Acute Myocardial

Infarction
By
Prof. Dr. OMAR EL-BAHI
Prof. of Cardiology
Alex. University
DEFINITION
 Third Universal Definition of
Myocardial Infarction
2012
ESC Clinical Practice
Guidelines

The latest MI consensus the third universal definition of

MI defines it according to standardized criteria and
emphasizes diagnosis of MI on the basis of cardiac
troponin (cTn) values.
History
The first clinical descriptions of MI are only around 100 years old. From this
first description it took some time until the first working group was set up by
the World Health Organization (WHO) in 1959 to define the disease acute
myocardial infarction (AMI) in order to study disease prevalence . This
definition was based on patient symptoms and ECG findings.
Later definitions of the WHO described AMI as a combination of two of three
characteristics: typical symptoms (i.e., chest discomfort), enzyme rise, and a
typical ECG pattern involving the development of Q waves, but still
myocardial infarction was mainly an ECG-based diagnosis.

Due to technological advances in more sensitive biomarkers and imaging

techniques and due to a need for a more precise and comparable definition,
The Joint ESC/ACC Committee published its first consensus document for the
redefinition of myocardial infarction in the year 2000 , with a more
pronounced biochemical approach demanding an elevation of cardiac
biomarkers before myocardial infarction could be diagnosed and a more
prospective approach considering rather ST-T-changes than Q-wave
development for categorization. With this definition, the STEMI was born.
The task force was then joined by the American Heart Association (AHA) and
the World Health Federation to become the global task force for the
definition of acute myocardial infarction.
This definition was updated by the same task force in 2007, giving cardiac
troponins a much higher significance than in the 2000 definition.
Additionally, different types of myocardial infarction were defined.

By now, cardiologists around the world had become used to using cardiac
biomarkers and particularly troponin for the diagnosis of AMI.
 Myocardial Injury versus
Myocardial Ischemia

Elevation of cardiac troponin indicates myocardial

necrosis :
*[if caused by myocardial ischemia defined as myocardial infarction,
*and if it is unrelated to ischemia, defined as myocardial injury.

DD of myocardial ischemia from myocardial injury is by:

*In the acute setting of myocardial ischemia presence of biomarker
dynamics(biomarker levels will change over time, i.e. a biomarker rise and/or
fall). *In chronic conditions and diseases causing myocardial
injurybiomarker levels will be more continuously elevated.
Definitions of
terms related to
reperfusion
therapy

2017 ESC Guidelines

for the management of
acute STEMI
 Classification
MI classification uses 5 categories according to the
myocardial lesion mechanism
Standard calibration of the ECG is 10 mm/mV.
Therefore 0.1mV = 1mm square on the vertical
axis.

[in the absence of (LVH) or (LBBB)].

In patients with inferior MI, it is recommended to record
right precordial leads (V3R and V4R) seeking ST-segment
elevation, to identify concomitant right ventricular (RV)
infarction.

Likewise, ST-segment depression in leads V1V3 suggests

myocardial ischaemia, especially when the terminal T-wave
is positive (ST-segment elevation equivalent), and
confirmation by concomitant ST-segment elevation
0.5mm recorded in leads V7V9 should be considered as a
means to identify posterior MI.

The presence of a Q-wave on the ECG should not

necessarily change the reperfusion strategy decision.

2017 ESC Guidelines for the

management of acute STEMI
2017 ESC Guidelines for the
management of acute STEMI
2017 ESC Guidelines for the
management of acute STEMI
Isolated posterior MI. In AMI of the inferior and basal portion of
the heart, often corresponding to the left circumflex territory, isolated ST-
segment depression 0.5mm in leads V1V3 represents the dominant
finding. These should be managed as a STEMI. The use of additional
posterior chest wall leads [elevation V7V9 0.5mm (1mm in men, 40years
old)] is recommended to detect ST-segment elevation consistent with inferior
and basal MI.
Left main coronary obstruction. The presence of ST
depression 1mm in six or more surface leads (inferolateral ST depression),
coupled with ST-segment elevation in aVR and/or V1, suggests multivessel
ischemia or left main coronary artery obstruction, particularly if the patient
presents with haemodynamic compromise.

