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Diagnosing Acute

Coronary Syndrome

Adapted from source


Risk Factors
 Smoking  Age-- > 45 for
 Hypertension male/55 for female
 Diabetes Mellitus  Chronic Kidney
Disease
 Dyslipidemia  Lack of regular
 Low HDL < 40 physical activity
 Elevated LDL / TG  Obesity
 Family History—event  Lack of Etoh intake
in first degree relative  Lack of diet rich in
>55 male/65 female fruit, veggies, fiber
ACUTE CORONARY SYNDROME

 No ST Elevation ST Elevation
Unstable Angina Myocardial Infarction
NSTEMI (Trop pos.)
ECG assessment

ST Elevation or new LBBB


STEMI

ST Depression or dynamic
T wave inversions
NSTEMI

Non-specific ECG
Unstable Angina
Unstable angina/NSTEMI
cardiac care
 Evaluate for conservative vs. invasive
therapy based upon:
• Risk of actual ACS
• TIMI risk score
• ACS risk categories per AHA guidelines

Low High
Intermediate
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
TIMI Risk Score
Predicts risk of death, new/recurrent MI, need for urgent
revascularization within 14 days
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)
 Surveillance in hospital
 Serial ECGs
 Serial Markers
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 (LMW or UFH)
 Clopidogrel
 20% reduction death/MI/Stroke – CURE trial
 1 month minimum duration and possibly up to 9 months
 Glycoprotein IIb/IIIa inhibitors ?
Biochemical markers
 Troponin: High sensitivity, high specificity
for myocardial tissue
 CK-MB: less tissue specific, but better
specificity for irreversible injury
 Myoglobin: for rapid diagnosis
Low-risk patients
 No recurrence of chest pain within
observational period
 No ST-segment depression
 Negative T waves, Flat T waves, Normal ECG
 No elevation of troponin
 Troponin twice negative

 Conservative strategy
High-risk patients
 Patients with recurrent ischemia
 Recurrent chest pain
 Dynamic ST-segment changes (ST- depression
or transient ST elevation)
 Early post infarction unstable angina
 Elevated troponin levels
 Diabetes
 Hemodynamic instability
 Major arrhythmias (VF, VT)
Acute Coronary Syndromes

ACS with persistent ACS without persistent


ST-segment ST-segment elevation
elevation

Troponin elevated Troponin elevated or not


Chest pain suggestive of ischemia

Immediate assessment within 10 Minutes

Initial labs Emergent History &


and tests care Physical
 12 lead ECG
 IV access  Establish
 Cardiac diagnosis
 Obtain initial cardiac
enzymes monitoring  Read ECG
 FBC, lipids, U+E,
 Oxygen  Identify
LFT, glucose, coags  Aspirin complications
 CXR  Nitrates  Assess for
reperfusion
Focused History
 Aid in diagnosis  Reperfusion
and rule out other questions
causes
 Palliative/Provocative  Timing of
factors presentation
 Quality of discomfort  ECG c/w STEMI
 Radiation  Contraindication to
fibrinolysis
 Symptoms associated
with discomfort  Degree of STEMI risk
 Cardiac risk factors
 Past medical history
-especially cardiac
Targeted Physical
 Examination  Recognize factors that
increase risk
 Vitals • Hypotension
 Cardiovascular • Tachycardia
system
• Pulmonary rales, JVP,
 Respiratory system pulmonary edema,
 Abdomen
• New murmurs/heart
 Neurological status sounds
• Diminished peripheral
pulses
• Signs of stroke
Non-ST-Segment Elevation MI
ST-Segment Elevation MI
New LBBB

QRS > 0.12 sec


L Axis deviation
Prominent R wave V1-V3
Prominent S wave 1, aVL, V5-V6

with t-wave inversion


STEMI cardiac care
 STEP 1: 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 (limb) or 2mm (chest)
 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 (e.g., AVM)
 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 months
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)
 Recent (within 2-4 weeks) internal bleeding
 Noncompressible vascular punctures
 For streptokinase: prior exposure (more than 5 days ago)
or prior allergic reaction to these agents, Aborigines
 Pregnancy
 Active peptic ulcer
 Current use of anticoagulants: the higher the INR, the
higher the risk of bleeding
STEMI cardiac care
 STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred if: PCI preferred if:


 <3 hours from onset  PCI available
 PCI not available/delayed  Door to balloon < 90min
• door to balloon >  Door to balloon minus
90min door to needle < 1hr
• door to balloon minus  Fibrinolysis
door to needle > 1hr contraindications
 Door to needle goal  Late Presentation > 3 hr
<30min  High risk STEMI
 No contraindications • Killup 3 or higher
 STEMI dx in doubt
Medical Therapy

 Morphine (class I, level C)


• Analgesia
• 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 recent ED meds, 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)
• Reassess for therapy as contraindications resolve

 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 (Clexane 30 mg iv or Heparin 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
• 24-48 hours of treatment
• Used in combo with aspirin and/or other platelet
inhibitors
• Changing from one to the other not recommended
 Clopidodrel (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
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
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
 HbA1c < 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)
LAD Stenosis, Wellens Syndrome
Positive Troponin-Non-cardiac
conditions
 Sepsis
 Aortic dissection
 SAH, ICH, seizure, stroke, preeclampsia
 Exacerbation COPD, Pulmonary Hypertension, PE
 Chemotherapy: Antracycline, Cyclophosphamide, 5-
FU, Cisplatin (toxic effect)
 GI-Bleeding (mismatch between oxygen demand
and supply of the myocardium)
 ESKD, rhabdomyelisis
 It is important to note that cardiac troponins are a marker of all heart
muscle damage, not just myocardial infarction. Other conditions that
directly or indirectly lead to heart muscle damage can also increase
troponin levels. Severe tachycardia (SVT, FAF) in an individual with
normal coronary arteries can also lead to increased troponins for
example, presumably due to increased oxygen demand and
inadequate supply to the heart muscle.

 Troponins are also increased in patients with heart failure, where


they also predict mortality and ventricular rhythm abnormalities.
They can rise in inflammatory conditions such as myocarditis and
pericarditis with heart muscle involvement (which is then termed
myopericarditis). Troponins can also indicate several forms of
cardiomyopathy, such as dilated cardiomyopathy,
hypertrophic cardiomyopathy or (left) ventricular hypertrophy,
peripartum cardiomyopathy, Takotsubo cardiomyopathy or
infiltrative disorders such as cardiac amyloidosis.

 Heart injury with increased troponins also occurs in cardiac


contusion, defibrillation and internal or external cardioversion.
Increased troponins are commonly increased in several procedures
such as cardiac surgery and heart transplantation, closure of atrial
septal defects, percutaneous coronary intervention or
radiofrequency ablation.

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