Myocardial Infarction https://medicalbooksvn.wordpress.com/

1. Hoang Cuong MD, Hanoi Medical University

2. MYOCARDIAL INFARCTION (MI) is a clinical syndrome that
results from occlusion of a coronary artery, with resultant
death of cardiac myocytes in the region supplied by that artery.
MI or heart attack is the irreversible damage of myocardial
tissue.
The degree of altered function depends on the area of heart
involved and the size of infarction.
Contractile function stops in the necrotic areas of the heart.
Obstruction in a coronary artery resulting from
atherosclerosis, a thrombus, or a spasm.

3. - Left main coronary artery (LMCA)→ The left ventricle and
left atrium.
• Left anterior descending artery (LDA)→ The front of the
left side of the heart.
• Circumflex artery (Cx)→ Outer side and back of the heart.
- Right coronary artery (RCA)→ Right ventricular, right
atrium, and SA, AV nodes, which regulate the heart rhythm.
• Right posterior descending artery and marginal artery→
Middle or septum of the heart.
- Smaller branches: obtuse marginal (OM), septal perforator
(SP), and diagonals.

5. The basis of anatomic, morphology, and diagnostic clinical information
• Transmural
• Non-Transmural (Subendocardial zones → Most vulnerable)
• Microscopic infarcts
• Type 1: Spontaneous MI (e.g... plaque, rupture, thrombotic occlusion,..)
• Type 2: Secondary to ischemia from a supply-and-demand mismatch
• Type 3: MI resulting in sudden cardiac death (without biomarkers)
• Type 4a: MI associated with percutaneous coronary intervention (PCI)
• Type 4b: MI associated with in-stent thrombosis
• Type 5: MI associated with coronary artery bypass surgery (CABS)
Anatomic or morphologic
Diagnostic clinical information

7. ST-segment elevation MI (STEMI)
• Transmural infarcts
• Full thickness of myocardial wall
involved ST elevation on ECG,
Q-waves.
Non-ST-segment elevation MI (NSTEMI)
• Subendocardial infarcts
• Subendocardium ( inner 1/3)
especially vulnerable to ischemia.
• ST depression on ECG.

8. Non-Modifiable
• Age: ≥45 years have eight times
greater risk for AMI.
• Male Gender: All age groups.
• Family History
Modifiable
• Tobacco Use: Damage blood vessel
walls.
• Diabetes Mellitus.
• Hypertension
• Hyperlipidemia: ↑ Cholesterol,
LDL, or triglycerides.
• Obesity
• Physical Inactivity
• Alcoholic Drinks

9. Change in
endothelium of
vessel
Narrowing of
vessel with
plaque
formation
Thrombus
formed
(Obstructs blood
flow to
myocardium)
Area of
ischemia, injury,
infarction
Can spread
through
thickness of
myocardial wall
Ventricular
Remodeling
• Mechanism
(CAD, spasm,
inflammation)
• Necrosis• Plaque ruptures • Subendocardial
layer

10. Coronary artery with atherosclerotic plaque.
The core of the atherosclerotic plaque houses
inflammatory cells and lipids which drive a chronic
inflammation within the artery wall
The atherosclerotic plaque is vulnerable (unstable).
Rupture or erosion may damage its cap, which
exposes highly thrombogenic materials. Such
materials activate platelets and coagulation factor.
Activation of platelets and coagulation factors results
in formation of a thrombus (atherothrombosis).
Myocardium supplied by this artery becomes
ischemic. Necrosis starts if flow is not restored within
30 minutes.

