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Non-ST-Segment Elevation Acute Coronary Syndromes: Risk Stratification Based on the ACC/AHA UA / NSTEMI Guidelines. ED Risk Stratification for Chest Pain. For the past 20 years. In 2002: Does this patient need fibrinolytic therapy?

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ED Risk Stratification for Chest Pain

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Non-ST-Segment ElevationAcute Coronary Syndromes:Risk Stratification Based on the ACC/AHA UA / NSTEMI Guidelines


ED Risk Stratification for Chest Pain

For the past 20 years . . .

In 2002:

  • Does this patient need fibrinolytic therapy?

  • Should this patient get anti-thrombin and anti-platelet agents?

  • Can I safely send this patient home?

R/O MI


ED  CCU  Cath Lab Risk Stratification for Chest Pain

Three levels of risk stratification are pertinent to the ED:

  • Low, intermediate, orhigh risk that ischemic symptoms are a result of CAD

  • Low, intermediate, or highrisk of short-term death or nonfatal MI from ACS

  • Dynamic, ongoing risk-oriented evaluation of low- or intermediate-risk patients for “conversion” to high-risk status that is linked to intensity of treatment


Chest Pain

History, Physical

EKG

Definite

Non-Cardiac

STEMI

UA/NSTEMI/

High Risk

Mod Risk

Low Risk

Initial Risk Stratification Scheme


Risk Stratification Tools in the ED

  • History and Physical

  • Standard ECG and Non-standard ECG leads

  • Cardiac Biomarkers

    • Troponin I or T, CK-MB, myoglobin

  • Predictive Indices / Schemes

  • Non-Invasive Imaging Studies

    • Echocardiogram

    • Exercise testing

    • Technetium-99m-sestamibi: stress and rest


I

IIa

IIb

III

Initial EvaluationRisk Stratification (1)

Early risk stratification by symptoms, physical findings, ECG, cardiac markers

12-lead ECG within 10 min for ongoing pain, or ASAP if pain has resolved at presentation

Cardiac markers, Troponins and CK-MB, for initial assessment

Monitoring, repeat ECG and cardiac markers in 6-12 hours, if initial results normal


I

IIa

IIb

III

Initial EvaluationRisk Stratification (2)

If <6 hours after symptom onset, add early myoglobin or CK-MB to troponin

C-reactive protein, other markers of inflammation

Total CK, SGOT, HBDH, LDH


Clinical Assessment (1)

  • Rapid, focused evaluation

    • Decisions based on this evaluation have substantial clinical and economic consequences

  • Are the symptoms a manifestation of ACS?

    • If so, what is the prognosis?

  • Identify signs of life-threatening instability

  • Triage to most appropriate area

    • Typically an ED or chest pain unit


Clinical Assessment (2)

  • Risk status determined in the ED by:

    • Assessment of anginal symptoms

    • Careful physical examination

    • Electrocardiogram

    • Cardiac biomarkers

    • CAD risk factors

    • Illicit drug use

  • Initial risk stratification assignment drives pace of subsequent evaluation and treatment


Clinical Assessment (3)

  • High-risk features apparent in the ED:

    • Accelerated pattern of angina

    • Ongoing rest pain > 20 min

    • Signs of CHF

    • Hemodynamic instability

    • Arrhythmias - Atrial or ventricular

    • Advanced age (> 75 years)

    • Ischemic ECG changes

    • Elevated cardiac markers


Electrocardiogram

  • Carries diagnostic and prognostic value

  • Especially valuable if captured during pain

  • ST-segment depression or transient ST-segment elevation are primary ECG markers of UA/NSTEMI

    • 75% of patients with + CK-MB do not develop Q waves

    • Differentiation between UA and NSTEMI relies upon positive biomarkers

    • Inverted T-waves suggestive of ischemia, particularly with good chest pain story


Six-Month Mortality by Baseline ECG Findings -GUSTO-IIb Results

10%

ST 

8%

ST 

6%

% Mortality

4%

NS ST-Ts

2%

0%

0

30

60

90

120

150

180

Days from Randomization

Savonitto, JAMA 1999


Biomarkers: CK/CKMB

  • Until recently the principal serum marker used in evaluation of ACS despite known limitations:

    • Low levels in healthy persons limits specificity

    • MB band may be elevated in skeletal muscle damage

    • Different MB isoforms exist in myocardium (MB2) and in plasma (MB1), and differentiating assay is not widely available


Biomarkers: Troponins

  • Very useful in diagnosis and prognosis of ACS

    • Normally not detectable in blood of healthy persons;

    • cTnI or cTnT can be positive with negative CK-MB = “minor myocardial damage”

