Acute Coronary

Syndrome
dr. Muhammad Ridwan, MAppSc, SpJP (K)

Bagian Kardiologi dan Kedokteran Vaskular FK Unsyiah

Bagian Fisiologi FK Unsyiah

2015
 Goals and Objectives
 Discuss the definition & pathophysiology of
ACS
 Recognize the clinical features of low,
intermediate and high risk ACS
 Be able to identify and treat patients
appropriate for a conservative or invasive
strategy
 Discuss new and controversial
pharmacological treatments
 INTRODUCTION
 Coronary Artery Disease – leading cause of morbidity & mortality in
industrialised nations.
 Although decrease in cardiovascular mortality  still major cause of
morbidity & burden of disease.

 South African perspective of cardiovascular disease:

 “A World in One Country” - Yusuf et al
 Epidemiological transitions of cardiovascular disease.
 HIGH RISK POPULATION FOR CAD/ACS:
INDIAN/WHITE/COLOURED

 INCREASING rate in Black population – lifestyle/socioeconomic changes,

urbanisation

 GF Jooste stats: 23.8% of admissions to resus. unit for chest pain/acs

related (stats 1Jan 2009 – 28 Feb 2009) 150/628 entries.

 In US – 2004 – 1.56 million admissions for ACS – 669 000 for unstable
angina, 896 000 for MI
 Higher prevelance for NSTEMI.
 DEFINITIONS

 CAD is a continuum of disease….

 Angina -> unstable angina -> AMI -> sudden cardiac death

 Acute coronary syndrome encompasses unstable angina, NSTEMI, STEMI

 Stable angina – transient episodic chest pain d/t myocardial ischaemia,

reproducible, frequency constant over time.usually relieved with rest/NTG.

 Classification of angina – Canadian Cardiovascular Society classification.

 Canadian Cardiovascular Association Classification of
Angina

CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY –

PAIN OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS

CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN

OCCURS ON MINIMAL EXERTION

CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT

PAIN, PAIN AT REST
 UNSTABLE ANGINA –
 Pain occurring at rest – duration > 20min, within one week of first visit
 New onset angina – ~ Class 2 severity, onset with last 2 months
 Worsening of chest pain – increase by at least 1 class, increases in
frequency, duration
 Angina becoming resistance to drugs that previously gave good control.

 NB! ECG – normal, ST depression(>0.5mm), T wave changes

 ACUTE MYOCARDIAL INFARCTION –
 ECC/ACC DEFN –rise and fall in cardiac enzymes with one or more of the
following:
 Ischaemic type chest pain/symptoms
 ECG changes – ST changes, pathological Q waves
 Coronary artery intervention data
 Pathological findings of an acute MI

 NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES
 STEMI = ST ELEVATION ON ECG + SYMPTOMS
 WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH
UNSTABLE ANGINA??

 5 -17% suffer an MI within a week after admission.

 3 -15% die within a year.
 ACS PATHOPHYSIOLOGY

 Distruption of coronary artery

plaque -> platelet
activation/aggregation /activation
of coagulation cascade ->
endothelial vasoconstriction -
>intraluminal
thrombus/embolisation ->
obstruction -> ACS
 Severity of coronary vessel
obstruction & extent of
myocardium involved determines
characteristics of clinical
presentation
 APPROACH
 Identifying those with chest pain suggestive of IHD/ACS.
 Thorough history required:
 Character of pain
 Onset and duration
 Location and radiation
 Aggravating and relieving factors
 Autonomic symptoms

 TYPICAL VS ATYPICAL HISTORY

 Failure to recognise symptoms other than chest pain -> approx 2 hr delay in
seeking medical attention
 CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN
(ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE)

CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF

ANGINA
TYPE OF PAIN DULL SHARP/STABBING
PRESSURE/CRUSHING
PAIN
DURATION 2-5 MIN, <20 MIN SECONDSTO
HOURS/CONTINUOUS
ONSET GRADUAL RAPID

LOCATION/CHEST WALL SUBSTERNAL, NOT LATERAL CHEST

TENDERNESS TENDER TO PALP. WALL/TENDER TO PALP.
REPRODUCIBALITY WITH WITH
EXERTION/ACTIVITY BREATHING/MOVING
AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT
 ATYPICAL PAIN

 RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:

 Diabetes, females, non white patients, elderly, dementia, no prior history of MI
 ATYPICAL SYMPTOMS:
 GIT symptoms
 Syncope
 SOB
 Pleuritic/positional pain
 Chest wall tenderness
 No chest pain/symptoms

