Luay Alkotob, MD, FACC

WHAT CAN I TALK TO YOU

ABOUT??????????

COOKING
ACUTE CORONARY
SYNDROME
All the Flavors
&
Ingredients
 NQW VASO-
SPASM QMI
MI
STEMI

Tako-
NSTE Tsubo
MI
 Algorithm for heart healthy living:
• The Japanese eat very little fat and suffer fewer heart attacks than the British or the
Americans.

• On the other hand, the French eat a lot of fat and also suffer fewer heart attacks than the
British or the Americans.

• The Japanese drink very little red wine and suffer fewer heart attacks than the British or
the Americans.

• The Italians drink generous amounts of red wine and also suffer fewer heart attacks than
the British or the Americans.

• Conclusion: Eat &drink what you like, It’s speaking English that kills you.

• ACC CURRENT JOURNAL REVIEW Nov/Dec 2002, 27.

 Hospitalizations in the U.S. Due to
ACS
Acute Coronary
Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million 0.33 million

Admissions per year Admissions per year

*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.
 Acute Coronary Syndrome

No ST Elevation ST Elevation

UA NSTEMI

Myocardial Infarction
Unstable Qw MI
Angina NQMI
 Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion

Thrombus Formation

Old
Terminology: UA NQMI STE-MI

New Non-ST-Segment Elevation Acute ST-Segment

Terminology: Coronary Syndrome (ACS) Elevation
(ACS)
 Other Etiologies

• Thromboembolism from plaque erosion

• Non–plaque-associated coronary thromboembolism
• Dynamic obstruction (spasm) of epicardial and/or
microvascular vessels
• Progressive mechanical obstruction to coronary flow
• Coronary arterial inflammation
• Secondary UA
• Coronary artery dissection
Pathology, Pathophysiology, and
Epidemiology
 The Vulnerable Plaque

Thin, Vulnerable,
Fibrous Cap

Large Lipid Core

Falk E, et al. Circulation. 1998;92:657-671.

Ruptured Plaque with Occlusive
Thrombus Formation

Thrombus
Formation

Falk E, et al. Circulation. 1998;92:657-671.

Atherothrombosis: Thrombus Superimposed
on Atherosclerotic Plaque

Falk E, et al. Circulation. 1998;92:657-671.

Available at: www.theheart.org.
 Characteristics of Unstable and
Stable Plaque

Unstable Stable
Lack of
Inflammatory inflammatory
cells cells
Thin Thick
Few fibrous cap More fibrous cap
SMCs SMCs

Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells
Libby P. Circulation. 1995;91:2844-2850.
Available at: www.theheart.org.
The Stable and
Unstable Plaque

Yeghiazarians Y, Braunstein JB, Askari A, et

al. Unstable angina pectoris. N Engl J Med.
2000;342:101-114.
 ACS Pathophysiology
Plaque Rupture, Thrombosis, and Microembolization
Quiescent plaque
Process Marker
Lipid core Plaque formation Cholesterol LDL

Vulnerable plaque C-Reactive Protein

Inflammation Adhesion Molecules
TF  Clotting
Multiple factors Interleukin 6, TNF
Cascade
Inflammation ? Infection sCD-40 ligand
Collagen 
platelet Plaque Rupture Modified LDL
activation
Foam Cells ? Macrophages
Macrophages Metalloproteinases
Metalloproteinases
Plaque rupture Platelet-thrombin micro-emboli
Thrombosis D-dimer, Complement,
Platelet Activation Fibrinogen, Troponin,
Thrombin CRP, CD40L

Courtesy of David Kandzari.

Systemic and Focal Plaque Rupture by IVUS in
ACS Patients Undergoing PCI
100 Analysis of 72 Arteries (n=24 TnI-positive ACS Patients)

79.0 %
% Plaque rupture

75 70.8 %

50
37.5 %

25

0
Plaque Plaque Plaque
rupture at rupture rupture in
site of culprit elsewhere different
lesion than site of artery than
culprit lesion culprit lesion

Rioufol G, et al. Circulation. 2002;106:804-808.

 Frequency of Multiple “Active” Plaques in
Patients With ACS
80% of Patients With 2 Plaques

30 N=24

25

20
Patients (%)

15

10

0
0 1 2 3 4 5
Frequency of multiple active plaque ruptures beyond the culprit lesion.

Rioufol G, et al. Circulation. 2002;106:804-808.