12. The natural course in total occlusions (transmural ischemia)

13. Early changes in infarction (minutes to days)
• Drop in tissue oxygen levels
• Rapid conversion from aerobic to anaerobic metabolism
o Impaired glycolysis and ATP production → impaired contractile protein function.
o Systolic dysfunction – loss of synchronous myocyte contraction →compromised cardiac
output.
o Diastolic dysfunction – reduced ventricular compliance (i.e. impaired relaxation) and
elevation of ventricular filling pressures.
• Accumulation of lactic acid and reduction in pH.
• Impairment of transmembrane Na-K-ATPase due to impaired ATP production.
o Increased intracellular Na+ → Intracellular edema.
o Increased extracellular K+ → Alteration in transmembrane potential → electrical
instability and susceptibility to arrhythmias.
o Increased intracellular Ca2+ → activation of degradative lipases and proteases → tissue
necrosis.
• Acute inflammatory response with infiltration of neutrophils leading to further tissue
damage

14. Late changes in infarction (days to weeks)
• Resorption of irreversibly injured/dead myocytes by macrophages
 Structural weakness of ventricular wall and susceptibility to myocardial wall rupture
• Fibrous tissue deposition and scarring
• Ventricular remodeling
 Infarct expansion—thinning and dilatation of necrotic tissue without additional necrosis.
 Increased ventricular wall stress
 Further impairment in systolic contractile function
 Increased likelihood of aneurysm formation
 Remodeling of non-infarcted ventricle
 Dilatation of overworked non-infarcted segments subjected to increased wall stress
 Enlargement initially compensatory to increased cardiac output via Frank-Starling
mechanism, but can eventually predispose to ventricular arrhythmias and lead to heart
failure.

18. Arrhythmias
• Electrical instability of ischemic myocardium.
• Interruption of perfusion to structures of the conduction pathway (i.e. SA, AV node,
bundle branches.
Congestive heart
failure
• Directly (systolic and diastolic dysfunction)
• Papillary muscle infarction or rupture → moderate to severe mitral
regurgitation.
Thromboembolism
• Intra-ventricular thrombus formation can arise from stasis of blood flow in regions
of impaired LV contraction.
Pericarditis • Early post-MI period when necrosis and neutrophilic infiltrates.
Ventricular aneurysm
• Develops as the ventricular wall is weakened but not perforated by the phagocytic
clearance of necrotic tissue.
Cardiac tamponade
• Hemorrhage into the pericardial space due to ventricular free wall rupture
→ severe restriction of ventricular filling; often lethal.
Cardiogenic shock
• Severely decreased cardiac output and hypotension with inadequate perfusion of
peripheral tissues.
• Self-perpetuating mechanism→ impaired contractility → hypotension,
decreased coronary perfusion → ↑ ischemic damage→ ↓ contractile function.

19. Chest pain/discomfort
Pain indicators Description
Location Behind side of sternum, left side of chest
Characterizes
Pressure, dull, squeezing, aching, crushing,
burning
“elephant sitting in the chest”
Duration >10-20 mins
Relieving
factors
No abatement of nitroglycerin, relieved with
analgesic /morphine.
Associated
symptoms
Weakness, dyspnea, fainting fit/ syncope/
Cold sweet, apprehensive.
Dyspnea, orthopnea, cough, wheezing,
nausea and vomiting, or abdominal bloating.

20. Chest pain/discomfort
Metabolic products such as lactate, serotonin and
adenosine accumulate locally and may activate
peripheral pain receptors in the C7 to T4
distribution
Some people (the elderly, people with diabetes, and
women) may have little or no chest pain. Or, they may
experience unusual symptoms (shortness of breath,
fatigue, weakness).
Levin’s sign: a person localizes the chest pain by clenching their fists
over their sternum

21. Tachycardia
 Dangerous arrhythmias can be precipitated by transient abnormalities of myocyte ion
transport and accumulation of local metabolites; increased sympathetic tone during
myocardial ischemia can also account for an increased heart rate.
Shortness of breath (dyspnea)
 The damage to the heart limits the output of the left ventricle, causing left ventricular failure
and consequent pulmonary edema
Nausea/vomiting
 Vomiting results as a reflex from severe pain.
 Vasovagal reflexes initiated from area of ischemia

22. Diaphoresis
Light-headedness
Palpitations
Massive surge of catecholamine from
the sympathetic nervous system
Loss of consciousness
 Inadequate blood flow to the brain and cardiogenic shock.
Sudden death
 Due to the development of ventricular fibrilation