 NRMI 2 STUDY – MI without chest pain -> increased risk of death (23% vs 9%)
 More complications – hypotension,heart failure, stroke
 Delayed ED presentation, delayed intervention
 RISK STRATIFICATION IN ACS

 Reasons :
 Provides prognostic information

 Determines treatment and level of intervention -> low risk patients –early
discharge, high risk -> admission to high care

 Helps decongest the ED and make available medical resources to more

needy patients

 Risk stratification should be ongoing – at admission, 6-8 hrs, 24hrs,

discharge
 TOOLS USED IN RISK STRATIFICATION

 HISTORY

 ECG

 BIOCHEMICAL MARKERS
 ECG

 First point of entry into ACS algorithm

 Abnormal or normal

 Neither 100% sensitive or 100% specific for AMI

 Single ECG for AMI – sensitivity of 60%, specificity 90%

 Represents single point in time –needs to be read in context

 Normal ECG does not exclude ACS – 1-6% proven to have AMI, 4%
unstable angina
 GUIDELINES:
 Initial 12 lead ECG – goal door to ECG time 10min, read by experienced
doctor (Class 1 B)
 If ECG not diagnostic/high suspicion of ACS – serial ECGs initially 15 -30
min intervals (Class 1 B)

 ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B)

 Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs

(Class 2a B)
 BIOCHEMICAL MARKERS

 IDEAL MARKER:
 High concentration in myocardium
 Myocardium specific
 Released early in injury
 Proportionate to injury
 Non expensive testing

 Troponins
 CKMB
 Myoglobin
 Other markers
 TROPONINS T/I

 Troponin T vs I –
 both equivalent in diagnostic and prognostic abilities ( except in renal
failure – Trop T less sensitive)

 Elevation ~ 2hrs to 12hrs

 ~30 – 40% of ACS patients without ST elevation – had normal CKMB but
elevated troponins on presentation

 Meta-analysis (Heindereich et al) – odds of death increased 3 to 8 fold with

positive troponin
 Mortality at 42 days in troponin positive patients
 MYOGLOBIN

 Rapid release within 2 hours

 Not cardiac specific

 Rule out for NSTEMI rather than rule in.

CKMB
Used in conjunction with troponins
Useful in diagnosing re-infarction
 MARKER CHANGE SCORES

 2 hour delta CKMB mass

 Aim – to exclude MI within 6hrs of symptom onset

 Determine changes in serum marker levels over certain time intervals –

delta values

 Increasing values while still within normal range suggestive of ischaemia –

more rapid anti- ischaemic mxn.
 OTHER MARKERS

 INDICATORS OF INFLAMMATION OR ACTIVATION OF

COAGULATION CASCADE:
 Myeloperoxidase, soluble CD40 ligand, IL6, hsCRP, d dimer, prothrombin
fragment 1 & 2

 Elevated before onset of irreversible injury

 Lack specificity

 Complex lab assays

 ISCHAEMIA MODIFIED ALBUMIN

 Measured with albumin cobalt binding assay

 In ischaemia -> decreased binding of albumin to cobalt
 Increased with minutes of ischaemia – elevated for 6-12hrs – gone by 24hrs
 ~90% negative predictive value
 Combined with myoglobin/CKMB/troponin – increases diagnostic
sensitivity of ischaemia by 40%
 Possible role for rule criteria in low risk patients
 Positive IMA – high risk patients – more aggressive mxn
 Positive in hypoxic disorders – poor specificity in this setting
 B –type Natriuretic Peptide:
 released from heart muscle in response to increased ventricular wall stress.
 Studies – BNP not a specific marker but a strong predictor of ACS
especially in patients with chest pain, no ECG changes, non diagnostic
troponins.
 Also positive in heart failure, PE, atrial arrythmias, renal failure

 Pregnancy Associated Plasma Protein A (PAPP-A):

 Released when plaque ruptures
 Predictor of ischaemia
 HEART FATTY ACID BINDING PROTEIN (HF ABP)
 Identifies AMI <4hrs after onset
 Protein involved in myocardial lipid synthesis, but also expressed outside
heart
 Therefore may be sensitive but not specific for injury
 Possible role in multi-marker strategy

 IMAGING MODALITIES
 Cardiac MRI
 Multidetector CT for coronary calcification
 Coronary CT angiography
 Undergoing clinical evaluation
 2007 ACC/AHA guidelines:
 Cardiac biomarkers measured in all patients with suspicion of ACS (Class
1 B)
 Troponin preferred marker( Class 1 B)
 If troponin negative within 6 hours of onset, repeat 8-12hours later(Class 1
B)
 Remeasuring of positive biomarkers to determine infarct size/necrosis
(Class 2a B)
 Patients presenting within 6 hours of symptom onset – myoglobin in
conjunction with troponin measured (Class 2b B)
 2hr delta CKMB/Delta troponin considered in <6hr presentation (Class 2b
B)
 BNP level – for global risk assessment(Class 2b B)
 Class 3 – AST/LDH/CK without CKMB
RISK STRATIFICATION MODELS
TIMI RISK SCORE –increase in mortality with increasing score ~40% all
cause mortality at 14 days for patients requiring urgent revascularisation
 WHICH MODEL IS MOST APPROPRIATE??