 3 principal presentations:

• Rest angina (angina commencing when the

patient is at rest)

• New-onset (less than 2 months) severe

angina

• Increasing angina
 Silent and Unrecognized Events

• The Framingham Study was the first to show that as

many as half of all MIs may be clinically silent and
unrecognized by the patient

• MI patients without chest discomfort were more

likely to be older, to be women, to have diabetes,
and/or to have prior heart failure [HF].
 SYMPTOMS SUGGESTIVE OF ACS

Definite ACS
Noncardiac Diagnosis Chronic Stable Possible ACS
Angina

No ST-Elevation ST-Elevation
Treatment as ACC/AHA Chronic
indicated by Stable Angina
alternative diagnosis Guidelines
ST and/or T wave changes
Nondiagnostic ECG
Normal initial serum Ongoing pain
cardiac biomarkers
Positive cardiac
biomarkers
Observe Hemodynamic
abnormalities
≥ 12 h from symptom onset
Evaluate for
reperfusion therapy

No recurrent pain; negative Recurrent ischemic pain or

follow-up studies positive follow-up studies
Diagnosis of ACS confirmed ACC/AHA STEMI
Stress study to provoke ischemia Guidelines

Consider evaluation of LV function if ischemia

is present (tests may be performed either
prior to discharge or as outpatient)

Negative Positive Admit to hospital

Potential diagnoses: nonischemic Diagnosis of ACS confirmed Manage via acute ischemia pathway
discomfort; low-risk ACS or highly likely

Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.

Arrangements for outpatient follow-up
 Management Plan

• Identification
• Risk Stratification
• Anti-ischemic therapy
• Anti-platelet therapy
• Anticoagulation therapy
• Lipid therapy
• Glucose & BP control
• Stop potentially harmful therapies
Feature High Risk
At least 1 of the following
features must be present:
History Accelerating tempo of
ischemic symptoms in
preceding 48 hrs
Character of Pain Prolonged ongoing (>20
min) rest pain
Clinical Findings •Pulmonary edema
•New or worsening MR
murmur
•S3 or new/worsening rale
•Hypotension, bradycardia,
tachycardia
•Age >75 years
ECG •Angina at rest with
transient ST-segment
changes >0.05 mV
•New or presumed new
BBB
•Sustained ventricular
tachycardia
Cardiac Markers Elevated (TnT or TnI >0.1
mg/mL)
Intermediate Risk
No high-risk feature but
must have 1 of the
following:
Prior MI, peripheral or
cerebrovascular disease,
CABG, or prior aspirin use
Prolonged (>20 min) rest
angina, now resolved, with
moderate or high likelihood
of CAD
Age > 70 years
•T-wave inversions >0.2
mV
•Pathological Q waves
Slightly elevated (TnT
>0.01 but <0.1 ng/mL)
Low Risk
No high- or intermediate-
risk feature but may have
any of the following
features:
New-onset or progressive
CCS Class III or IV angina
the past 2 weeks
Normal or unchanged ECG
during an episode of chest
discomfort
Normal
Variables Used in the TIMI Risk Score

•Age ≥ 65 years
•At least 3 risk factors for CAD
•Prior coronary stenosis of ≥ 50%
•ST-segment deviation on ECG presentation
•At least 2 anginal events in prior 24 hours
•Use of aspirin in prior 7 days
•Elevated serum cardiac biomarkers

Antman EM, et al. JAMA 2000;284:835–42.

TIMI = Thrombolysis in Myocardial Infarction.
 TIMI Risk Score
TIMI All-Cause Mortality, New or Recurrent MI, or Severe
Risk Recurrent Ischemia Requiring Urgent Revascularization
Score Through 14 Days After Randomization %
0-1 4.7
2 8.3
3 13.2
4 19.9
5 26.2
6-7 40.9

Antman EM, et al. JAMA 2000;284:835–42.

Timing of Release of Various Biomarkers After Acute Myocardial Infarction

Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157

 B-Type Natriuretic Peptide

•B-type natriuretic peptide (BNP): new biomarker of considerable

interest
•BNP is a cardiac neurohormone released on ventricular myocyte
stretch as proBNP, which is enzymatically cleaved to the N-
terminal proBNP (NT-pro-BNP) and, subsequently, to BNP
•Natriuretic peptides are strong predictors of both short- and long-
term mortality in patients with STEMI and UA/NSTEMI
•Recommend: Measurement of BNP or NT-pro-BNP may be
considered to supplement assessment of global risk in patients with
suspected ACS (Class IIb, LOE: B)

Galvani M, et al. Circulation 2004;110:128–34.