2017 ESC Guidelines for the

management of acute STEMI
 Atypical ECG presentations that should prompt a primary
PCI strategy in patients with on-going symptoms
consistent with myocardial ischaemia

It may be difficult to
detect transmural
ischaemia in patients
with chest pain and
RBBB. Therefore, a
primary PCI strategy
should be considered
when persistent
ischaemic symptoms
occur in the presence
of RBBB

2017 ESC Guidelines for the

management of acute STEMI
Acute myocardial infarction (MI) is defined as death or
necrosis of myocardial cells.
Critical myocardial ischemia may occur as a result of:
1- decreased myocardial oxygen and nutrients:
a) a thrombus on an ulcerated or unstable plaque
b) (> 75%) fixed coronary artery stenosis due to atherosclerosis
c) dynamic stenosis associated with coronary vasospasm
2- increased myocardial metabolic demand:
a) extremes of physical exertion.
b) severe hypertension
c) hypertrophic obstructive cardiomyopathy
d) severe aortic stenosis.
I) Based on morphologic standpoint :
1- A transmural MI :(ischemic necrosis of the full thickness of the
affected muscle from the endocardium to the epicardium.
2- A nontransmural MI:
ischemic necrosis is limited to either the endocardium or the
endocardium and myocardium. is limited to either the
endocardium or the endocardium and myocardium.
II) based on clinical diagnostic criteria:
1) Q waves MI
2) Non Q waves MI
III) A more common clinical diagnostic classification:
1) ST elevation MI.
2) Non - ST elevation MI.
CAUSE
The most common etiology of MI is a
thrombus superimposed on a ruptured
or unstable atherosclerotic plaque.
PATHOPHYSIOLOGY
Mechanisms of Occlusion:
* Most MIs are caused by a disruption in the vascular endothelium
unstable plaque stimulates the formation of an intracoronary thrombus,
coronary artery blood flow occlusion. If such an occlusion persists long
enough (20 to 40 min), irreversible myocardial cell damage and cell death
will occur .
* The two primary characteristics of atherosclerotic plaque are :
1) fibromuscular cap
2) lipid-rich core.
* Plaque erosion may occur due to the actions of metalloproteases
collagenases and proteases thinning of the overlying
fibromuscular cap.
* disruption of the endothelium and fissuring or rupture of the
fibromuscular cap
Mechanisms of Myocardial Damage:
The severity of an MI is dependent on three factors:
1) the level of the occlusion
2) length of time of the occlusion,
3) collateral circulation .
after a 6- to 8-hour period of coronary occlusion,
most of the distal myocardium has died.
Risk Factors:
Six primary risk factors have been identified:
1) High Blood Cholesterol.
2) Diabetes Mellitus
3) Hypertension
4) Tobacco Use
5) Male Gender
6) Family History
 SIGNS
AND
SYMPTOMS
Table 1:
Signs and Symptoms of a Myocardial Infarction
Chest pain described as a pressure sensation, fullness, or squeezing in
the midportion of the thorax
Radiation of chest pain into the jaw/teeth, shoulder, arm, and/or
back
Associated dyspnea or shortness of breath
Associated epigastric discomfort with or without nausea and vomiting
Associated diaphoresis or sweating
Syncope or near-syncope without other cause
Impairment of cognitive function without other cause
DIAGNOSIS
I) Classical chest pain.
Ask:
Nature and location of the pain.
Duration of the pain.
Other associated symptoms-sweating, nausea, shortness of
breath, palpitations.
Past medical history (particularly heart disease, high
cholesterol).
Family history (particularly heart disease).
Smoker?
 Myocardial Infarction
Typical presentation:
Sustained central chest pain not relieved by
saling GTN.
Other features that may be present:
Collapse cardiac arrest, breathlessness,
anxiety/fear that dying, nausea vomiting,
sweating, pain in 1 or both arms, jaw, back
or upper abdomen.
Note: May occasionally be silent especially
in patients with DM.
II) Electrocardiography
III) Blood Tests
Table 2:
Normal Values of Blood Tests to
Detect Myocardial Infarction
Analysis Normal Range
Total creatinine
30-200 U/L
phosphokinase (CPK(
CPK, MB fraction 0,0-8,8 ng/mL

CPK, MB fraction percent of total CPK 0-4 %

CPK, MB2 fraction <1 U/L

Troponin I 0,0-0,4 ng/mL
Troponin T 0,0-0,1 ng/mL
Common Causes Of Chest Pain
Myocardial infarction.
Unstable angina.
Pulmonary embolism.
Pericarditis.
Pleurisy.
Pneumothorax.
Dissecting thoracic aortic aneurysm.
Oesophageal spasm.
Musculoskeletal disorders .
IV- Echocardiography :
The presence of wall motion abnormalities
on the echocardiogram
THERAPY
 Emergency care

* Relief of pain, breathlessness, and anxiety

* Cardiac arrest
Relief of pain is very important, because the pain is
associated with sympathetic activation, which causes
vasoconstriction and increases the workload of the heart.