23. Diagnostic of myocardial infarction is based on the following three components
 Cardiac Troponin ─ Elevation of cardiac troponins in peripheral blood is
mandatory to establish a diagnosis of myocardial infarction
 ECG ─ ST elevations, ST depressions, T-wave inversions and pathological Q-
waves.
 Symptoms ─ Typical ischemic chest pain, or with dyspnea, nausea, unexplained
weakness, or a combination of these symptoms.
► The diagnosis requires elevated levels of cardiac troponins and display either
symptoms or ECG changes consistent with myocardial infarction/ischemia. Most
patients, however, display both ECG changes and symptoms.

24. Cardiac troponin I:
• Appears 4 hrs after MI; Peaks in 24 hrs.
• ↑ for 7-10 days.
• More specific than other protein markers.
Creatinine kinase (CK-MB):
• Appears 6 to 12, peaks in 16 to 24hrs after MI.
• Returns to normal 48 to 72 hrs after MI.
• Useful in diagnosing re-infarction following acute MI
because levels return to normal after 48hr.
In the first 6 hours, ECG is the gold standard.
ECG changes:
• ST elevation (STEMI, transmural infarct).
• ST depression (NSTEMI, subendocardial infarct).
• Hyperacute (peaked) T waves, T-wave inversion.
• New LBBB, and pathologic Q waves or poor R wave
progression
→ Evolving or old transmural infarct

25. ECG criteria for the diagnosis of acute STEMI
New ST segment elevations in at least two anatomically contiguous leads:
• Men age ≥40 years: ≥2 mm in V2-V3 and ≥1 mm in all other leads.
• Men age <40 years: ≥2.5 mm in V2-V3 and ≥1 mm in all other leads.
• Women (any age): ≥1.5 mm in V2-V3 and ≥1 mm in all other leads.
• Men & women V4R and V3R : ≥0.5 mm, except from men <30 years in whom the
criteria is ≥1 mm.
• Men & women V7-V9: ≥0.5 mm.
ECG criteria for ischemic ST segment depression:
• New horizontal or downsloping ST segment depressions
≥0.5mm in at least two anatomically contiguous leads.
ECG criteria for ischemic ST segment depression:
• T-wave inversion ≥1mm in at least two anatomically contiguous lead. These leads
must have evident R-waves, or R-wave larger than S-waves.
ECG criteria for pathological Q-waves (Q-wave infarction):
• Any Q-wave in leads V2 to V3 ≥0.02s or QS complex in V2 and V3; or Q wave
≥0.03s and ≥0.1mV deep or QS complex in all other leads.

26. Ischemic ST-T changes
Myocardial ischemia causes changes to the ST segment and T-wave (ST-changes):
 The ST segment may be either elevated or depressed (in relation to the PR segment)
→ST segment elevation and ST segment depression.
 The T-wave may diminish in amplitude (flat T-waves), become negative (T-wave
inversion) or even increase markedly in amplitude (hyperacute T-wave).

27. Transmural ischemia (STEMI)
Subendocardial ischemia (NSTEMI)

28. Post-Ischemic T-wave changes
ST Elevation MI Non-ST Elevation Infarction
Ischemia ST depression, peaked T-waves,
then T-wave inversion
Ischemia ST-depression and T-wave
inversion
Infarction ST elevation and appearance of Q-
waves
Infarction ST depression & T-wave inversion
Fibrosis ST segments and T-waves return
to normal, but Q-waves persist
Fibrosis ST returns to baseline, but T-wave
inversion persist

