Acute Coronary Syndrome

Mustika Mahbubi
 Overview of 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; 115:69171.
Acute Coronary Syndrome
Definition: a constellation of symptoms related to
obstruction of coronary arteries with chest pain being
the most common symptom in addition to nausea,
vomiting, diaphoresis etc.

Chest pain concerned for ACS is often radiating to the

left arm or angle of the jaw, pressure-like in
character, and associated with nausea and sweating.
Chest pain is often categorized into typical and
atypical angina.
 Acute Coronary Syndrome (ACS)

Definition: The spectrum of acute ischemia related syndromes ranging from

UA to MI with or without ST elevation that are secondary to acute plaque
rupture or plaque erosion.

[----UA---------NSTEMI----------STEMI----]
Acute coronary syndrome
Based on ECG and cardiac enzymes, ACS is classified into:
STEMI: ST elevation, elevated cardiac enzymes
NSTEMI: ST depression, T-wave inversion, elevated cardiac
enzymes
Unstable Angina: Non specific EKG changes, normal cardiac
enzymes
Unstable Angina
Occurs at rest and prolonged, usually lasting >20 minutes
New onset angina that limits activity
Increasing angina: Pain that occurs more frequently, lasts
longer periods or is increasingly limiting the patients activity
Pathophysiology of Stable Angina and
ACS
Pathophysiology ACS

Decreased O2 Supply

Asymptomatic
Flow- limiting stenosis

Myocardial Infarction
Anemia
Plaque rupture/clot

Increased O2 Demand

Angina
O2 supply/demand mismatchIschemia

Myocardial ischemianecrosis
 Pathophysiology of ACS
Evolution of Coronary Thrombosis
Unstable
NSTEMI STEMI
Angina Non-occlusive
thrombus
Non sufficient to cause Complete thrombus
occlusive tissue damage & occlusion
thrombus mild
myocardial ST elevations on
Non specific necrosis ECG or new LBBB
ECG
ST depression +/- Elevated cardiac
Normal T wave inversion enzymes
cardiac on
enzymes ECG More severe
symptoms
Elevated cardiac
enzymes
 Diagnosis of ACS
At least 2 of the following
History ( angina or angina
equivalent)
Acute ischemic ECG changes
Typical rise and fall of cardiac
markers
Absence of another identifiable
etiology
Initial Evaluation and management of Non ST-
elevation ACS

Initial Evaluation and Management

History and Physical

ECG
Cardiac Biomarkers

Establish the Likelihood that

Clinical Presentation Risk Stratify for Short-term
Represents an ACS Adverse Outcomes
Secondary to CAD
 Likelihood of ACS by Hx/PE
History/Examination Suggesting AMI
Pain in Chest or Left Arm LR 2.7
CP Radiation
Right Shoulder LR 2.9 (1.4-6.0)
Left Arm
LR 2.3 (1.7-3.1)
Both Left & Right Arm
Diaphoresis LR 7.1 (3.6-14.2)
3rd Heart Sound LR 2.0 (1.9-2.2)
SBP < 80 mm Hg LR 3.2 (1.6-6.5)
Pulmonary Crackles LR 3.1 (1.8-5.2)
LR 2.1 (1.4-3.1)

Panju AA. JAMA.

1998;280:1256.
 Likelihood of ACS by Hx/PE

ClinicalExamination Against AMI

Pleuritic Chest Pain
Sharp or Stabbing Pain
LR 0.2 (0.2-0.3)
Positional Chest Pain LR 0.3 (0.2-0.5)
Reproducible Chest Pain
LR 0.3 (0.2-0.4)
Panju AA. JAMA. 1998;280:1256.
LR 0.2-0.4
EKG
STEMI:
Q waves , ST elevations, hyper acute T waves; followed by T wave inversions.
Clinically significant ST segment elevations:
> than 1 mm (0.1 mV) in at least two anatomical contiguous leads
or 2 mm (0.2 mV) in two contiguous precordial leads (V2 and V3)

