MOCHAMMAD FATHONI

DEPART. OF CARDIOLOGY,
MEDICAL FACULTY,
SEBELAS MARET UNIVERSITY,
Dr. MOEWARDI HOSPITAL, SOLO

FAST RESPONSE OF

Acute Coronary Syndrome

16 Sept.2012
 Acute Coronary Syndrome
 Clinical syndromes caused by acute myocardial ischemia
 Unstable angina

 Angina at rest or new onset angina, accelerating

symptoms
 No detectable increase of biomarkers

 Non-ST-elevation MI

 Angina at rest or new onset angina, accelerating

symptoms
 Detectable release of biomarkers

 ST-elevation MI

 Clinical presentation of acute myocardial infarction with

EKG evidence of ST-segment elevation
 Acute Coronary Syndromes

 Unstable Angina
Similar
 Non-ST-Segment pathophysiology
Elevation MI Similar presentation
(NSTEMI) and early
management rules
 ST-Segment Elevation
MI (STEMI)
STEMI requires
evaluation for acute
reperfusion and
intervention
 Diagnosis of Acute MI
STEMI / NSTEMI
 At least 2 of the
following
Ischemic
symptoms
Diagnostic ECG
changes
Serum cardiac
marker elevations
 Diagnosis of Angina
 Typical angina : three of the following
 Substernal chest discomfort
 Onset with exertion or emotional stress
 Relief with rest or nitroglycerin

 Atypical angina
 2 of the above criteria

 Noncardiac chest pain

 1 of the aboveTypical angina—All
 Diagnosis of Unstable Angina
 Patients with typical angina - An episode of angina
 Increased in severity or duration

 Has onset at rest or at a low level of exertion

 Unrelieved by the amount of nitroglycerin or rest

that had previously relieved the pain
 Patients not known to have typical angina
 First episode with usual activity or at rest within
the previous two weeks
 Prolonged pain at rest
U NSTABLE
NSTEMI STEMI
ANGINA
Non Occluding thrombus Complete thrombus
occlusive sufficient to cause occlusion
tissue damage & mild
thrombus
myocardial necrosis ST elevations on
Non specific ECG or new LBBB
ST depression +/-
ECG T wave inversion on Elevated cardiac
ECG enzymes
Normal Elevated cardiac More severe
cardiac enzymes symptoms
enzymes
Troponin
Ttt I
rise
 Expanding Risk Factors
 Smoking
 Hypertension
 Diabetes Mellitus
 Dyslipidemia
 Low HDL < 40
 Elevated LDL / TG
 Family History—event
in first degree relative
>55 male/65 female
 Age-- > 45 for
male/55 for female
 Chronic Kidney
Disease
 Lack of regular
physical activity
 Obesity
 Lack of diet rich in
fruit, veggies, fiber
Take note of these common signs of an acute
coronary syndrome:
•Chest pain or discomfort, which may involve
pressure, tightness or fullness
•Pain or discomfort in one or both arms, the jaw,
neck, back or stomach
•Shortness of breath
•Feeling dizzy or lightheaded
•Nausea
•Sweating
These symptoms should be taken seriously. If you
experience chest pain or other symptoms, call 118
immediately.
118
Acute Management

 Initial evaluation
& stabilization
 Efficient risk
stratification
 Focused cardiac
care
 Evaluation
 Efficient & direct history Occurs
 Initiate stabilization simultaneously
interventions

Plan for moving rapidly to Directed Therapies

indicated cardiac care are
Time Sensitive!
 Chest pain suggestive of ischemia

Immediate assessment within 10 Minutes

Initial labs Emergent History &
and tests care Physical
 12 lead ECG  IV access  Establish

 Obtain initial  Cardiac diagnosis

cardiac enzymes monitoring  Read ECG

 electrolytes, cbc  Oxygen  Identify

lipids, bun/cr,  Aspirin complications

glucose, coags  Nitrates  Assess for

 CXR reperfusion
 Focused History
 Aid in diagnosis and rule out
other causes  Reperfusion questions
 Palliative/Provocative
factors  Timing of
 Quality of discomfort presentation
 Radiation  ECG c/w STEMI
 Symptoms associated
 Contraindication to
with discomfort
fibrinolysis
 Cardiac risk factors
 Degree of STEMI
 Past medical history -
risk
especially cardiac
 Targeted Physical
 Recognize factors that
 Examination
increase risk
 Vitals
 Hypotension
 Cardiovascular
 Tachycardia
system
 Pulmonary rales,
 Respiratory
system  Pulmonary edema,
 Abdomen
 New murmurs/heart sounds
 Diminished peripheral pulse
 Neurological
status  Signs of stroke