32. The electrocardiographic natural course of ST-elevation myocardial infarction (STEMI)
The patient typically presents somewhere between these
NormalECG
HyperacuteT-wavesoccur
secondsafterocclusion
arise.Thesepersistonlyfor
afewminutes.
HyperacuteT-waves
diminish.Withinminutes
theST-segmentbecomes
elevates.
PathologicalQ-wavesoccur
within6to16hours.ST-
segmentelevationsbeginto
normalize.
Continuenormalizationof
theST-segmentelevations.
Q-wavesbecomedeeper.
Post-ischemicT-wave
inversionstarts.
PathologicalQ-wavesand
T-inversions.
T-waveinversionsnormalize
withinafewweeks(theymay
occasionallypersistmuch
longer,orevenbecome
permanent).Q-eavesare
generallypermanent,butmay
occasionallynormalizewithin
ayear

34. STEMI without ST elevations on ECG
• Transmural ischemia located in the posterolateral region of the left ventricle.
This referred to as posterior, or posterolateral, or inferobasal STEMI.
• Right ventricular infarction (STEMI): No lead in the 12-lead ECG is adequate to
detect right ventricular infarction.
Hyperacute T-waves
• Large T-waves occur in several conditions such as hyperkalemia, early
repolarization and male/female pattern. However, transmural ischemia may cause
hyperacute T-waves, which are very large, broad based, symmetric T-waves.
The mechanism from STEMI to asystole and death

35. Localization of MI
Localization – Left Coronary Artery (LCA)
Left Main
(proximal LCA)
occlusion
Left Circumflex
(LCX) occlusion
Left Anterior
Descending
(LAD) occlusion
Extensive Anterior
Injury
Lateral Injury Anteroseptal
Injury
Localization – Right Coronary Artery (RCA)
Proximal RCA occlusion Posterior descending artery
(PDA) occlusion
- Right Ventricle Injured
- Posterior wall of left
ventricle injured
- Inferior wall of left
ventricle injured
Inferior wall of left ventricle
injured

36. Localization Summary Prevalence of Culprit Artery
Left Coronary Artery
• Septal
• Anterior
• Lateral
• Possibly Inferior
Right Coronary Artery
• Right Ventricular Infarct
• Inferior
• Posterior
RCA 45%
LCx 12%
LAD 36%
Prevalence of STEMI
Inferior 58%
Anterior 39%
Other 3%

37. Localization of MI
aVL
Lateral
II
Inferior
V1
Septal
V4
Anterior
I
Lateral
aVF
Inferior
V2
Septal
V5
Lateral
-aVR
III
Inferior
V3
Anterior
V6
Lateral

38. Localization of MI: The implications of ST-segment elevation
Localization ST elevation
Reciprocal ST
depression
Coronary Artery
Anterior MI V1-V6 None LAD
Septal MI
V1-V4, disappearance
of septum Q in leads
V5, V6
None LAD
Lateral MI I, aVL, V5, V6
II, III, aVF (inferior
leads)
LCX
Inferior MI II, III, aVF I, aVL (lateral lead)
RCA (80%) or LCX
(20%)
Posterior MI V7,V8, V9
High R in V1-V3 with
ST depression V1-V3
>2mm (mirror view)
RCA or LCX
Right Ventricle MI V1, V4R I, aVL RCA
Atrial MI PTa in I, V5, V6 PTa in I, II, or III RCA

39. Localization Criteria: Occluded artery to the ECG
Localization of LAD
ECG changes
Look at
Proximal LAD
(above D1 and 1st septal)
Mid LDA
(between 1st septal and D1)
Distal LAD
(below septal 1 and D1)
V1-V4 ST ↑ ST ↑ ST ↑
II, III, aVF ST ↓
ST ↑
(III esp.)
ST isoelectric or ↑
aVR ST ↑ ST ↑ ST ↓
V5, V6 ST ↓
aVL ST ↓
Conduction
defects
RBBB
LAFB

40. Localization Criteria: Occluded artery to the ECG
Localization of LAD
ST ↓
II, III and aVF
ST ↓
III>II, II maybe ♀♂
ST inferior leads
Not depressed, eventually ↑

41. Localization Criteria: Occluded artery to the ECG
Localization of LAD ASMI
ST elevate in V1-V4
Reciprocal ST depression in II, III, aVF
Present Absent
ST elevation in V1, aVR
AbsentPresent
Proximal LAD Mid LAD Distal LAD
Recommendations: I, aVL, V1-V4: Extensive anterior wall infarction due to occlusion of
proximal LAD
V3-V6, II, aVF: AWMI due to mid/distal occlusion of LAD

