programs for
  high-risk patients (e.g. recent acute coronary
  syndrome or revascularization, HF)

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Exercise Evidence Mortality Risk
Observational study of self-reported physical
activity in 772 men with established coronary
heart disease Light or moderate
exercise is associated with lower risk
Wannamethee SG et al. Circulation
20001021358-1363
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• Renin-Angiotensin-Aldosterone System Blockers
  Recommendations

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ACE Inhibitor Recommendations
Use in all patients with LVEF lt 40, and those
with diabetes or chronic kidney disease
indefinitely, unless contraindicated Consider
for all other patients Among lower risk
patients with normal LVEF where cardiovascular
risk factors are well controlled and where
revascularization has been performed, their use
may be considered optional
ACEAngiotensin converting enzyme, LVEF left
ventricular ejection fraction
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The Spectrum of ACS

• STEMI

Non-cardiacchest pain
Stableangina
NSTEMI
UA
Atypical pain
Ongoing pain
Rest pain, Post-MI, DM, Prior Aspirin
Exertional pain
Clinical finding
ST-T wave changes
ST elevation
Negative
EKG
Negative
Positive
Serum markers
Lowprobability
Medium-high risk
STEMI
Low risk
Risk assessment
Diagnostic rule out MI/ACS pathway
Aspirin, heparin/low-molecular-weight heparin
(LMWH) clopidogrelAnti-ischemic Rx Early
conservative therapy
ThrombolysisPrimary PCI
Negative
Aspirin GP IIb/IIIa inhibitor clopidogrel
heparin/ LMWH anti-ischemic RxEarly invasive Rx
Discharge
DMdiabetes mellitus. Cannon, Braunwald. Heart
Disease. 2001.
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Acute Coronary Syndromes Management of STEMI
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Balloon angioplasty
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Stents
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Acute Coronary Syndromes Management of
UA/NSTEMI
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Acute Management of UA/NSTEMI

• Anti-Ischemic Therapy
• Oxygen, bed rest, ECG monitoring
• Nitroglycerin
• ?-Blockers
• ACE inhibitors

• Antithrombotic Therapy
• Antiplatelet therapy
• Anticoagulant therapy

UA, unstable angina NSTEMI, non-ST-segment
elevation myocardial infarction ECG,
electrocardiogram ACE, angiotensin-converting
enzyme. Braunwald E, et al. J Am Coll Cardiol.
200036970-1062.
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Rationale for Use Pharmacologic Intervention in
Thrombosis
Coagulation cascade
Platelets
Collagen
Leukocytes
Platelets A2 vWF ADP Activated platelets Fibrinog
en cross-linking Platelet aggregation
LMWH
Tissue factor Factor Xa Prothrombin Thrombin
TFPI
LMWH UFH
Thromboxane
Thienopyridines
Aspirin
GP IIb/IIIa inhibitors
Anti-thrombin
LMWH UFH
Anti-thrombin
Direct thrombin inhibitors
Fibrin
Fibrinogen
Thrombus
Fibrin degradation
Plasmin
UFHunfractionated heparin. LMWHlow-molecular-wei
ght heparin ADPadenosine diphosphate. TFPItissue
factor pathway inhibitor Selwyn A. Am J
Cardiol. 2003913H-11H.
Thrombolytics
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Efficacy of Aspirin Doses on Vascular Events in
High Risk Patients
Aspirin Dose Trials OR ()
Odds Ratio
5001500 mg 34 19
160325 mg 19 26
75150 mg 12 32
lt75 mg 3 13
Any aspirin 65 23
0
0.5
1.5
1.0
2.0
Anti - platelet Better
Anti - platelet Worse
Odds reduction.
Treatment effect P lt 0.0001.
Adapted with permission from the BMJ Publishing
Group. Anti-thrombotic Trialists Collaboration.
BMJ. 200232471-86.
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Comparison of Heparin ASA vs ASA Alone
B
Theroux
B
RISC
B
Cohen 1990
B
ATACS
B
Holdright
B
Gurfinkel
Summary Relative Risk
B
0.67 (0.44-0.1.02)
0.1
1
10
RR Death/MI
ASA Alone 68/65510.4
Heparin ASA 55/6987.9
ASA, acetylsalicylic acid RISC, Research on
InStability in Coronary artery disease ATACS,
Antithrombotic Therapy in Acute Company
Syndromes RR, relative risk MI, myocardial
infarction. Oler A, et al. JAMA.
1996276811-815. (with permission)
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TIMI IIB/ESSENCE MetanalysisEnoxaparin vs
Unfractionated Heparin
TIMI, Thrombosis in Myocardial Infarction
ESSENCE, Efficacy and Safety of Subcutaneous
Enozapam in NonQ-Wave Coronary Events UHF,
unfractionated heparin ENOX, enoxaparin MI,
myocardial infarction OR, odds ratio. Antman EM,
et al. Circulation. 19991001602-1608. (with
permission)
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LMWH Limitations

