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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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Ed risk stratification for chest pain

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


Ed risk stratification for chest pain

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

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


Ed risk stratification for chest pain

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

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


Initial evaluation risk stratification 1

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


Initial evaluation risk stratification 2

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

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

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

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

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

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

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

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

Troponin as a Marker of Increased Risk in ACS


Long term survival and troponin t status

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

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

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


Ed risk stratification for chest pain

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

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

“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

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

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

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


Immediate management

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

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

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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