Titrated intravenous (i.v.) opioids (e.g. morphine) are the

analgesics most commonly used in this context.

However, morphine use is associated with a slower

uptake, delayed onset of action, and diminished effects of
oral antiplatelet agents (i.e. clopidogrel, ticagrelor, and
prasugrel), which may lead to early treatment failure in
susceptible individuals.

2017 ESC Guidelines for the

management of acute STEMI
Oxygen is indicated in hypoxic patients with arterial
oxygen saturation (SaO2) < 90%. There is some evidence
suggesting that hyperoxia may be harmful in patients with
uncomplicated MI, presumably due to increased
myocardial injury. Thus, routine oxygen is not
recommended when SaO2 is90%.

Anxiety is a natural response to the pain and the

circumstances surrounding an MI. Reassurance of
patients and those closely associated with them is of
great importance.
A mild tranquillizer (usually a benzodiazepine) should be
considered in anxious patients.

2017 ESC Guidelines for the

management of acute STEMI
In patients
following cardiac
arrest
and STEMI on the
ECG,
primary PCI is the
strategy of .
Choice and should
be
considered in
survivors
of cardiac arrest
2017 ESC2h).
(within Guidelines for the
management of acute STEMI
IRA = infarct related artery *
TNK-tPA = Tenecteplase tissue plasminogen activator *
From: 2017 ESC Guidelines for the management of AMI in patients presenting with
STEMI. The Task Force for the management of AMI in patients presenting with
STEMI of the (ESC)..
From: 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting
with ST-segment elevationThe Task Force for the management of acute myocardial infarction in
patients presenting with ST-segment elevation of the European Society of Cardiology (ESC)
Eur Heart J. Published online August 26, 2017..
Organization of ST-segment elevation
myocardial infarction treatment in networks
To maximize staff experience, primary PCI centres should
perform the procedure systematically on a 24/7 basis for
all STEMI patients. Other models, although not ideal, may
include weekly or daily rotation of primary PCI centres or
multiple primary PCI centres in the same region. Hospitals
that cannot offer a 24/7 service for primary PCI should be
allowed to perform primary PCI in patients already
admitted for another reason who develop STEMI during
their hospital stay. However, these hospitals should be
discouraged from initiating a service limited to daytime-
or within-hours primary PCI, as this may generate
confusion with the EMS operators and may affect the
STEMI diagnosis-to-reperfusion time and the quality of
intervention of focused 24/7 true primary PCI centres.
Primary percutaneous
coronary intervention
and adjunctive therapy
Primary PCI is the preferred reperfusion strategy in patients with
STEMI within 12h of symptom onset, provided it can be performed
expeditiously (i.e. 120min from STEMI diagnosis) by an experienced
team.

However, in some circumstances, primary PCI is not an immediate option

and fibrinolysis could be initiated expeditiously. The extent to
which the PCI-related time delay diminishes the advantages of PCI over
fibrinolysis has been widely debated.

Rescue PCI is indicated in the case of failed fibrinolysis (i.e. ST-

segment resolution < 50% within 6090min of fibrinolytic administration),
or in the presence of haemodynamic or electrical instability, worsening
ischaemia, or persistent chest pain.

To shorten time to treatment, fibrinolysis should be administered in the

pre-hospital setting if possible. Patients should be transferred to a PCI-
capable facility as soon as possible after bolus of lytics administration.
Routine early PCI strategy is indicated after successful
fibrinolysis (preferably 224h after fibrinolysis).

There is general agreement that a primary PCI strategy should

also be followed for patients with symptoms lasting >12h in
the presence of: (1) ECG evidence of on-going ischaemia;
(2) on-going or recurrent pain and dynamic ECG changes; and
(3) on-going or recurrent pain, symptoms, and signs of heart failure,
shock, or malignant arrhythmias.

However, there is no consensus as to whether PCI is also

beneficial in patients presenting >12h from symptom onset
in the absence of clinical and/or electrocardiographic evidence of
on-going ischaemia.
A meta-analysis of trials testing whether late recanalization of an
occluded IRA is beneficial showed no benefit of reperfusion.
Therefore, routine PCI of an occluded IRA in asymptomatic
patients >48h after onset of symptoms is not indicated.
These patients should be managed like all patients with chronic total
occlusion, in which revascularization should be considered in the
presence of symptoms or objective evidence of viability/ischaemia in
the territory of the occluded artery.
Recommendations for reperfusion therapy
Recommendations for reperfusion therapy
Summary of important time targets
Procedural aspects of primary PCI
 (1) Access route
Over recent years, several studies have provided robust evidence in favour
of the radial approach as the default access site in ACS patients
undergoing primary PCI by experienced radial operators. The (MATRIX)
trial recruited 8404 ACS patients (48% STEMI) who were randomly allocated
to trans radial or trans femoral access. Radial access was
associated with lower risks of access site bleeding, vascular
complications, and need for transfusion.

