Management of Acute

Coronary Syndrome
 Objective
Definition
Pathophysiology
Different Types of ACS
Diagnosis of ACS
Initial Management
Risk Stratification
Different case scenarios
Invasive vs Conservative Strategies.
Secondary Prevention.
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
Flow- limiting stenosis
Anemia
Plaque rupture/clot

Increased O2 Demand

O2 supply/demand
mismatch→Ischemia
A
Myocardial nA
ischemia→necrosis gisy
nm
Pathophysiology of ACSEvolution of
Coronary Thrombosis
Unstable
STEMI
Angina NSTEMI
Non Non-occlusive Complete
occlusive thrombus thrombus
thrombus sufficient to cause occlusion
Non specific tissue damage & ST elevations
ECG mild on
Normal myocardial ECG or new
cardiac necrosis LBBB
enzymes ST depression +/- Elevated
T wave inversion cardiac
on enzymes
ECG More severe
Elevated cardiac symptoms
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 Risk Stratify for Short-term

Clinical Presentation Adverse Outcomes
Represents an ACS
Secondary to CAD
Location of Pain
 Likelihood of ACS by Hx/PE
History/Examination Suggesting AMI
Pain in Chest or Left Arm
CP Radiation LR 2.7
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 –
Pleuritic Chest Pain
Against AMI
Sharp or Stabbing Pain
Positional Chest Pain
Reproducible Chest Pain
LR 0.2 (0.2-0.3)
LR 0.3 (0.2-0.5)
LR 0.3 (0.2-0.4)
Panju AA. JAMA. 1998;280:1256.
LR 0.2-0.4
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.
 I aV V V
Inferior Wall MI
I R 1 4
I aV V V
I L 2 5
I aV V V
II F
aV V3 V6
I R 1 4 Lateral Wall MI
I aV V V
I L 2 5
I aV V V
I aV V V
I F 3 6 Anteroseptal
I R 1 4
I aV V V MI
I L 2 5
 Posterior MI
ST elevation in inferior & ST depresssion in
lead V1-V2

Always get Posterior ECG:

V7- Posterior Axillary line
V8- B/w V7 & V9
V9- Inerscapular border
 Right Sided EKG
ST elevation in RV 4 is suggestive
of RV MI

RVI occurs
around 40% in
V V
inferior MI’s
2 1 Hypotension

R R
Jugular vein distention
Dry lung sounds
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
%

%
%

%
%
83 17 14 13 5 6
1 4 8 4 0 7
≥

M
o
rt
 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.

 CASE 1
65 year Pakistani male
Known case of DM -20 years, HTN -15 years, Hyperlipidemic
Presented with ER with complaint of Epigestric pain,
Nausea and One episode of Vomiting and Dizziness.
BP: 80/60 mmHg
Treated by GP with IV Fluids , Metoclopromide, PPI and
Antacid
BP improved 110/70 mmHg, No vomiting but still persisting
pain in epigestric region.
ECG
 Case 2
58 year Indian male
Known case of DM and HTN for more than
10 years.
Presented to ER with c/o Left sided
intermittent Chest pain for last 03 days and
more pain for last 02 Hrs.
ECG
Troponin was Negative and pain was relieved
after 10-15 minutes in ER

What to do Next?
Patient came after 03 Hrs with same pain but
severe in intensity.
2 ECG
nd
 Case
72 year male
Known case of HTN and Ex-Smoker.
Presented to ER with Dizziness , sweating for
3 Hrs.
On arrival BP: 160/90 mmHg, HR: 85/min
and he was sweating
ECG
 CASE
45 year male
Smoker , DM and Obese
Recent History of Hospitalization for
Pneumonia.
Presented to ER with 05 Hr History of Left
Chest pain and Shortness of Breath.
O/E : BP 100/70 mmHg, HR :110 /min
R/R 35/min, O2 Sat: 90% on room air.
CVS Ex: S1+S2 , Chest Ex: Scattered Crackles
more on Left Chest
 Case
32 yo female with crushing cp, sob and
diaphoresis
Meds/PMH/Soc Hx/Past Surg Hx all negative
120/70, 90, 18, RA Sat=97%
Case
Case : EKG After 1 NTG