Note: LBBB and pacemakers can interfere with diagnosis of MI on EKG

EKG
NSTEMI:
ST depressions (0.5 mm at least) or T wave inversions ( 1.0 mm
at least) without Q waves in 2 contiguous leads with
prominent R wave or R/S ratio >1.
Isolated T wave inversions:
can correlate with increased risk for MI
may represent Wellens syndrome:
critical LAD stenosis
>2mm inversions in anterior precordial leads
Unstable Angina:
May present with nonspecific or transient ST segment
depressions or elevations
 Risk Stratification by ECG
CAVEATS cont.
1 ECG cannot exclude AMI

Brief sample of a dynamic process

Small regions of ischemia or infarction may be missed

Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40.

How Sensitive is the ECG Alone?
Cardiac Enzymes
Troponin is primarily used for diagnosing MI because it has
good sensitivity and specificity.
CK-MB is more useful in certain situations such as post
reperfusion MI or if troponin test is not available
Other conditions can cause elevation in troponin such as
renal failure or heart failure
The increasing troponin trend is the important thing to look
for in diagnosing MI. Order Troponin together with ECG when
doing serial testing to rule out ACS.
 Timing of Release of Various Biomarkers
After Acute Myocardial Infarction

Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3 rd ed. Rochester, MN: Mayo
Clinic Scientific Press and New York: Informa Healthcare USA, 2007:77380.
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1e157, Figure 5.
 Risk Stratification by Troponin
%

%
Mortality at 42 Days

%
%

%
%
831 174 148 134 50 67

Non ACS causes of Troponin Elevation
1. Trauma (including contusion; ablation; pacing; ICD firings,, endomyocardial biopsy,
cardiac surgery, after-interventional closure of ASDs)
2. Congestive heart failure (acute and chronic)
3. Aortic valve disease and HOCM with significant LVH
4. Hypertension
5. Hypotension, often with arrhythmias
6. Noncardiac surgery
7. Renal failure
8. Critically ill patients, especially with diabetes, respiratory failure
9. Drug toxicity (eg, adriamycin, 5 FU, herceptin, snake venoms)
10. Hypothyroidism
11. Coronary vasospasm, including apical ballooning syndrome
12. Inflammatory diseases (eg, myocarditis, Kawasaki disease, smallpox vaccination,
13. Post-PCI
14. Pulmonary embolism, severe pulmonary hypertension
15. Sepsis
16. Burns, especially if TBSA greater than 30%
17. Infiltrative diseases: amyloidosis, hemachromatosis, sarcoidosis, and scleroderma
18. Acute neurologic disease, including CVA, subarchnoid bleeds
19. Rhabdomyolysis with cardiac injury
20. Transplant vasculopathy
21. Vital exhaustion

Modified from Apple FS, et al Heart J. 2002;144:981-986.

Early Invasive

Conservative
Unstable angina/NSTEMI cardiac care
Evaluate for conservative vs. invasive strategy based upon:
Likelihood of actual ACS
Risk stratification by TIMI risk score
ACS risk categories per AHA guidelines

Low High
Intermediate
 TIMI Risk Score
Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14
days
 TIMI Risk Score
T: Troponin elevation (or CK-MB elevation)
H: History or CAD (>50% Stenosis)
R: Risk Factors: > 3 (HTN, Hyperlipidemia, Family Hx, DM II, Active Smoker)

E: EKG changes: ST elevation or depression 0.5 mm concordant leads

A2:Aspirin use within the past 7 days; Age over 65
T: Two or more episodes of CP within 2 hours
 Deciding between Early Invasive vs a Conservative Strategies

Definitive/Possible ACS
Initiate ASA, BB, Nitrates,
Anticoagulants, Telemetry

Early Invasive Strategy Conservative Strategy

Hemodynamic instability
TIMI Risk Score >3
New ST segment Elecrical instability

Refractory angina
TIMI Risk Score <3 (Esp. Women)
deviation No ST segment deviation
Positive biomarkersPCI in past 6 months