42. Localization Criteria: Occluded artery to the ECG
Inferior MI
ST Elevation in II, III, aVF
RCA OR LCx
ST ↑ III>II
ST ↓ I, aVL
ST ↑ II>III
ST ↑ I, aVL

43. Serum markers
• The appearance of certain proteins in the blood after myocardial cell death is a very
sensitive and reliable indicator of MI.
• Myocardial cell death leads to elevated serum levels of myoglobin, troponin, lactate
dehydrogenase, and creatine kinase (isoform).
• Cardiac biomarkers have slightly different amino acid sequence than other cell types.
→ Myocytes contain the isoforms CK-MB, troponin I, and troponin T.
• CK-MB → highly specific indicator of MI, remains elevated for only 48-72 hours after MI.
• Troponin I and T (comprise part of the cardiac cell contractile apparatus)→ markers of
choice for detecting MI, remain elevated for a longer period.
• Cardiac troponins I and T → highly sensitive and specific for cardiac cell death, but less
helpful in detecting new infarction (reinfarction).
• Cardiac myoglobin levels → elevated in serum very quickly, helpful in early detection;
but, less specific than the other markers.
→ All serum markers are useful diagnostically only during the acute period of MI.

45. • We recommend using cardiac troponins in preference to creatine kinase MB for
diagnostic and prognostic purposes. For most settings, it is unnecessary to obtain both
values.
• Myoglobin and lactate dehydrogenase should no longer be used for the evaluation of
patients with acute coronary syndrome and/or possible acute myocardial infarction.
While there are theoretical advantages of other cardiac biomarkers, such heart-type
fatty acid binding protein and copeptin, available data suggest that cardiac troponin
outperforms each of them in almost every specific way. Their use is not encouraged.
Source: Uptodate.com
Why troponin is preferred?
• Diagnosis:
 Because of their increased sensitivity and specificity compared with CK-MB and other markers.
 With regard to specificity, troponin elevations are almost always specific for cardiac injury,
except for the infrequent analytical false positives caused by fibrin interference and/or cross-
reacting antibodies. CK-MB is not specific for cardiac injury, as a small amount is found in
skeletal muscle
• Prognosis:
 Troponin measurements have enhanced prognostic value compared with CK-MB
measurements in patients with a non-ST elevation acute coronary syndrome (ACS).

46. Treatment options and their role in the management of acute coronary syndromes.
Therapy in ACS is targeted at providing measures that improve the balance between
myocardial oxygen supply and demand, stabilizing the intracoronary thrombus that in
initiated the syndrome and ultimately, restoring blood flow to the ischemic
myocardium.
• Immediate adjunctive treatment.
• Antiplatelet therapy.
• Anticoagulant therapy.
• Fibrinolysis.
• Primary percutaneous coronary intervention (PCI)
• Surgical revascularization.

47. Immediate adjunctive treatment
Nitrates
↓ angina symptoms by inducing coronary vasodilation and
improving myocardial O2 supply, and by ↓ myocardial O2
demand by ↓ preload through venodilatation.
Beta blockers
↓ myocardial O2 demand by ↓ heart rate and contractility; in
addition, also contribute to electrical stability.
Calcium channel blockers
↓ myocardial O2 demand by ↓ heart rate and contractility, ↓
wall stress via ↓ blood pressure, and ↓ preload via
venodilatation.
Morphine ↓ myocardial oxygen demands by ↓ chest pain and anxiety.
Oxygen Improves oxygen supply in patients with hypoxemia.