Diagnosis?
 Prinzmetal's Angina
Coronary artery spasm
Typically occurs at rest
2/3rds have CAD
Spasm can be induced during angiogram
Rx with nitrates and Ca channel blockers
 Case
50 yo male pressure like chest pain
PMH: DM, Htn, Elevated cholesterol
Meds: Insulin, HCTZ, Tenormin, Lipitor
130/70, 70, 18, RA Sat=96%
Exam: nl
EKG with CP
Pain Free After 1 NTG

Diagnosis?
 Wellens Syndrome
Isoelectric or minimally  ST followed by
concave or straight ST and a symmetrically
inverted T wave
Most common V2-V3, and V4-V6
Highly suggestive critical LAD stenosis

http://
Diagnostic limitations
History:
25% have ‘atypical’ histories
ECG:
55% of pts with AMI have a
normal 1ST 12-lead ECG
Convential Cardiac Markers:
Normal for the first 3- 4 hours
Combined Sensitivities for ACS
Early
Invasive

Conservati
ve
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 Hig
Intermed h
iate
 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 TIMI Risk Score <3 (Esp. Women)
New ST segment instability
deviation Elecrical instability
No ST segment deviation
Positive biomarkers Refractory angina Negative Biomarkers
PCI in past 6 months
CABG
EF <40%

Coronary angiography Recurrent Signs/Symptoms Remains Stable

(24-48 hours) Heart failure ↓
Assess EF and/or Stress Testing
Arrhythmias
↓
EF<40% OR Positive stress
Go to Angiography
Specifics of Early Hospital Care

Anti-Ischemic Therapy
Anti-Platelet Therapy
Anticoagulant Therapy
 Early Hospital CareAnti-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 CareAnti-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 CareAnticoagulant
Therapy
Class I
Unfractionated Heparin
Enoxaparin
Bivalarudin
Fondaparinux

Relative choice depends on invasive vs

conservative strategy and bleeding risk
Early Hospital CareStatin Therapy

MIRACL TrialInclusion 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%
1
5
14.8%

Atorvastatin
1
0
Time to first occurrence of:
Death (any cause)
Nonfatal MI
5 Resuscitated cardiac arrest
Worsening angina with new Relative risk = 0.84P = .048
objective evidence and urgent 95% CI 0.701-0.999
rehospitalization
C
0
u
0 4 8 1 1
m 2 6
u Time Since Randomization (weeks)
l
Schwartz
a GG, et al. JAMA. 2001;285:1711-1718.
t
 Statin Evidence: MIRACL Study
Fatal and Nonfatal Stroke
2

Placebo
1
.
5

1
Atorvastatin

0
.
Relative risk = 0.49
5 P = .04
C 95% CI 0.24-0.98
u
m 0
u 0 4 8 1 1
l 2 6
Time Since Randomization (weeks)
a
t DD, et al. Circulation. 2002;106:1690-1695.
Waters S2
i 4
 PROVE-IT Trial
All-Cause Death or Major CV Events in All Randomized Subjects

3
0
Pravastatin
2 40mg
5 (26.3%)
2
% 0
Atorvastatin
with 1 80mg
Even 5 (22.4%)
t 1
0
16% RR
5
(P =
0.005)
0
0 3 6 9 1 1 1 2 2 2 3
2 5 8 1 4 7 0
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
 Secondary PreventionClass 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
 Secondary PreventionClass III

Hormone Replacement Therapy

Antioxidants (Vit C, Vit E)
Folic Acid
New and Controversial
Drug Therapies
 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
J Am Coll Cardiol. 2016;68(10):1082-1115. oi:10.1016/j.jacc.2016.03.513
J Am Coll Cardiol. 2016;67(7):853-879. doi:10.1016/j.jacc.2015.09.011
Waters DD, et al. Circulation. 2002;106:1690-1695.
Panju AA. JAMA. 1998;280:1256
Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40
Am J Med 2002, 90:1264-1265
Ann Emerg Med 2005; 45:581-585
Ann Int Med 2003; 139:979-986
N Engl J Med. 2001;344:1939-1942
Questions?