 ECG assessment

ST Elevation or new LBBB

STEMI

ST Depression or dynamic
T wave inversions
NSTEMI

Non-specific ECG
Unstable Angina
Normal or non-diagnostic EKG
ST Depression or Dynamic T wave
Inversions
ST-Segment Elevation MI
 Cardiac markers
 CK-MB isoenzyme
 Troponin ( T, I)
 Rises 4-6 hours after
 Very specific and more injury and peaks at 24
sensitive than CK hours
 Rises 4-8 hours after  Remains elevated 36-48
injury hours
 May remain elevated  Positive if CK/MB > 5%
for up to two weeks of total CK and 2 times
 Can provide prognostic normal
information  Elevation can be
 Troponin T may be predictive of mortality
elevated with renal dz,  False positives with
poly/dermatomyositis exercise, trauma, muscle
 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, 2007:773–80.
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
 Risk Stratification
Based on initial
Evaluation, ECG, and
STEMI Cardiac markers
Patient?
YES NO

- Assess for reperfusion UA or NSTEMI

- Select & implement - Evaluate for Invasive
reperfusion therapy vs. conservative
- Directed medical treatment
therapy - Directed medical
therapy
 Risk Stratification to Determine the Likelihood of
Acute Coronary Syndrome
Assessment Findings Findings Findings
indicating HIGH indicating indicating LOW
likelihood of ACS INTERMEDIATE likelihood of ACS
likelihood of ACS in absence of
in absence of high- or
high-likelihood intermediate-
findings likelihood findings
History Chest or left arm Chest or left arm Probable ischemic
pain or pain or symptoms
discomfort as discomfort as Recent cocaine
chief symptom chief symptom use
Reproduction of Age > 50 years
previous
documented
angina
Known history of
coronary artery
disease,
including
myocardial
Risk Stratification to Determine the Likelihood of
Acute Coronary Syndrome

Physical New transient Extracardiac Chest

examination mitral vascular discomfort
regurgitation, disease reproduced by
hypotension, palpation
diaphoresis,
pulmonary
edema or rales
ECG New or Fixed Q waves T-wave
presumably Abnormal ST flattening or
new transient segments or T inversion of T
ST-segment waves not waves in leads
deviation (> documented to with dominant R
0.05 mV) or T- be new waves
wave inversion Normal ECG
(> 0.2 mV) with
symptoms
Serum cardiac Elevated Normal Normal
Table 1. Short-Term Risk of Death or Nonfatal MI in Patients With UA

Low Risk (No

Intermediate high- or
High Risk (At Risk (No high- intermediate-risk
least 1 of the risk feature but feature but may
following must have 1 of have any of the
features must be the following following
Feature present) features) features)
Accelerating Prior MI,
History
tempo of peripheral or
ischemic cerebrovascular
symptoms in disease, or
preceding 48 hrs CABG; prior
aspirin use
Table 1. Short-Term Risk of Death or Nonfatal MI in Patients With UA

Low Risk (No

Intermediate high- or
High Risk (At Risk (No high- intermediate-risk
least 1 of the risk feature but feature but may
following must have 1 of have any of the
features must be the following following
Feature present) features) features)
Character of Prolonged Rest angina (<20 New-onset CCS
pain ongoing (>20 min or relieved Class III or IV
min) rest pain with rest or angina in the
no relieved sublingual NTG past 2 wk with
with rest or moderate or
sublingual NTG high likelihood
of CAD
 Intermediate Risk
High Risk (At least (No high-risk Low Risk (No high- or
intermediate-risk
1 of the following feature but must
feature but may have
features must be have 1 of the any of the following
Feature present) following features) features)

ECG findings Angina at rest with T-wave inversions Normal or

transient ST- >0.2 mV unchanged ECG
segment changes during an episode
>0.05 mV of chest
discomfort
Bundle-branch Pathological Q
block, new or waves
presumed new
Sustain VT
 Intermediate Risk
High Risk (At least (No high-risk Low Risk (No high- or
intermediate-risk
1 of the following feature but must
feature but may have
features must be have 1 of the any of the following
Feature present) following features) features)

Cardiac markers Markedly elevated Slightly elevated Normal

(eg, TnI >0.1 (eg, Tn I >0.01 but
ng/mL) <0.1 ng/mL)

C
 Cardiac Care Goals
Decrease amount of myocardial
necrosis
Preserve LV function

Prevent major adverse cardiac

events
Treat life threatening complications
 STEMI CARDIAC CARE
Assessment
 Time since onset of symptoms
 90 min for PCI / 12 hours for fibrinolysis

 Is this high risk STEMI?