48. Antiplatelet therapy
Aspirin
Prevents further thrombus formation by inhibiting platelet
synthesis of thromboxane A2, an important mediator of
platelet activation.
Clopidogrel ( or other ADP
receptor blockers)
Inhibit ADP-mediated activation of platelet, thereby
preventing expansion of the existing thrombus; have
superior outcomes when used in combination with Aspirin
GP IIb/IIIa inhibitors
Potent antiplatelet agents that block the final common
pathway of platelet aggregation; often used in patients
undergoing PCI as they are very effective in reducing cardiac
events in these patients.

49. Anticoagulant therapy
UPH (Unfractionated
heparin) or LMWH (low
molecular weight heparin)
UFH an LMWH, which preferentially bind to
antithrombin III and factor Xa, respectively, slow
thrombin formation and impede clot development.
Recombinant tissue-type
plasminogen activators
(tPA, rPA and TNK-tPA)
Transform the inactive precursor plasminogen into the
active protease plasmin, which lyses fibrin clots, thereby
accelerating lysis of the occlusive intracoronary thrombus
and restoring blood flow.
Fibrinolysis

50. Primary percutaneous coronary intervention (PCI)
Plain old balloon
angioplasty (POBA)
Inflation of a balloon within a stenosed coronary artery
mechanically dilates the affected vessel to restore blood flow,
both by compressing the atherosclerotic plaque and
stretching the underlying media.
Bare metal stent
Mechanically maintain the patency of coronary arteries
occluded by atherosclerotic plaques.
Drug-eluting stents
In addition to maintaining patency, these stents release
antiproliferative agents such as sirolimus or paclitaxel, which
prevent neointimal proliferation (migration of smooth
muscle cells and production of extracellular matrix), thereby
decreasing the rate of in-stent restenosis

51. Surgical revascularization
Coronary artery bypass
graft (CABG)
Restores coronary blood flow by using a healthy patent
artery to bridge circulation around an occlusive lesion
within an atherosclerotic coronary vessel.

52. Acute Myocardial Infarction Management
Pre-hospital management
• Arrange an emergency ambulance if AMI is suspected. Take an ECG as soon as possible but do
not delay transfer to hospital
• Cardiopulmonary resuscitation and defibrillation in the event of a cardiac arrest.
• Oxygen: do not routinely administer oxygen but monitor oxygen saturation using pulse
oximetry as soon as possible.
• Pain relief with GTN sublingual/spray and/or an intravenous opioid 2.5-5g diamorphine or 5-
10 mg morphine IV with an anti-emetic. Avoid IM injections, as absorption is unreliable and the
injection site may bleed if the patient later receives thrombolytic therapy.
• A mild tranquillizer (usually a benzodiazepine) should be considered in anxious patients.
• Aspirin 300 mg orally (dispersible or chewed).
• Insert a Venflon® for intravenous access and take blood tests for FBC, renal function and
electrolytes, glucose, lipid, clotting screen, CRP and cardial enzymes (troponin I or T).
• Pre-hospital thrombolysis is indicated if the time from the initial call to arrival at hospital is
likely to be over 30 minutes.
• When primary PCI cannot be provided within 120 minutes of ECG diagnosis→ patients with
STEMI should receive immediate (pre-hospital or admission) thrombolytic therapy.

53. Acute Myocardial Infarction Management
Pre-hospital management
• The NICE recommends using IV bolus (reteplase or tenecteplase) rather than an infusion for
pre-hospital thrombolysis.
Recommendation: Hypoxaemia Class Level
• Oxygen is indicated in patients with hypoxaemia (SaO2 <90% or PaO2 <60
mmHg)
I C
• Routine oxygen is not recommended in patients with SaO2 ≥90% III B
Recommendation: Symptoms Class Level
• Titrated i.v opioids should be considered to relieve pain. IIa C
• A mild tranquillizer (usually a benzodiazepine) should be considered in
very anxious patients.
IIa C