LOE = level of evidence.
Initial Therapies and Management
 ACC/AHA Class I Recommendations for
Initial Management and
Anti-Ischemic Therapy
• Bed rest
• Continuous ECG Monitoring
• Supplemental O2 to maintain SaO2 >90%
• NTG (IV or PO as dictated clinically)
• Beta-blockers (PO)
• IV Morphine prn pain, anxiety, and/or CHF
• IABP for hemodynamic instability
• ACEI for persistent hypertension in patients with LV
systolic dysfunction or CHF

Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf.

 Other modalities
• A 92-year old man saw MD for annual PE.
• A few days later the doctor saw the man walking down
the street with a gorgeous lady on his arm.
• At his follow up visit the doctor said:
– "You're really doing great aren't you?" The
– "Just doing what you said, Doctor, 'Get a hot mama and be
cheerful.' "
• "But I didn't say that,"
• "I said, 'You've got a heart murmur, be careful!"
 Anti-Ischemic Therapy

I IIa IIb III Bed/chair rest with continuous ECG monitoring is

recommended for all UA/NSTEMI patients during
the early hospital phase.

Supplemental oxygen should be administered to

I IIa IIb III patients with UA/NSTEMI with an arterial saturation
< 90%, respiratory distress, or other high-risk
features for hypoxemia. (Pulse oximetry is useful for
continuous measurement of SaO2.)
 Anti-Ischemic Therapy

I IIa IIb III Patients with UA/NSTEMI with ongoing ischemic

discomfort should receive sublingual NTG (0.4 mg)
every 5 min for a total of 3 doses, after which
assessment should be made about the need for
intravenous NTG, if not contraindicated.

Intravenous NTG is indicated in the first 48 h after

I IIa IIb III UA/NSTEMI for treatment of persistent ischemia, heart
failure (HF), or hypertension. The decision to
administer intravenous NTG and the dose used should
not preclude therapy with other proven mortality-
reducing interventions such as beta blockers or
angiotensin-converting enzyme (ACE) inhibitors.
 Anti-Ischemic Therapy

Oral beta-blocker therapy should be initiated within

I IIa IIb III the first 24 h for patients who do not have 1 or more
of the following: 1) signs of HF, 2) evidence of a
low-output state, 3) increased risk* for cardiogenic
shock, or 4) other relative contraindications to beta
blockade (PR interval greater than 0.24 s, second or
Major third degree heart block, active asthma, or reactive
Change airway disease).
 Anti-Ischemic Therapy

In UA/NSTEMI patients with continuing or

I IIa IIb III frequently recurring ischemia and in whom beta
blockers are contraindicated, a nondihydropyridine
calcium channel blocker (e.g., verapamil or
diltiazem) should be given as initial therapy in the
absence of clinically significant LV dysfunction or
other contraindications.
 Anti-Ischemic Therapy

I IIa IIb III An ACE inhibitor should be administered orally

within the first 24 h to UA/NSTEMI patients with
pulmonary congestion or LV ejection fraction
(LVEF) ≤ 40%, in the absence of hypotension
Major (systolic blood pressure < 100 mm Hg or < 30 mm
Change Hg below baseline) or known contraindications to
that class of medications.

I IIa IIb III An angiotensin receptor blocker should be

administered to UA/NSTEMI patients who are
intolerant of ACE inhibitors and have either clinical
or radiological signs of HF or LVEF ≤ 40%.
New
 Anti-Ischemic Therapy

I IIa IIb III

It is reasonable to administer supplemental oxygen to
all patients with UA/NSTEMI during the first 6 h
after presentation.

New

I IIa IIb III

In the absence of contradictions to its use, it is
reasonable to administer morphine sulfate
intravenously to UA/NSTEMI patients if there is
uncontrolled ischemic chest discomfort despite NTG,
I → IIa provided that additional therapy is used to manage
the underlying ischemia.
 Anti-Ischemic Therapy

It is reasonable to administer intravenous beta

I IIa IIb III blockers at the time of presentation for hypertension
to UA/NSTEMI patients who do not have 1 or more
of the following: 1) signs of HF, 2) evidence of a
low-output state, 3) increased risk* for cardiogenic
shock, or 4) other relative contraindications to beta
I → IIa blockade (PR interval greater than 0.24 s, second or
third degree heart block, active asthma, or reactive
airway disease).