 KILLIP classification
 If higher risk may manage with more invasive rx

 Determine if fibrinolysis candidate

 Meets criteria with no contraindications

 Determine if PCI candidate

 Based on availability and time to balloon rx
 Fibrinolysis indications
 ST segment elevation >1mm in
two contiguous leads
 New LBBB

 Symptoms consistent with

ischemia
 Symptom onset less than 12 hrs
prior to presentation
 Absolute contraindications for fibrinolysis
therapy in patients with acute STEMI
 Any prior ICH
 Known structural cerebral vascular lesion
 Known malignant intracranial neoplasm
(primary or metastatic)
 Ischemic stroke within 3 months EXCEPT acute
ischemic stroke within 3 hours
 Suspected aortic dissection
 Active bleeding or bleeding diathesis (excluding
menses)
 Significant closed-head or facial trauma within 3 mont.
Relative contraindications for fibrinolysis
therapy in patients with acute STEMI
 History of chronic, severe, poorly controlled
hypertension
 Severe uncontrolled hypertension on
presentation (SBP greater than 180 mm Hg
or DBP greater than 110 mmHg)
 History of prior ischemic stroke greater than
3 months, dementia, or known intracranial
pathology not covered in contraindications
 Traumatic or prolonged (greater than 10
minutes) CPR or major surgery (less than 3
weeks)
Relative contraindications for
fibrinolysis therapy in patients with
acute STEMI
 Recent (within 2-4 weeks) internal bleeding
 Noncompressible vascular punctures
 For streptokinase/anistreplase: prior
exposure (more than 5 days ago) or prior
allergic reaction to these agents
 Pregnancy
 Active peptic ulcer
 Current use of anticoagulants: the higher
the INR, the higher the risk of bleeding
 SUMMARY
 ACS includes UA, NSTEMI, and STEMI
 Assesment the diagnosis of ACS
 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
 SUMMARY
STEMI CARE CVICU
 Monitor for complications:
 recurrent ischemia, cardiogenic shock, ICH, arrhythmias

 Review guidelines for specific management of

complications & other specific clinical scenarios
 PCI after fibrinolysis, emergent CABG, etc…

 Decision making for risk stratification at hospital

discharge and/or need for CABG
THANK YOU
FOR YOUR
ATTENTION
 STEMI cardiac care
 STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred if: PCI preferred if:

 <3 hours from onset
 PCI not available/delayed
 door to balloon > 90min
 door to balloon minus
door to needle > 1hr
 Door to needle goal <30min
 No contraindications
 PCI available
 Door to balloon < 90min
 Door to balloon minus
door to needle < 1hr
 Fibrinolysis
contraindications
 Late Presentation > 3 hr
 High risk STEMI
 Killip 3 or higher
 STEMI dx in doubt
Comparing outcomes
 Medical Therapy
MONA + BAH
 Morphine (class I, level C)
 Analgesia 2-5 mg , maximum 20 mg /day
 Reduce pain/anxiety—decrease sympathetic tone, systemic
vascular resistance and oxygen demand
 Careful with hypotension, hypovolemia, respiratory
depression

 Oxygen (2-4 liters/minute) (class I, level C)

 Up to 70% of ACS patient demonstrate hypoxemia
 May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation
 Nitroglycerin (class I, level B)
 Analgesia—titrate infusion to keep patient pain free
 Dilates coronary vessels—increase blood flow
 Reduces systemic vascular resistance and preload
 Careful with hypotension, bradycardia, tachycardia, RV
infarction

 Aspirin (160-325mg chewed & swallowed) (class I, level A)

 Irreversible inhibition of platelet aggregation
 Stabilize plaque and arrest thrombus
 Reduce mortality in patients with STEMI
 Careful with active PUD, hypersensitivity, bleeding
disorders
 Beta-Blockers (class I, level A)
 14% reduction in mortality risk at 7 days at 23% long term
mortality reduction in STEMI
 Approximate 13% reduction in risk of progression to MI
in patients with threatening or evolving MI symptoms
 Be aware of contraindications (CHF, Heart block,
Hypotension)

 ACE-Inhibitors / ARB (class I, level A)