    • Predictive of MI and death when elevated, independent of CK-MB levels

    • Elevated troponins validated as a predictor of enhanced treatment benefit from aggressive therapies (LMW heparins, GP IIb/IIIa inhibitors, early invasive strategy)


Troponin as a Marker of Increased Risk in ACS


Long Term Survival and Troponin-T Status

GUSTO-IIa Results

1-Year Mortality Rates:

Troponin-T Positive: 14%

Troponin-T Negative: 5%

TnT -

p < 0.001

TnT +


Biomarkers: Myoglobin

  • Utility limited by release kinetics (early) and by lack of cardiac specificity

  • Isolated elevation of myoglobin 4-8 hours after pain onset with a a non-diagnostic ECG must be supplemented by a more cardiac-specific marker

  • Sufficiently sensitive that a negative myoglobin 4-8 hours after pain onset is useful in excluding myocardial necrosis


Integration of Biomarkers with Clinical History

  • Time since symptom onset should be a factor in marker selection and in repeat assay strategy

  • Elevated serum levels of troponins persist for 7-14 days after initial release

  • Delta values, as close as 2 hours apart, may be sufficiently sensitive to assist with serial evaluations

  • Serial cardiac marker strategy not specified


Myoglobin

CK-MB (mass)

Troponin T

Myoglobin

CK-MB (mass)

Troponin T

100%

100%

75%

75%

50%

50%

25%

25%

0%

0%

3

4

5

6

8

12

3

4

5

6

8

12

Serial Cardiac Markers

Serial Testing in 309 Patients with Suspected MI

Sensitivity

Hours After Symptom Onset

Hours After Symptom Onset

Hours After Symptom Onset

Winter, Circulation, 1995


Biomarkers: Bedside Testing

  • Consideration of bedside marker assay recommended when hospital lab turnaround time > 30-60 minutes

  • Ready-for-use availability must be balanced against need for stringent QC and training of ED personnel, CLIA concerns, political hazards, etc

  • Prognostic value limited because many assays are qualitative, not quantitative


“Vein-to-Brain” Reporting Times for Cardiac Markers - St. Agnes Hospital

Bedside Test (mean=15 mins)

Laboratory Test (mean=128 mins)

180

160

140

120

100

Reporting Times (mins)

"Vein-to Brain"

80

60

40

20

n = 939

SD = 46.74

0

Test Type

Christenson R: Md Med 2001 Spring:Suppl:98-103


Distribution of Reporting Times for Cardiac Markers - St. Agnes Hospital

284 mins = Latest Reporting Time

(201.3 mins)

95th percentile

(147 mins)

75th percentile

(Median , 117 mins)

50th percentile

Range of Lab Reporting Times

(85 mins)

25th percentile

(62.6 mins)

5th percentile

40 mins = Earliest Reporting Time

Christenson R: Md Med 2001 Spring:Suppl:98-103


Noninvasive Studies

  • Guidelines do not consider use of these tests in the ED setting, although:

    • Many EDs now use rest sestamibi scanning in the risk stratification process

    • Stress testing used after patients have “ruled out”

  • Reality dictates that appropriate provocative testing often not likely after patient leaves ED

    • ED is the “first, last, and best shot” at intervening in patients with risk concerns


Predictive Indices - Risk Scores in the ED

  • Combine clinical history, physical exam findings, ECG signs of ischemia, and cardiac marker results

    • PURSUIT and TIMI Risk Scores

  • Therapies such as LMW heparin and GP IIb/IIIa inhibitors have greater benefit in patients with higher risk scores

  • Have not been tested prospectively in the ED

  • Risk scores not specifically recommended by the ACC/AHA Guidelines


I

IIa

IIb

III

Immediate Management

Classify as non-cardiac, chronic stable angina, possible ACS, or definite ACS

Evaluate for immediate reperfusion therapy if definite ACS and ST-segment  present

Pharmacological or exercise stress test, if possible ACS and serial biomarkers and ECGs are normal

Admit pts with definite ACS, ongoing pain,  biomarkers, new ST  or deep T-wave inversion, abnormal hemodynamics, or (+) stress test


The “Key” to Risk Stratification

  • Link ongoing evaluation of risk to changes in intensity of therapy

  • Develop risk stratification schemes that reflect capabilities of ED and needs/preferences of cardiologists

  • Develop treatment pathways that provide for independent response of emergency physicians to recognition of higher risk levels


The “Rallying Cry” for CRUSADE . . .

. . . starts with a successful risk stratification strategy

A seamless transition of optimal care—diagnostic and therapeutic—from the ED to the Cardiology Service . . .


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