*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age
greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60,
increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32.
ClOpidogrel and Metoprolol in Myocardial
Infarction Trial (COMMIT)
•45,852 patients within 24 h acute MI
― 93% STEMI or LBBB
•Up to 15 mg IV → 500 mg po metoprolol daily vs placebo
•Co-primary outcomes
― death, reinfarction, or cardiac arrest
― death from any cause to discharge or up to 4 wk in hospital
•Neither co-primary outcome ↓ by metoprolol
― 5 fewer reinfarctions, 5 fewer VF
― 11 more/1000 → cardiogenic shock
 Risk cardiogenic shock especially with initial hemodynamic
instability
― moderate late benefit with relative stability
•Recommend: start -blocker po when hemodynamically stable

Chen ZM, et al. Lancet 2005;366:1622–32.

 Anti-Ischemic Therapy

I IIa IIb III Immediate-release dihydropyridine calcium

antagonists should not be administered to patients
with UA/NSTEMI in the absence of a beta blocker.

An intravenous ACE inhibitor should not be given to

I IIa IIb III
patients within the first 24 h of UA/NSTEMI because
of the increased risk of hypotension. (A possible
exception may be patients with refractory
hypertension.)
New
Platelets and Anti-Platelet
Therapies
 Pathogenesis of Acute
Coronary Syndromes:
Plaque The integral role of
Fissure or platelets
Rupture
Platelet
Adhesion

Platelet
Activation

Platelet
Aggregation

Thrombotic
Occlusion
 The Role of Platelets in
Atherothrombosis
1 Adhesion 3Aggregation

2 Activation
 Collagen Arachidonic
Epinephrine
Acid
•Aspirin
ADP
Thrombin
•Ticlopidine •Heparin
•Clopidogrel •LMW Heparin
•Direct Thrombin
Inhibitors
The
Platelet

IIb/IIIa
receptors
•GP IIb/IIIa inhibitors fibrin
 Antiplatelet Therapy

I IIa IIb III Aspirin should be administered to UA/NSTEMI

patients as soon as possible after hospital
presentation and continued indefinitely in patients
not known to be intolerant of that medication. (Box
A)

I IIa IIb III Clopidogrel (loading dose [LD] followed by daily

maintenance dose)* should be administered to
UA/NSTEMI patients who are unable to take ASA
because of hypersensitivity or major gastrointestinal
intolerance. (Box A)
LD added

*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks
used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of
clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive
clinical efficacy and the safety of higher oral loading doses have not been rigorously established.
 Antiplatelet Therapy

I IIa IIb III In UA/NSTEMI patients with a history of

gastrointestinal bleeding, when ASA and clopidogrel
are administered alone or in combination, drugs to
minimize the risk of recurrent gastrointestinal
bleeding (e.g., proton-pump inhibitors) should be
New prescribed concomitantly.
 Treatment of Unstable Angina
Results of a study from the Montreal Heart Institute

% Developing MI 12
10
8
6
4
2
0
placebo aspirin heparin ASA+hep

Treatment

Theroux P, Quimet H, McCans J, et al. N Engl J Med. 1988;319:1105-1111.

 The Primary Composite End Point
in the CURE Trial
14 Placebo 20%
+ Aspirin RRR
12
% With Event

10 P=.00009
8 Clopidogrel
+ Aspirin
6
4

0 3 6 9 12

Follow-up
(months)
Yusuf S, Zhao F, Mehta SR, et al. N Engl J Med. 2001;345:494-502.
PRISM-PLUS: MI/Death Event Rates
Placebo + heparin
Aggrastat + heparin
RR=30%
15 P=0.03
RR=43%
P=0.006 11.9
% Patients

10 RR=66%
P=0.01 8.3 8.7

4.9
5
2.6
0.9
0
2 Days 7 Days 30 Days
Data from PRISM-PLUS Study Investigators. N Engl J Med. 1998;338:1488-1497.
PURSUIT Primary End Point

N Engl J Med. 1998;339:436-443

 Intracoronary Stenting and
Antitithrombotic Regimen–Rapid Early Action for Coronary
Treatment (ISAR-REACT)-2

•2,022 patients within 48 h high-risk UA/NSTEMI

•ASA + clopidogrel + abciximab vs ASA + clopidogrel
•600 mg LD clopidogrel ≥ 2 h before PCI → abciximab or placebo
•↓ Death, MI, or urgent TVR by 30 d with abciximab
― ↓ If cTnT +; no diff if cTnT –
•No diff major/minor bleeding
•Recommend: GP IIb/IIIa + clopidogrel if inv strategy used and
high risk (Class IIa, LOE: B)

Kastrati A, et al. JAMA 2006;295:1531–8.

