Acute coronary syndrome : Acute coronary syndrome : Risk stratification – Risk stratification –

markers of myocardial necrosismarkers of myocardial necrosis

Paul CalleEmergency Department

Ghent University HospitalBelgium

IntroductionIntroduction

ACS in ED is frequent, often difficult to recognize, a major cause of morbidity and mortality with prognosis related to early treatment

high risk of suboptimal care with poor outcome

high need for management strategy

ACS classification (focus on ECG and troponin) ST-elevation myocardial infarction (STEMI) non-STEMI

(includes "micro-infarctions", i.e. no ECG changes, no CK-MB , only troponin )

unstable angina (no troponin )

New criteria for acute, evolving or recent MINew criteria for acute, evolving or recent MI

Either one of the following criteria satisfies the diagnosis for an acute, evolving or recent MI :1. Typical rise and gradual fall (troponin) or more rapid rise

and fall (CK-MB) of biochemical markers of myocardialnecrosis with at least one of the following:

a) ischemic symptoms;b) development of pathologic Q waves on the ECG;c) ECG changes indicative of ischemia (ST segment

elevation or depression); ord) coronary artery intervention (e.g. coronary

angioplasty).

2. Pathologic findings of an acute MI

Illustrative figures (USA) ACS accounts for only 20% among 6 million

chest pain patients in ED costs to rule out ACS : 500 to 5,000 S missed ACS diagnosis in ED : 2 to 5%,

with 30 day mortality rate of 10% missed MI diagnosis in ED : 40% of mal-

practice awards against emergency physicians at least 20% of non-ACS patients with chest

pain suffer from (potentially) life threatening diseases : aortic dissection, pulmonary embolism, stable angina, pneumothorax, ...

Risk stratificationRisk stratification

Patient presents with chest pain or potential chest pain equivalent (e.g. jaw, shoulder, arm, back, or epigastric pain, unexplained dyspnea, syncope, palpitations)

Chest pain triage and ECG (< 10 min)

Physician's history Physician's physical examination

Prompt 12- or 15-lead ECG

Prompt differentiation

ST-segment elevation meeting fibrinolytic criteria or new/presumably new

LBBB or evidence of acute posterior MI

ST-segment depression > 0.5 mm or transient ST-segment elevation

not meeting fibrinolytic criteria (ECG or clinical evidence

of unstable angina)

Very low suspicion

of ACS

(modified from Pollack et al,2003)

ECG is nondiagnostic or normal

Clinical suspicionof ACS

Nature of presenting episode and time course Cardiac risk factors (previous MI, hypertension,

lipids, smoking, diabetes, family history) and related past medical (atherosclerotic cardio-vascular disease, CVA, peripheral vascular disease) and surgical history (percutaneous coronary intervention, CABG)

Comorbidities and quick review of systems (to suggest alternative diagnoses, such as lung infection or infarction, chest wall or gastro-intestinal pain)

(Pollack et al,2003)

Physician's historyPhysician's history

Evaluate hemodynamic status and perfusion

Lung auscultation for rales, ronchi, ... Evaluate for possible alternative

diagnoses (e.g. chest wall pain, pneumonia, pulmonary embolism, [evidence of DVT])

Cardiac examination

(Pollack et al,2003)

Physician's physical examination

ECG for acute chest painECG for acute chest pain

Not a perfect diagnostic tool (specificity-sensitivity) 10% of new ST-elevations are not caused by MI Up to 50% of MI patients present with normal or

inconclusive ECG (e.g. previous MI, LV hypertrophy) 2% of patients with normal ECG will develop MI

15-lead ECG for right ventricular or posterior MI Request previous ECG for comparison Serial ECGs (and continuous ST-monitoring?)

improve sensitivity

Risk stratificationRisk stratification

Patient presents with chest pain or potential chest pain equivalent (e.g. jaw, shoulder, arm, back, or epigastric pain, unexplained dyspnea, syncope, palpitations)

Chest pain triage and ECG (< 10 min)

Physician's history Physician's physical examination

Prompt 12- or 15-lead ECG

Prompt differentiation

ST-segment elevation meeting fibrinolytic criteria or new/presumably new

LBBB or evidence of acute posterior MI

ST-segment depression > 0.5 mm or transient ST-segment elevation

not meeting fibrinolytic criteria (ECG or clinical evidence

of unstable angina)

Very low suspicion

of ACS

(modified from Pollack et al,2003)

ECG is nondiagnostic or normal

Clinical suspicionof ACS

Markers and/or ECG to rule out ACS or to guide strategy therapy

Markers and ECG to confirm MI and to determine prognosis

The perfect markerThe perfect marker

Marker for myocardial necrosis, and also for cardiac ischemia

Linear relationship between blood levels and extent of myocardial injury (and prognosis)

100% sensitive 100% specific Immediate increase (+ constant blood level for

hours to days) Test kits : reliable, rapid, universally available and

inexpensive

What about troponin T and What about troponin T and II ? ?

Very high sensitivity for myocardial necrosis Related to prognosis

Not 100% specific for atherosclerotic coronary artery disease myocarditis, cardiomyopathy, myocardial contusion, ... renal failure, auto-immune diseases, ...)

Up to 6 hours before raised blood levelsno early MI diagnosis possible

Raised blood levels for many daystroublesome diagnosis of re-infarction

BUT

Role for myoglobin ?Role for myoglobin ?

Initial elevation : 1 to 4h after onsetbetter early marker than troponins

BUT : early myoglobin is less sensitive and less specific (due to skeletal muscletrauma) than late troponindecisions mainly based on clinical skills, ECG and late troponin (exceptrarely for reperfusion therapy)

Duration of elevation : 24 – 48huseful for re-infarction diagnosis

Role for CK-MB ?Role for CK-MB ?

Initial elevation comparable with troponins

Less sensitive than troponins

High specificity (comparable with troponins)

Rapid rise and fall (instead of gradual fall for troponins) allowing more accurate estimation of MI extent

ED strategy in chest pain patientsED strategy in chest pain patients

Patient presents with chest pain or potential chest pain equivalent (e.g. jaw, shoulder, arm, back, or epigastric pain, unexplained dyspnea, syncope, palpitations)

Chest pain triage and ECG (< 10 min)

Physician's history Physician's physical examination

Prompt 12- or 15-lead ECG

Prompt differentiation

STEMI Non-STEMIunstable angina

Other causes of chest pain

(modified from Pollack et al,2003)

Start appropriate treatment and send patient to CCU or cath lab

Suspicion of ACS

Continuous risk-oriented ACS

evaluation and treatment in ED

Diagnostic workup and treatment as indicated in ICU, ward, ED or as

outpatient

TIMI risk scoreTIMI risk score1 point each for presence of :

Age > 65 years Documented prior coronary artery stenosis > 50% Three or more conventional cardiac risk factors (e.g. age, sex,

family history, hyperlipidemia, diabetes, smoking, obesity) Use of aspirin in the preceding 7 days Two or more anginal events in the preceding 24h ST-segment deviation (transient elevation or persistent

depression) Increased cardiac biomarkers

Score 5 – 7 :high risk

Score 3 – 4 :intermediate risk

Score 0 – 2 :low risk

(Pollack et al, 2003)

ConclusionsConclusions The diagnosis of ACS during the first few hours of

evolution is a difficult task that challenges the best of (emergency) physicians.

Critical decisions should be based on much more elements than biomarkers.

For emergency physicians, the most difficult and medicolegally risky decisions center on how to minimize the costs to the healthcare system without jeopardizing the quality of care provided to patients with atypical symptoms and/or inconclusive ECG.

Chest pain center