56. Acute Myocardial Infarction Management
In-hospital management
Definitions of terms related to reperfusion therapy
Primary PCI
Emergent PCI with balloon, stent, or other approved device,
performed on the IRA without previous fibrinolytic treatment.
Primary PCI strategy Emergent coronary angiography and PCI of the IRA if indicated.
Rescue PCI
Emergent PCI performed as soon as possible in the case of failed
fibrinolytic treatment.
Routine early PCI strategy
after fibrinolysis
Coronary angiography, with PCI of the IRA if indicated, performed
between 2 and 24 hours after successful fibrinolysis.
Pharmacoinvasive strategy
Fibrinolysis combined with rescue PCI (in case of failed fibrinolysis)
or routine early PCI strategy ( in case of successful fibrinolysis)

57. Acute Myocardial Infarction Management
In-hospital management
Recommendations for reperfusion therapy Class Level
• Reperfusion therapy is indicated in all patients with symptoms of ischemia of ≤12h
duration and persistent ST-segment elevation.
I A
• A primary PCI strategy is recommended over fibrinolysis within indicated timeframes. I A
• If timely primary PCI cannot be performed after STEMI diagnosis, fibrinolytic therapy is
recommended within 12 h of symptom onset in patients without contraindications.
I A
• In the absence of ST-segment elevation, a primary PCI strategy is indicated in patients
with suspected ongoing ischemic symptoms suggestive of MI and at least one of the
following criteria present:
o Haemodynamic instability or cardiogenic shock
o Recurrent or ongoing chest pain refraction to medical treatment
o Life-threatening arrhythmias or cardiac arrest.
o Mechanical complications or MI
o Acute heart failure
o Recurrent dynamic ST-segment or T-wave changes, particularly with intermittent ST-
segment elevation.
I C

58. Acute Myocardial Infarction Management
In-hospital management
Recommendations for reperfusion therapy Class Level
• Early angiography (within 24h) is recommended if symptoms are completely
relieved and ST-segment elevation is completely normalized spontaneously or
after nitroglycerin administration (provided there is no recurrence of symptoms
or ST-segment elevation)
I C
• In patients with time from symptom onset >12h, a primary PCI strategy is
indicated in the presence of going symptoms suggestive of ischaemia,
haemodynamic instability, or life-threatening arrhythmias.
I C
• A routine primary PCI strategy should be considered in patients presenting late
(12-48h) after symptom onset.
IIa B
• In asymptomatic patients, routine PCI of an occluded IRA>48h after onset of
STEMI is not indicated.
III A

60. In-hospital management
Intervals Time targets
Maximum time from FMC to ECG and diagnosis ≤10 min
Maximum expected delay from STEMI diagnosis to primary PCI (wire
crossing) to choose primary PCI strategy over fibrinolysis (if this target time
cannot be met, consider fibrinolysis)
≤120 min
Maximum time from STEMI diagnosis to wire crossing in patients presenting
at primary PCI hospitals
≤60 min
Maximum time from STEMI diagnosis to wire crossing in transferred patients ≤90 min
Maximum time from STEMI diagnosis to bolus or infusion start of fibrinolysis
in patients unable to meet primary PCI target times
≤10 min
Time delay from start of fibrinolysis to evaluation of its efficacy (success or
failure)
60-90 min
Time delay from start of fibrinolysis to angiography (if fibrinolysis is
successful)
2-24 hours

62. In-hospital management
Recommendations for reperfusion therapy Class Level
IRA strategy
• Primary PCI of the IRA is indicated. I A
• New coronary angiography with PCI if indicated is recommended in patients
with symptoms or signs of recurrent or remaining ischaemia after primary PCI
I C
IRA technique
• Stenting is recommended (over balloon angioplasty) for primary PCI. I A
• Stenting with new-generation DES is recommended over BMS for primary PCI I A
• Radial access is recommended over femoral access if performed by an
experienced radial operator.
I A
• Routine use of thrombus aspiration is not recommended. III A
• Routine use of deferred stenting is not recommended. III B
Primary percutaneous coronary intervention
and adjunctive therapy

