Non-ST-segment

Elevation Acute Coronary

Syndrome (ACS) =
Unstable angina (UA) and
NSTEMI
 Acute Coronary Syndromes
Unstable Angina
Similar pathophysiology
(UA)
Non-ST-Segment Similar presentation and early
management rules
Elevation MI
(NSTEMI) STEMI requires evaluation for
acute reperfusion intervention

ST-Segment
Elevation MI
(STEMI)
 Pathophysiology
Usually acute thrombosis induced by a ruptured
or eroded atherosclerotic plaque (unstable plaque),
with or without concomitant vasoconstriction
partly blocks the artery, interrupting blood supply to
heart muscle (myocardial ischaemia)

Unstable angina myocardial ischaemia with no

evidence of heart muscle death (myocardial
necrosis)

NSTEMI myocardial ischaemia with

evidence of myocardial necrosis
Vulnerable Plaque
Stable Unstable Non-Q Q wave
Angina Angina wave MI MI

CAD UA/NSTEMI STEMI

Days- Mins-
weeks hours

Antithrombotic Thrombolysis
Therapy Primary PCI
 Acute Evaluation of ACS
Presentation Chest pain or Short of Breath

ST-segment ST-segment
ECG Normal Depression Elevation

Markers + + +

Diagnosis Unstable
Rule-Out Acute MI
Angina
 Clinical presentation
Chest pain: retro-sternal pressure or
heaviness radiating to the left arm, neck or
jaws
Prolonged (20 min) anginal pain at rest
De novo severe angina
Recent destabilisation of previously stable
angina
Post MI angina
 Clinical presentation
Other symptoms: diaphoresis, nausea,
dyspnoea, abdominal pain, syncope

Atypical complains: younger (25-40 years)

and older (>75 years) patients, women,
patients with diabetes, chronic renal failure
or dementia
Braunwald
Severity Classification
Clinical Circumstances of (UA)

A B C
Develops in presence Develops in the Develops within 2 weeks after
of extracardiac absence of extracardiac acute myocardial infarction
condition that condition (primary UA) (postinfarction UA)
intensifies myocardial
ischemia (secondary
UA)

I - New onset of severe IA IB IC

angina or accelerated
angina; no rest pain

II - Angina at rest within IIA IIB IIC

past month but not within

preceding 48 hr (angina at
rest, subacute)

III - Angina at rest within IIIA IIIB IIIC

48 hr (angina at rest,
acute)
 Diagnostic tools
Physical examination
ECG
Biochemical markers
Echocardiography
Imaging of the coronary anatomy
(coronarography, angio CT, MRI)
 ECG
Should be obtained within 10min of first medical contact

Consider additional leads, if normal

Comparison with previous ECG - if obtainable useful

Always serial ECGs or continuous monitoring

A normal ECG does not exclude the diagnosis (hidden

ischaemia in CX and right ventricular involvement).
 ECG
ST segment shifts: ST depression,
transient ST elevation
T- wave changes:
inversion (deep symmetrical inversion),
flat T wave,
pseudo-normalisation
Normal
 Biomarkers
Troponins

CK-MB

Others
 Biomarkers - Troponins
The preferred biomarker for myocardial necrosis is
cardiac Troponin

An increased value for cardiac Troponin is defined as a

measurement exceeding the 99th percentile of a normal
reference population (URL upper reference limit)