 2007 ACS/AHA GUIDELINES:

 Risk stratification models useful in decision making with regard to
treatment options ( Class 2a B)
 TIMI vs GRACE vs PURSUIT

 PURSUIT & GRACE risk scores allow better discrimination of in hospital

and 1 year mortality in patients compared to TIMI. (Andrew et al, Risk
scores for risk stratification in ACS …)

 What’s appropriate in our setting???

MANAGEMENT ALGORITHM
Gold Standard for Treatment of ACS

ACC/AHA 2007 Guidelines for the Management of

Patients With Unstable Angina/Non–ST-Elevation
Myocardial Infarction

http://circ.ahajournals.org/cgi/content/full/102/10/1193
Algorithm for evaluation and management of patients suspected of having ACS.
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.
 ACS Overview

 Overview of ACS
 Assessment of “Likelihood of ACS”
 Early Risk Stratification
 Invasive vs Conservative Strategy
 Pharmacotherapy
 Long-term Therapy/Secondary Prevention
 Scope of the Problem
 5 million ER visits nationwide for CP
 800,000 experience an MI each year
 213,000 die from their event
 ½ of those die before reaching the ER

 Pre-CCU, mortality for MI was >30%

 Fell to 15% with CCU
 With current interventions, in hospital mortality of
STEMI is 6-7%
 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; 115:69–171.
 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----]
Pathophysiology of Stable Angina and ACS

Pathophysiology ACS

Decreased O2 Supply

Asymptomatic
•Flow- limiting stenosis
•Anemia
•Plaque rupture/clot

Angina
Increased O2 Demand

O2 supply/demand mismatch→Ischemia

Myocardial ischemia→necrosis
 Pathophysiology of ACS
Evolution of Coronary Thrombosis
Unstable
NSTEMI STEMI
Angina
Non-occlusive
thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus tissue damage & mild
myocardial necrosis ST elevations on
Non specific ECG or new LBBB
ECG ST depression +/-
T wave inversion on Elevated cardiac
Normal cardiac ECG enzymes
enzymes
Elevated cardiac More severe
enzymes symptoms
 STEMI
 Name 3 situations in which you cannot
diagnose STEMI
 STEMI
 Name 3 situations in which you cannot
diagnose STEMI

 Left Ventricular Hypertrophy

 Chronic or Rate Dependent LBBB

 Paced Rhythm
 Cardiac Catheterization
 Name the only 3 situations that demand
emergent cardiac catheterization.
 Cardiac Catheterization
 Name the only 3 situations that demand
emergent cardiac catheterization.

 STEMI or new LBBB

 ACS with hemodynamic or electrical instability
despite optimal medical management
 Uncontrolled CP despite optimal medical
management
 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 LR 7.1 (3.6-14.2)
 Diaphoresis LR 2.0 (1.9-2.2)
 3rd Heart Sound LR 3.2 (1.6-6.5)
 SBP < 80 mm Hg LR 3.1 (1.8-5.2)
 Pulmonary Crackles LR 2.1 (1.4-3.1)

Panju AA. JAMA. 1998;280:1256.

 Likelihood of ACS by Hx/PE

 Clinical Examination – Against AMI

 Pleuritic Chest Pain LR 0.2 (0.2-0.3)
 Sharp or Stabbing Pain LR 0.3 (0.2-0.5)
 Positional Chest Pain LR 0.3 (0.2-0.4)
 Reproducible Chest Pain
LR 0.2-0.4

Panju AA. JAMA. 1998;280:1256.

 Risk Stratification by ECG

 Simple, quick, noninvasive tool

 Universally available, cheap
 Correlates with risk and prognosis
 Guides treatment decisions
 Can identify alternative causes
 Risk Stratification by ECG
 ECG Findings and Associated LR for AMI
 New ST-E > 1mm LR 5.7-53.9
 New Q waves LR 5.3-24.8
 Any ST-E LR 11.2 (7.1-17.8)
 New Conduction Defect LR 6.3 ( 2.5-15.7)
 New ST-D LR 3.0-5.2

 NORMAL ECG LR 0.1-0.4

Panju AA. JAMA. 1998;280:1256.