 Start in patients with anterior MI, pulmonary congestion,
LVEF < 40% in absence of contraindication/hypotension
 Start in first 24 hours
 ARB as substitute for patients unable to use ACE-I
 Heparin (class I, level C to class IIa, level C)
 LMWH or UFH (max 4000u bolus, 1000u/hr)
 Indirect inhibitor of thrombin
 less supporting evidence of benefit in era of reperfusion

 Adjunct to surgical revascularization and thrombolytic /

PCI reperfusion
 Coordinate with PCI team (UFH preferred)

 Used in combo with aspirin and/or other platelet inhibitors

 Changing from one to the other not recommended

 Additional medication therapy
 Clopidogrel (class I, level B)
 Irreversible inhibition of platelet aggregation
 Used in support of cath / PCI intervention or if
unable to take aspirin
 3 to 12 month duration depending on scenario

 Glycoprotein IIb/IIIa inhibitors

(class IIa, level B)
 Inhibition of platelet aggregation at final common
pathway
 In support of PCI intervention as early as possible
prior to PCI
 Additional medication therapy

 Aldosterone blockers (class I, level A)

 Post-STEMI patients
No significant renal failure (cr < 2.5
men or 2.0 for women)
No hyperkalemis > 5.0

LVEF < 40%

Symptomatic CHF or DM
 STEMI care CCU
 Monitor for complications:
 recurrent ischemia, cardiogenic shock, ICH, arrhythmias

 Review guidelines for specific management of

complications & other specific clinical scenarios
 PCI after fibrinolysis, emergent CABG, etc…

 Decision making for risk stratification at hospital

discharge and/or need for CABG
 Unstable angina/NSTEMI
cardiac care
 Evaluate for conservative vs. invasive therapy
based upon:
 Riskof actual ACS
 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
 ACS risk criteria
Low Risk ACS Intermediate Risk
No intermediate or high ACS
risk factors Moderate to high likelihood
of CAD
<10 minutes rest pain
>10 minutes rest pain,
Non-diagnositic ECG now resolved

Non-elevated cardiac T-wave inversion > 2mm

markers
Slightly elevated cardiac
Age < 70 years markers
 High Risk ACS
Elevated cardiac markers
New or presumed new ST depression
Recurrent ischemia despite therapy
Recurrent ischemia with heart failure
High risk findings on non-invasive stress test
Depressed systolic left ventricular function
Hemodynamic instability
Sustained Ventricular tachycardia
PCI with 6 months
Prior Bypass surgery
 Low Intermediate High
risk risk risk

Chest Pain
center
Conservative Invasive
therapy therapy
 Invasive therapy option
UA/NSTEMI
 Coronary angiography and revascularization
within 12 to 48 hours after presentation to ED
 For high risk ACS (class I, level A)
 MONA + BAH (UFH)
 Clopidogrel
 20% reduction death/MI/Stroke – CURE trial
 1 month minimum duration and possibly up to 9 months
 Glycoprotein IIb/IIIa inhibitors
 Conservative Therapy for
UA/NSTEMI
 Early revascularization or PCI not planned
 MONA + BAH (LMW or UFH)
 Clopidogrel
 Glycoprotein IIb/IIIa inhibitors
 Only in certain circumstances (planning PCI, elevated TnI/T)
 Surveillence in hospital
 Serial ECGs
 Serial Markers
 Secondary Prevention
 Disease
 HTN, DM, HLP

 Behavioral
 smoking, diet, physical activity, weight

 Cognitive
 Education, cardiac rehab program
 Secondary Prevention
disease management
 Blood Pressure
 Goals < 140/90 or <130/80 in DM /CKD
 Maximize use of beta-blockers & ACE-I

 Lipids
 LDL < 100 (70) ; TG < 200
 Maximize use of statins; consider fibrates/niacin first
line for TG>500; consider omega-3 fatty acids

 Diabetes
 A1c < 7%
 Secondary prevention
behavioral intervention
 Smoking cessation
 Cessation-class, meds, counseling
 Physical Activity
 Goal 30 - 60 minutes daily
 Risk assessment prior to initiation

 Diet
 DASH diet, fiber, omega-3 fatty acids
 <7% total calories from saturated fats
 Medication Checklist
after ACS
 Antiplatelet agent
 Aspirin* and/or Clopidorgrel
 Lipid lowering agent
 Statin*
 Fibrate / Niacin / Omega-3

 Antihypertensive agent
 Beta blocker*
 ACE-I*/ARB
 Aldactone (as appropriate)
 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
THANK YOU
FOR YOUR
ATTENTION