The (MATRIX) trial reinforced previous observations from (RIVAL)

trial, and the (RIFLE-STEACS) trial.
(2) New-generation DES have shown superior safety and
improved efficacy compared with first-generation DES, in particular
with respect to lower risks of stent thrombosis and recurrent MI.
(COMFORTABLE AMI) trial & (EXAMINATION) trial.

Routine use of (3) deferred stenting is not recommended.

In the Taste and TOTAL trials, (4) routine thrombus

aspiration is not recommended, but in cases of large
residual thrombus burden after opening the vessel with a
guide wire or a balloon, thrombus aspiration may be
considered.
Procedural aspects of the primary PCI strategy
Peri-procedural and post-procedural
antithrombotic therapy in patients undergoing
primary PCI
Peri-procedural and post-procedural
antithrombotic therapy in patients undergoing
primary PCI
Doses of antiplatelet
and anticoagulant
cotherapies in patients
undergoing primary PCI
or not reperfused
Doses of
antiplatelet
and anticoagulant
cotherapies in
patients undergoing
primary PCI
or not reperfused
Doses of antiplatelet and anticoagulant cotherapies in
patients undergoing primary PCI or not reperfused
Therapies to reduce infarct size and micro vascular
obstruction [MVO]
Final infarct size and MVO are major independent predictors of long-
term mortality and heart failure in survivors of STEMI.

MVO is defined as inadequate myocardial perfusion after

successful mechanical opening of the IRA, and is caused by several
factors.
MVO is diagnosed immediately after PCI when:
1] post-procedural angiographic TIMI flow is<3, or
2] in case of a TIMI flow of 3 when myocardial blush grade is 0 or 1, or
3] when ST resolution within 6090min of the procedure is<70%.

Other non-invasive techniques to diagnose MVO are late gadolinium

enhancement (LGE) CMR (the current state of the art for MVO
identification and quantification), contrast echocardiography, single-
photon emission computed tomography (SPECT), and positron
emission tomography (PET).
Therapies to reduce infarct size and micro vascular
obstruction [MVO]

Different strategies, such as coronary post-conditioning, remote

ischaemic conditioning, early i.v. metoprolol, GP IIb/IIIa inhibitors,
drugs targeting mitochondrial integrity or nitric oxide pathways,
adenosine, glucose modulators, hypothermia, and others, have been
shown to be beneficial in pre-clinical and small-scale clinical
trials,217,219 but still there is no therapy aimed at reducing
ischaemia/reperfusion injury (MI size) that is clearly associated with
improved clinical outcomes. The reduction of ischaemia/reperfusion
injury in general, and MVO in particular, remains an unmet need to
further improve long-term ventricular function in STEMI.
Fibrinolysis and
pharmacoinvasive
strategy
Benefit and indication of fibrinolysis
Doses of fibrinolytic agents and antithrombotic co-
therapies
multiple bleeding risk scores outperform CHA2DS2-VASc [Cardiac
failure, Hypertension, Age 75 (Doubled), Diabetes, Stroke (Doubled)
VAScular disease, Age 6574 and Sex category (Female)] in predicting
bleeding risk.

For most patients, triple therapy (in the form of oral anticoagulation,
aspirin, and clopidogrel) should be considered for 6months. Then, oral
anticoagulation plus aspirin or clopidogrel should be considered for an
additional 6months. After 1year, it is indicated to maintain only oral
anticoagulation.