LD = loading dose; LOE = level of evidence.
Contraindications to GP IIb/IIIa Rx
• Active or recent bleeding (4-6 weeks)
• Severe hypertension (SBP >180-200 mm Hg; DBP >110
mm Hg)
• Any hemorrhagic CVA (+/- intracranial neoplasm, AVM,
or aneurysm)
• Any CVA within 30 days–2 years
• Major surgery or trauma within 4-6 weeks
• Thrombocytopenia ( <100,000/mm3 )
• Bleeding diathesis/warfarin with elevated INR
• (Doses must be avoided with renal insufficiency or failure)
Antithrombin Therapy Studies and
Recommendations
Comparison of Heparin + ASA vs ASA Alone
Theroux

RISC

Cohen 1990

ATACS

Holdright
Gurfinkel
Summary Relative Risk
0.67 (0.44-0.1.02)
0.1 1 10
Heparin + ASA RR: ASA Alone
55/698=7.9% Death/MI 68/655=10.4%

Oler A, Whooley MA, Oler J, et al. Adding heparin to aspirin reduces the incidence of myocardial
infarction and death in patients with unstable angina: a meta-analysis. JAMA. 1996;276:811-815.
 ESSENCE Results
Unfractionated Heparin
30% Enoxaparin (Lovenox)
25%
Recurrent Angina
Death, MI or

20%
15%
P = 0.02
10%
Risk Reduction 16.2%
5%
0
5 9 13 17 21 25 29
Days After Randomization
 TIMI 11B: Enoxaparin vs. Heparin in
NSTE-ACS
20
Unfractionated Heparin 16.7 %
Urgent Revascularization

16 Enoxaparin (Lovenox)
Death, MI or

12 14.2 %

8
p = 0.03
4 Relative Risk Reduction = 15%

0 2 4 6 8 10 12 14
Days
Adapted from Antman EM, et al. Circulation. 1999;100:1593-1601.
ACC/AHA Recommendations for Antithrombin
Therapy in Patients with NSTE-ACS
• Class I
– Anticoagulation with subcutaneous LMWH or intravenous
UFH should be added to antiplatelet therapy
– Dose of UFH 60-70 U/kg (max 5000) IV followed by
infusion of 12-15 U/kg/hr (initial max 1000 U/hr) titrated
to aPTT 1.5-2.5 times control
– Dose of enoxaparin 1 mg/kg subcutaneously q12 hr; the
first dose may be preceded by a 30-mg IV bolus
• Class IIa
– Enoxaparin is preferable to UFH as an anticoagulant unless
CABG is planned within 24 hours

Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf.

Lipid Control
 Heart Protection Study (HPS)

•20,536 patients with CHD

•Simvastatin (40 mg qd) vs placebo
•↓ Total mortality by simvastatin
― ↓ Total CHD, total stroke, revascularization
― ↑ Benefit over time, irrespective of initial cholesterol level
and in broad spectrum of patients (e.g., women, elderly
& patients with diabetes)
•Recommend: Statin in all patients at discharge regardless of
baseline LDL-C (Class I, LOE: A)

Heart Protection Collaborative Group. Lancet 2002;360:7–22.

LOE = level of evidence.
Stopping Potentially Harmful Meds

• COX II inhibitors

• Roziglitizone

• HRT
Invasive vs Conservative Strategy
for UA/NSTEMI ISAR-
COOL
2003 RITA-3
VANQWISH

MATE VINO

TIMI IIIB TRUCS

TACTICS-
TIMI 18
FRISC II

Conservative Invasive

Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.

 Special Cases

• Cocain and Amphetamines

• Vaso spasm

• Small vessel disease

• Takatsubo

• Acute Pericarditis
Elevated serum cardiac troponin concentration in the
absence of an acute coronary syndrome

• Elevation in the general population

• Demand ischemia
• Critical illness 
• Tachycardia
• Left ventricular hypertrophy 
• Coronary vasospasm
• Acute stroke
• Direct myocardial damage 
• Heart failure
• Pulmonary disease
• Chronic kidney disease
STEMI
Primary PCI
 Primary PCI
I IIa IIb III STEMI patients presenting to a hospital with PCI
capability should be treated with primary PCI within
90 min of first medical contact as a systems goal.