 Risk Stratification by ECG
CAVEATS

 1-8% AMI have a normal ECG

 Only Approx 50% of AMI patients have

diagnostic changes on their initial ECG

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

 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?
How Predictive is NTG response?
 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. 3rd ed. Rochester, MN:
Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80.
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
 Risk Stratification by Troponin
8 7.5 %
7
6.0 %
Mortality at 42 Days

6
5
4 3.4 % 3.7 %
3
2
1.7 %
1.0 %
1
831 174 148 134 50 67
0
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0  9.0

Cardiac troponin I (ng/ml)

 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.

Combined Sensitivities for ACS
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

• TIMI Risk Score >3 •Hemodynamic instability
•Elecrical instability
• New ST segment
•Refractory angina
•TIMI Risk Score <3 (Esp. Women)
deviation
•PCI in past 6 months •No ST segment deviation
• Positive biomarkers
•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
Specifics of Early Hospital Care

Anti-Ischemic Therapy
Anti-Platelet Therapy

Anticoagulant Therapy
 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-Ischemic Therapy
 Class III
 Nitrates if BP<90 mmHg or RV infarction
 Nitrates within 24-hrs of Sildenafil or 48 hrs of Tadalafil
 Immediate release dihydropyradine Ca-blockers in the
absence of B-Blocker therapy
 IV ACE-inhibitors
 IV B-blockers in patients with acute HF, Low output state
or cardiogenic shock, PR interval >0.24 sec, 2nd or 3rd
degree heart block, active asthma, or reactive airway
disease
 NSAIDS and Cox-2 inhibitors
 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

 Statin Evidence: MIRACL Study
Primary Efficacy Measure
Placebo 17.4%
15
14.8%
Cumulative Incidence (%)

Atorvastatin
10

Time to first occurrence of:

• Death (any cause)
• Nonfatal MI
5
• Resuscitated cardiac arrest
• Worsening angina with new Relative risk = 0.84
objective evidence and P = .048
urgent rehospitalization 95% CI 0.701-0.999
0
0 4 8 12 16
Time Since Randomization (weeks)

Schwartz GG, et al. JAMA. 2001;285:1711-1718.

 Statin Evidence: MIRACL Study
Fatal and Nonfatal Stroke
2
Cumulative Incidence (%)

1.5
Placebo

1
Atorvastatin

0.5
Relative risk = 0.49
P = .04
95% CI 0.24-0.98
0
0 4 8 12 16
Time Since Randomization (weeks)
Waters DD, et al. Circulation. 2002;106:1690-1695. S24
 PROVE-IT Trial
All-Cause Death or Major CV Events
in All Randomized Subjects
30
Pravastatin 40mg
25 (26.3%)

20
%
Atorvastatin 80mg
with 15 (22.4%)
Event
10
16% RR
5 (P =
0.005)
0
0 3 6 9 12 15 18 21 24 27 30
Months of Follow-up
 Summary of PROVE-IT Results
In patients recently hospitalized within 10 days for an
acute coronary syndrome:
 “Intensive” high-dose LDL-C lowering (median LDL-C 62
mg/dL) compared to “moderate” standard-dose lipid-lowering
therapy (median LDL-C 95 mg/dL) reduced the risk of all cause
mortality or major cardiac events by 16% (p=0.005)
 Benefits emerged within 30 days post ACS with continued benefit
observed throughout the 2.5 years of follow-up
 Benefits were consistent across all cardiovascular endpoints,
except stroke, and most clinical subgroups
Invasive vs Conservative
Strategies
 Invasive vs Conservative Strategy
Clinical Trials
ISAR-
COOL

VANQWISH (98) ICTUS (05) RITA-3 (02)

MATE VINO

TIMI IIIB (94) TRUCS

TACTICS-
TIMI 18 (01)
Weight of FRISC II (99)
the evidence

Conservative Invasive
Strategy Favored No difference Strategy Favored
N=920 N=2,874 N=7,018
How Early is Early?
 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
New UA/NSTEMI
Patient Groups at
Discharge

Medical Therapy Bare Metal Stent Drug Eluting

without Stent Group Stent Group

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

Indication for
Anticoagulation?

Yes No
Add: Warfarin (INR 2.0 to 2.5) Continue with dual antiplatelet
(Class IIb, LOE: B) therapy as above

Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 11. INR = international normalized ratio; LOE = level of evidence.
 Secondary Prevention
Class III

 Hormone Replacement Therapy

 Antioxidants (Vit C, Vit E)
 Folic Acid
 Summary
 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
Questions?