In cases of very high bleeding risk, triple therapy can be reduced to

1month after STEMI, continuing on dual therapy (oral anticoagulation plus
aspirin or clopidogrel) up to 1year, and thereafter only anticoagulation.
 Elderly patients
a higher proportion of elderly patients is expected to
present with STEMI.

atypical symptoms diagnosis of MI may be delayed or

missed.

more comorbidities and are less likely to receive

reperfusion therapy.

at particular risk of bleeding and other complications from

acute therapies because bleeding risk increases with age,
renal function tends to decrease, and the prevalence of
comorbidities is high.

using radial access whenever possible. There is no upper

age limit with respect to reperfusion, especially with
primary PCI.
 Patients with diabetes

atypical chest pain.

delayed initiation of treatment.
more diffuse atherosclerotic disease.
 Comparison of the various pharmacotherapy for
type 2 diabetes mellitus

Sulfonylureas TZDs
GLP-1
AGIs
DPP-4 agonists SGLT-2
Meglitinide
Metformin 2nd Rosigl Piogli inhibito glucagon- inhibitor alpha-
s
1st gen and 3rd itazon tazon rs like s glucosidas
gen e e peptide-1 e inhibitors

Relative
glycemic +++ +++ + +++ ++ +++ ++ ++
efficacy

Effect on Loss/
Gain Gain Gain Gain Gain Neutral Loss Loss Neutral
weight neutral

Likely
Overall CV Neutra Cauti
Benefit Caution No data benefi Neutral Benefit Benefit No data
safety l on
t

Association
GI
with
Significant Profound effects,
Lactic Hypoglyce increased
side hypoglycemia, acute GI effects
acidosis mia fracture risk,
effects secondary failure pancrea
bladder
titisa
cancera
Recommended doses of antithrombotic agents in the
acute care of patients with chronic kidney disease
 Non-reperfused patients
Patients who, for specific reasons (e.g. long delay), fail to receive
reperfusion therapy within the recommended time (first 12h) should
immediately be evaluated clinically to rule out the presence of clinical,
haemodynamic, or electrical instability.

A primary PCI strategy is indicated [class I] in the presence of signs

or symptoms suggestive of on-going myocardial ischaemia, heart
failure, haemodynamic instability, or life-threatening arrhythmias,

and should be considered [class IIa] in stable asymptomatic

patients between 1248h after symptom onset.

After that time, either a non-invasive test for the presence of residual
myocardial ischaemia/viability to decide a late invasive strategy or
elective coronary angiography should be considered [class IIa].

However, routine PCI is not indicated [class III] in totally occluded

IRA beyond the first 48h from symptom onset due to the increased
risk of late complications
I) Antiplatelet Agents:
- Aspirin in a dose of at least 160 mg and up to 325 mg
- Aspirin interferes with function of the enzyme cyclo-
oxygenase
& Inhibits the formation of thromboxane A2.
- Aspirin prevents additional platelet activation
& Interferes with platelet adhesion and cohesion.
Other antiplatelet agentsincluding clopidogrel, and
dipyridamole-for patients who have a true allergy to
aspirin
II) Supplemental Oxygen:
To patients with symptoms and/or
signs of pulmonary edema or pulse
oximetry reading less than 90% blood
oxygen saturation.
III) Nitrates:
Nitrates are metabolized to nitric oxide in the vascular
endothelium. Nitric oxide relaxes vascular smooth muscle
and dilates the blood vessel lumen.
Table 3:
Nitroglycerine Dosing Schedule
in Myocardial Infarction

Nitroglycerine Formulation Dosing

Sublingual tablet 0,2-0,6 mg every 5 minutes
Spray 0,4 mg every 5 minutes
Transdermal or paste 0,2-0,8 mg/hour
Intravenous 0,5-200 mcg/minute
IV) Beta-blockers :
Therapy is recommended within 12 hours of MI
Beta blockade decreases the rate and force of myocardial
contraction and decreases overall myocardial oxygen demand .
Table 4:
Selective Beta-1-blockers Dosing
Beta-1-blocker
Metoprolol 25-200 mg every 12 hours
Atenolol 25-200 mg every 24 hours
Esmolol 50-300 mcg/kg/minute intravenously
Betaxolol 5-20 mg every 24 hours
Bisoprolol 5-20 mg every 24 hours
Acebutolol 200-600 mg every 12 hours
V) Heparin:
1- Unfractionated Heparin
2- Low-molecular-weight Heparin (LMWH)

VI) Fibrinolytic therapy is indicated for

patients with a presentation compatible with MI
and ST segment elevation greater than 0.1 mV
in 2 contiguous EKG leads, or new onset of a
bundle branch block, who present less than 12
hours but not more than 24 hours after
symptom onset.
VII) Percutaneous Coronary Intervention:
The use of stents with PCI for MI is superior
to the use of PCI without stents, primarily
because stenting reduces the need for
subsequent target-vessel revascularization.

VIII) Glycoprotein IIb/IIIa Antagonists

IX) Surgical Revascularization:

- coronary artery bypass grafting (CABG)
2017 ESC Guidelines for the
management of acute STEMI