I IIa IIb III STEMI patients presenting to a hospital without PCI

capability, and who cannot be transferred to a PCI
center and undergo PCI within 90 min of first medical
contact, should be treated with fibrinolytic therapy
within 30 min of hospital presentation as a systems
goal, unless fibrinolytic therapy is contraindicated.
 Options for Transport of Patients With
STEMI and Initial Reperfusion Treatment
Hospital fibrinolysis:
Door-to-Needle
within 30 min.
Not PCI
capable

Onset of 9-1-1 EMS on-scene EMS Inter-

symptoms of EMS • Encourage 12-lead ECGs. Triage Hospital
STEMI Dispatch • Consider prehospital fibrinolytic if Plan Transfer
capable and EMS-to-needle within
30 min.
PCI
capable
GOALS
5 8
min. EMS Transport
min.
Patient EMS Prehospital fibrinolysis EMS transport
EMS-to-needle EMS-to-balloon within 90 min.
within 30 min. Patient self-transport
Dispatch Hospital door-to-balloon
1 min. within 90 min.

Golden Hour = first 60 min. Total ischemic time: within 120 min.
Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at
http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001. Figure 1.
Facilitated PCI
 Meta-analysis: Facilitated PCI vs
Primary PCI

Mortality Reinfarction Major Bleeding

Lytic alone 1.43 1.81

(1.01-2.02) (1.19-2.77)
N=2953
1.03 1.40
IIb/IIIa alone (0.49-2.17) (0.49-3.98)
N=1148
3.07 1.03
Lytic +IIb/IIIa (0.18-52.0) (0.15-7.13)
N=399

All 1.38 1.71 1.51

(N=4500) (1.01-1.87) (1.16 - 2.51) (1.10 - 2.08 )

0.1 1 10 0.1 1 10 0.1 1 10

Fac. PCI PPCI Fac. PCI PPCI Fac. PCI PPCI
Better Better Better Better Better Better

Keeley E, et al. Lancet 2006;367:579.

 Facilitated PCI
I IIa IIb III A planned reperfusion strategy using full-dose fibrinolytic
therapy followed by immediate PCI is not recommended
and may be harmful.

I IIa IIb III Facilitated PCI using regimens other than full-dose
fibrinolytic therapy might be considered as a reperfusion
strategy when all of the following are present:
a. Patients are at high risk,
b. PCI is not immediately available within 90 minutes, and
c. Bleeding risk is low (younger age, absence of poorly
controlled hypertension, normal body weight).
 Rescue PCI

A strategy of coronary angiography with intent to

I IIa IIb III
perform rescue PCI is reasonable for patients in
whom fibrinolytic therapy has failed (ST-segment
elevation < 50% resolved after 90 min following
initiation of fibrinolytic therapy in the lead
showing the worst initial elevation) and a moderate
or large area of myocardium at risk [anterior MI,
inferior MI with right ventricular involvement or
precordial ST-segment depression].
 Occluded Artery Trial (OAT)
Eligibility:
• Confirmed Index MI
• Total IRA occlusion
• 3-28 days (>24 hours)
Exclusion criteria:
• Significant left main or 3 vessel
CAD
• Hemodynamic or electrical
instability
• Rest or low-threshold angina
• NYHA Class III-IV HF or shock
Hochman JS, et al. Am Heart J 2005;150:627-42;
Hochman JS, et al. N Engl J Med 2006;355:2395-407.
RESULTS
2166 randomized
1082 PCI + optimal medical therapy
1084 Optimal medical therapy (MED)
Death, MI, CHF Class IV
4 year event rate:
17.2% PCI vs 15.6% MED
Hazard Ratio: PCI vs MED=1.16;
95% Cl (0.92, 1.45); p=0.20
Fatal and Non fatal MI
4 year event rate:
7.0% PCI vs 5.3% MED
Hazard Ratio: PCI vs MED=1.36;
95% Cl (0.92, 2.00); p=0.13
 Late PCI after Fibrinolysis or for Patients Not
Undergoing Primary Reperfusion

I IIa IIb III

PCI of a hemodynamically significant stenosis in a
patent infarct artery > 24 hours after STEMI may be
considered as part of a invasive strategy.

I IIa IIb III PCI of a totally occluded infarct artery > 24 hours
after STEMI is not recommended in asymptomatic
patients with 1- or 2-vessel disease if they are
hemodynamically and electrically stable and do not
have evidence of severe ischemia.
 Preventive treatment

Cardiologist Available for

• Cardiologist needed for a
reasonable compensation,
very busy practice
car cleaning and
transmission too