• Indirect inhibition dependent on antithrombin
• Inability to inhibit clot-bound thrombin
• Catheterization lab slower onset, longer
  half-life, and with enoxaparin, no standard test
  to measure levels/effect
• CABG concerns regarding the long half-life
• Monitoring for Factor Xa possible, but what is
  the therapeutic target, increased time, expense?
• Not all LMWHs are the same

CABGcoronary artery bypass graft.
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CURE Primary Endpoint MI/Stroke/CV Death
0.14
Placebo Aspirin
20 Relative-riskReduction
0.12
0.10
Plt0.001 N12,562
0.08
Clopidogrel Aspirin
Cumulative Hazard Rate
0.06
0.04
0.02
0.00
9
0
6
12
3
Months of Follow-Up
Other standard therapies were used as
appropriate. CVcardiovascular. CURE Trial
Investigators. N Engl J Med. 2001345494-502.
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Early Use of GP IIb/IIIa Inhibition Improves PCI
CAPTURE, PURSUIT, PRISM-PLUS
Post-PCI
Before PCI
10
10
8.0
8
8
Death/MI
6
6
Death/MI
n12,296 p0.001
4.9
4.3
4
4
2.9
n2754 p0.001
2
2
0
0
24 h
48 h
24 h
48 h
72 h
0
PCI
Boersma E, et al. Circulation. 19991002045-2048.
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In-hospital Mortality is Lower With Early GP
IIb/IIIa Inhibitor Use (within 24 hrs)
? 42? plt0.0001
Includes patients who received late GP IIb/IIIa
inhibitor (gt 24 hrs) therapy.
Unadjusted for risk.
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TIMI Risk Score for UA/NSTEMI 7 Independent
Predictors

• Aged 65 years
• 3 CAD risk factors
• Prior CAD (stenosis gt50)
• Aspirin in last 7 days
• gt2 anginal events in 24 hours
• ST deviation
• Elevated cardiac markers (CK-MB or troponin)

TIMI, thrombosis in myocardial infarction UA,
unstable angina NSTEMI, nonST-segment elevation
myocardial infarction CAD, coronary artery
disease.Antman EM, et al. JAMA. 2000284835-842.
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TIMI risk score predicts 30 day mortality after a
myocardial infarction                          
                                                  
   The TIMI risk score has a continuous
association with 30-day mortality in patients
with an ST elevation (STE) myocardial infarction
who are eligible for fibrinolytic therapy.
Morrow, DA, Antman, EM, Charlesworth, A, et al
Circulation 2000 1022031.
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TIMI risk score predicts 14 day outcome for
NSTEMI and UA                                  
                                            
The TIMI risk score has a
continuous association with 14-day mortality,
recurrent MI and target vessel revascularization
in patients with an NSTEMI and unstable angina
(UA)
Antman, EM, Cohen, et al, JAMA 2000 284835.
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Chest Pain Classification/Triage

• Class I
• Class II
• Class III
• Class IV
• Class V
• Class x

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Class I

• STEMI
• Chest pain with STE or new LBBB
• Acute revascularization followed by CICU
  admission

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Class II

• Unstable Angina/NSTEMI (high risk)
• Positive initial cardiac markers
• ST depression gt 1mm in two contiguous leads
• TIMI risk score gt 5
• Continued angina requiring IV NTG drip
• CHF
• SBP lt 90mmHg or gt 180mmHg
• New mitral regurgitaiton
• Recent ACS (lt 30 days)
• Admit to CICU by cardiology

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Class III

• Unstable Angina
• No initial increase in cardiac markers
• Normal ECG or ST depression lt 1mm
• No CHF
• No recent ACS
• TIMI risk score 3-4
• Admit to telemetry by cardiology

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Class IV

• Unstable Angina with normal ECG
• No initial increase in cardiac markers
• No history of CAD
• TIMI risk score lt 3
• No ongoing or recurring pain
• Admit to Chest Pain Service or Chest Pain Center
  in ER

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Class V

• Non-cardiac Chest Pain
• Workup in ER with appropriate referral

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Class x

• Critical causes of acute chest pain other than
  ACS or ACS combined with other acute
  critical/life-threatening illnesses
• Admit to intensive care (MICU, SICU or CICU) as
  appropriate

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Chest pain algorithm