CABG Negative Biomarkers
EF <40%

Remains Stable
Recurrent Signs/Symptoms
Coronary angiography Heart failure Assess EF and/or Stress Testing
(24-48 hours) Arrhythmias
EF<40% OR Positive stress
Go to Angiography
 Early Hospital Care
Anti-Ischemic Therapy
Class I
Bed/Chair rest and Telemetry
Oxygen (maintain saturation >90%)
Nitrates (SLx3 Oral/topical. IV for ongoing iscemia, heart failure, hypertension)
Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa
indication)
Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-
blockers
ACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other
pts) (ARBs for those intolerant)
Statins
 Early Hospital Care
Anti-Platelet Therapy
Class I
Aspirin (162-325 mg), non enteric coated
Clopidogrel for those with Aspirin allergy/intolerance (300-600 mg load and 75
mg/d)
GI prophylaxis if a Hx of GI bleed
GP IIb/IIIa inhibitors should be evaluated based on whether an invasive or
conservative strategy is used
GP IIb/IIIa inhibitors recommended for all diabetics and all patient in early
invasive arm
 Early Hospital Care
Anticoagulant Therapy
Class I
Unfractionated Heparin
Enoxaparin
Bivalarudin
Fondaparinux

Relative choice depends on invasive vs conservative strategy and bleeding risk

 Early Hospital Care
Statin Therapy

MIRACL Trial
Inclusion Criteria
3086 patients with Non ST ACS
Total cholesterol <270 mg/dl
No planned PCI
Randomized to Atorvastatin vs Placebo
Drug started at 24-96 hours
 Secondary Prevention
Class I Indications
Aspirin
Beta-blockers: (all pts, slow titration with moderate to severe failure
ACE-Inhibitors: CHF, EF<40%, HTN, DM

(All pts-Class IIa) ARB when intolerant to ACE. (Class IIa as alternative to
ACEI)
Aldosterone blockade: An ACEI, CHF with either EF<40% or DM and if CrCl>30
ml/min and K<5.0 mEq/L
Statins
Standard Risk Factor Management
Long-Term Antithrombotic Therapy at Hospital Discharge
after UA/NSTEMI
UA/NSTEMI
Patient Groups
at Discharge

Medical Bare Metal Drug Eluting

Therapy Stent Group Stent Group
without Stent

ASA 75 to 162 mg/d ASA 162 to 325 mg/d for at ASA 162 to 325 mg/d for
indefinitely (Class I, LOE: least 1 month, then 75 to 162 at least 3 to 6 months,
A) mg/d indefinitely (Class I, then 75 to 162 mg/d
LOE: A) indefinitely
& (Class I, LOE: A)
&
Clopidogrel 75 mg/d at &
Clopidogrel 75 mg/d for at
least 1 month (Class I, LOE:
least 1 month and up to 1 Clopidogrel 75 mg/d for at
A) and up to 1 year (Class
year least 1 year (Class I, LOE:
I, LOE: B)
(Class I, LOE:B) B)
Indication for
Anticoagulation?

Yes No
Add: Warfarin (INR 2.0 to 2.5) Continue with dual
(Class IIb, LOE: B) antiplatelet therapy as
above
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1e157, Figure 11. INR = international normalized ratio; LOE = level of evidence.
Sedikit tentang APS
 Stable Angina
Non-Invasive Evaluation
N o n d is a b lin g A n g in a

R e s t in g L V F u n c t i o n
( C lin ic a l A s s e s s m e n t)

L V D y s f u n c t io n N o r m a l L V F u n c t io n

C o r o n a r y A r t e r io g r a p h y S t r e s s T e s t in g

H ig h R is k L o w R is k

C o r o n a r y A r t e r io g r a p h y M e d ic a l T h e r a p y

S t a b le R e c u r r e n t A n g in a

M e d ic a l T h e r a p y C o r o n a r y A r t e r io g r a p h y

N.A.N 2009
 Stable Angina
Current Pharmacotherapy
Beta-blockers
Calcium channel blockers
Nitrates
Aspirin
Statins
? ACE inhibitors