63. In-hospital management
Antiplatelet therapy
• A potent P2Y12 inhibitor (prasugrel or ticagrelor), or Clopidogrel if these are not available or are
contraindicated, is recommended before (or at latest at the time of ) PCI and maintained over 12
months, unless there are contraindications such as excessive risk of bleeding.
I A
• Aspirin (oral or i.v if unable to swallow) is recommended as soon as possible for all patients without
contraindications.
I B
• GP IIb/IIIa inhibitors should be considered for bailout if there is evidence of no-reflow or a
thrombotic complication.
IIa C
• Cangrelor may be considered in patients who have not received P2Y12 receptor inhibitors. IIb A
Anticoagulant therapy
• Anticoagulant is recommended for all patients in addition to antiplatelet therapy during primary
PCI.
I C
• Routine use of UFH is recommended. I C
• In patients with heparin-induced thrombocytopenia, bivalirudin is recommended as the
anticoagulant agent during primary PCI.
I C
• Routine use of enoxaparin i.v. should be considered. IIa A
• Routine use of bivalirudin should be considered. IIa A
• Fondaparinux is not recommended for primary PCI. III B
Peri- and Post-procedural antithrombotic therapy
Class Level

64. In-hospital management Fibrinolysis and Pharmacoinvasive strategy
Recommendations Class Level
When fibrinolysis is the reperfusion strategy, it is recommended to initiate this treatment as
soon as possible after STEMI diagnosis, preferably in the pre-hospital setting.
I A
A fibrin-specific agent (i.e. tenecteplase, alteplase, or reteplase) is recommended I B
A half-dose of tenecteplase should be considered in patients ≥75 years of age. IIa B
Anteplate co-therapy with fibrinolysis
Oral or i.v. aspirin is indicated. I B
Clopidogrel is indicated in addition to aspirin. I A
DAPT (in the form of aspirin plus a P2Y12 inhibitor) is indicated for up to 1 year in patients
undergoing fibrinolysis and subsequent PCI.
I C
Anticoagulation co-therapy with fibrinolysis
Anticoagulation is recommended in patients treated with lytics until revascularization (if
performed) or for the duration of hospital stay up to 8 days. The anticoagulant can be:
• Enoxaparin i.v. followed by s.c. (preferred over UFH) I A
• UFH given as a weight-adjusted i.v. bolus followed by infusion. I B
• In patients treated with streptokinase: Fondaparinux i.v. bolus followed by an s.c. dose 24
later.
IIa B

65. In-hospital management Fibrinolysis and Pharmacoinvasive strategy
Recommendations Class Level
Transfer after fibrinolysis
Transfer to a PCI-capable Centre following fibrinolysis is indicated in all patients
immediately after fibrinolysis
I A
Interventions following fibrinolysis
Emergency angiography and PCI if indicated is commended in patients with heart
failure/shock.
I I
Rescue PCI is indicated immediately when fibrinolysis has failed (<50% ST-segment
resolution at 60-90 min) or at any time in the presence of haemodynamic or electrical
instability, or worsening ischaemia.
I A
Angiography and PCI of the IRA, if indicated, is recommended between 2 and 24 after
successful fibrinolysis.
I A
Emergency angiography and PCI if needed is indicated in the case of recurrent ischaemia or
evidence of reocclusion after initial successful fibrinolysis.
I C

66. In-hospital management Fibrinolysis and Pharmacoinvasive strategy
Contra-indications to fibrinolytic therapy
Absolute Relative
Previous ICH or stroke of unknown origin at anytime. Transient Ischaemic attack in the preceding 6 months
Ischaemic stroke in the preceding 6 months. Oral anticoagulant therapy
Central nervous system damage or neoplasms or
arteriovenous malformation
Pregnancy or within 1 week postpartum
Recent major trauma/surgery/head injury (within the
preceding month)
Refractory hypertension (SBP>180 mmHg and/or
DBP>110mmHg)
GI bleeding within the past month Advanced liver disease
Known bleeding disorder (excluding menses) Infective endocarditis
Aortic dissection Active peptic ulcer
Non-compressible Prolonged or traumatic resuscitation
Non-compressible punctures in the pass 24 hours (e.g.
liver biopsy, lumbar puncture0