Troponin T may be elevated with severe congestive HF,

Ao dissection, cardiac contusion, cardioversion, ablation,
pacing, myocarditis, pulmonary cembolism, severe
pulmonary HT, hypertensive crisis, tachy-/
bradyarrhythmias, hypothyroidism, renal dz, stroke,
subarachnoid haemorrhage, infiltrative dz (amyloidosis,
haemochromatosis, sarcoidosis),
 Biomarkers - Troponins
cTn I
normal values: 0 - 0.1 ng/ml
onset: 4-6 hrs, peak: 12-24 hrs, return to
normal: 4-7 days)

cTn T
normal values: 0 - 0.2 ng/ml
onset: 3-4 hrs, peak: 10-24 hrs, return to
normal: 10-14 days
 Biomarkers CK-MB
Rises 4-6 hours after injury and peaks at 24
hours
Remains elevated 36-48 hours
Positive if CK/MB > 5% of total CK and 2
times normal
Elevation can be predictive of mortality
False positives with exercise, trauma, muscle
dz, DM,
 DIAGNOSTIC TOOLS
Echocardiography - used early in all patients:
Evaluation of global LV function.
Diagnose regional hypokinesia by wall motion analysis.
Rule out some differential diagnosis.

Stress testing (e.g. exercise ECG) to rule out obstructive CAD

in pain free patients with normal ECG and negative biomarkers.

Multislice Cardiac CT useful and recommended to rule out CAD

as cause of pain in patients with low to intermediate likelihood
of CAD and when troponin and ECG are inconclusive.
 Coronary angiography

Should be performed urgently for

diagnostic purpose in patients at high risk.
Ischaemic risk (GRACE score).
 Markers of increased risk
Clinical
Continuous or frequent episodes of pain.

Tachycardia.

Hypotension.

Heart failure.

Electrocardiogram:
ST-segment depression or T-wave inversion on admission.

Deep T- wave inversion in anterior leads.

ST-segment depression 0.1mV or 0.05 mV in two or

more contiguous leads.

ST-segment elevation (0.1 mV) in lead aVR.
 TREATMENT -Antischaemic Therapy

Nitrates (oral or intravenous) to relieve angina.

adrenergic blocker (BB)
in patients with tachycardia and/or hypertension.
all patients with LV dysfunction.
Continue BB in patients on chronic treatment unless
Kilip class III with heart failure.
Non-dihydropyridine calcium channel blocker
considered in patients without heart failure with
continued symptoms already on BB or with
Contraindication to BB.
 TREATMENT - Antiplatelet treatment
Aspirin lifelong for all.
A P2Y12 inhibitor should be added and kept for 12 months unless
there are contraindications such as excessive bleeding risk.
Ticagrelor indicated in all-comers

prasugrel only prior PCI in clopidogrel nave patients without

prior stroke/TIA whose anatomy is known,

clopidogrel if ticagrelor and prasugrel are not an option.

Glycoprotein IIb/IIIa in high risk PCI patients, but not routinely

upstream.
A proton pump inhibitor in combination with DAPT is
recommended in patients at risk with a previous history of
gastrointestinal haemorrhage or peptic ulcer.
 TREATMENT - Anticoagulation
Fondaparinux best benefit/ risk profile.

Add UFH on top of fondaparinux in patients undergoing PCI.

Enoxaparin in low bleeding risk patients.

Other low molecular weight heparins or unfractionated

heparin are less recommended options

Bivalirudin in high risk bleeding as alternative to GP IIb/IIIa +

UFH in patients undergoing PCI.
TREATMENT - Invasive management
Timing of revascularization customized according to risk

Within 72 hours all patients at risk, but

Within 2 hours for very high risk patients (life-threatening

symptoms)
Within 24 hours for patients with high risk criteria

(GRACE score > 140, troponin release, ST-T changes)

Prefer DES stents for PCI.

Non invasive evaluation for low risk patients.

 TREATMENT - Long term
management, secondary prevention
Statins for all initiated early with aim of LDL < 70 mg/Dl

Beta adrenergic blockers to all with LVEF < 40%.

ACE inhibitors to all with LVEF < 40%, patients with symptomatic heart
failure, hypertension, diabetes or kidney disease. Consider ACE inhibitors
for all other as a general preventive medication.

ARB with proven efficiency to ACE intolerant patients.

Aldosterone antagonists to patients already on BB/ACEI with LVEF < 35%.

intervention on diet, exercise and lifestyle