Acute ST-elevation

myocardial infarction
(STEMI)
Assoc Prof Serban Balanescu, MD
 Acute MI: definition
Focal myocardial cell death due to acute severe and

prolonged ischemia mostly determined by:

Acute coronary occlusion:

thrombosis on an atherosclerotic plaque or

embolization

Coronary spasm acute vasoconstriction

Different association of the two

 Classification of acute MI

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
 Prevalence of AMI in USA

Mozaffarian D et al. AHA Heart Disease and Stroke Statistics. Circulation 2015;132.

different statistic data show that death by MI is responsible of 20-25% of total mortality.
In Romania, in 1992, 58% of death occurred because of cardiovascular causes, and 25% was
due to AMI.
Circadian pattern of the occurrence of MI
 Etiology
A. non atherosclerotic obstructive CAD:
a) Coronary vasculitis (large epicardial vessels):
- lues
- chronic infection (TB, Salmonella, leper)
- poly-arteritis nodosa
- Wegeners granulomatosis
- Takayasu disease
- Systemic lupus erythematosus
b) Wall thickening or intimal proliferation (small intramural coronary vessels):
- coronary X sdr (small coronary vessel disease)
- amyloidosis, muco polysaccharidosis
- oral contraceptives and smoking
- post irradiation coronary fibrosis
c) extrinsic compression:
- tumors (subepicardial metastasis)
- Valsalva sinus aneurysm
B. coronary embolization:
- infective endocarditis
- mitral valve prolapse
- left trial appendage of left ventricular thrombus
- atrial myxoma
- intraoperatory or coronary angiography embolization
- papilary fibroelastoma of aortic cusps
 Etiology
C. Traumatic:
- coronary dissection postangioplasty
- aortic dissection type A
- myocardial contusion; other, penetrating trauma
D. congenital coronary anomalies:
a) abnormal origin in the aortic root
- in the controlateral Valsalva sinus (LCA or RCA)
- single coronary artery
b) Coronary origin of LM in the pulmonary artery (ALCAPA)
c) arterio-venous coronary fistulas
E. in situ coronary thrombosis:
- policythemia vera
- primary idiopathic thrombocytosis
- disseminated intravascular coagulation
F. Other:
- coronary spasm with normal coronary arteries (Prinzmetal)
- NSTEMI with severe LV hypertrophy in different conditions
associated to prolonged mechanic overload or hypoxia
 Pathology
3 main morphologic stages:
Acute myocardial necrosis
Myocardial resorbtion and invasion with inflammatory cells (neutrophils, etc)
Irregular progressive scarring; patchy, irregular, isles of viable myocardium
interspersed with scars

Morphology dynamics:
Progressive necrosis starts ~ 1h, complete at 4-6 h after occlusion can be
seen as bluish discoloration of myocardium
24-48 h necrotic myocardium purple red, fibrinous subepicardial reaction
2-7 days peripheral haemorrhagic contour, some yellow streaks inside
1- 4 weeks necrotic myocites invaded by macrophages, inflammatory cells
1 - 3 months myocardial necrosis is replaced by white scar (fibrous tissue)
stunned miocardium: viable but non functional myocardium at the periphery of
necrotic zone
Can evolve towards necrosis or recovery
 Anteroseptal MI: gross pathology

Apex
Mid-ventricular
section
Antero-lateral MI

Sub endocardial layers:

usually the most severely
ischemic
Gross pathology of RV myocardial infarction
 AMI: light microscopy

AMI day 1 from onset

MI 3 months after acute

disease

AMI day 3 from onset

Antero-lateral acute MI with intra
myocardial hemorrhage
 Ventricular remodeling
Infarct zone expansion - progressive

Aneurysm formation
Starts as early as 24-48h
 Pathophysiology of AMI

Complicated atherosclerotic plaque

Microcirculation IRA

Myocardial necrosis Capillaries

Myocardium
 Pathophysiology of AMI: complicated
atherosclerotic plaque
intrinsic plaque vulnerability
Large lipid core
Thin fibrous cap
Many inflammatory cells
Biomechanical causes:
BP
HR
Vasospasm
Plaques frequently rupture at dawn:
circadian rhythm of
platelet aggregation
PAI, endogenous fibrinolysis
serum epinephrine
 Vulnerable plaque
thrombosis
Erosion:
- 25% of lesions
- associated with smoking
- more frequent in F

Rupture:
- 75% of lesions; n = 298 pts
- abnormal lipid prophile

Arbustini E et al. Heart 1999;82:269.

 Acute coronary sdr by
ruptured plaque thrombosis spasm

Luminal obstruction Clinical syndrome

Temporary or non-occlusive Unstable angina ,

NSTEMI

Persistent, occlusive STEMI

Modulating factor: the presence of collateral vessels: one of

the main determinants of the volume of myocardial necrosis
Distal embolization
in AMI

Consequence of:
plaque ulceration
reperfusion
Pathophysiology of MI: myocardial necrosis and
its consequences
diastolic dysfunction
Segmentary systolic dysfunction
Systolic dysfunction is
proportional with the volume of
myocardial necrosis:
< 20% of LV mass: no LVF
20-40% of LV mass: LVF clinically
relevant
> 40% of LV mass: cardiogenic shock
The increase of serum enzymes is
proportional with necrosis extent
 Killip classification of MI (clinical)
Functional class Clinical signs Mortality

Class I - No signs of heart failure 5-7%

(noncomplicated AMI)

Class II - Wet pulmonary rales on both

inferior 1/3 of the lungs and/or
10-15%
(mild-to-moderate HF) 3rd heart sound with tachycardia

Class III - Wet pulmonary rales up to both

suprascapular spaces; frank
20-50%
(severe congestive HF cardiogenic pulmonary edema
acute pulmonary
edema)

Class IV -- Peripheral hypoperfusion, cold,

wet skin, confusion)
60-80%
(cardiogenic shock) -- Systemic hypotension (SBP
90 mmHg)
- tachycardia
 Forrester hemodynamic classification
Cardiac Index

18 mmHg
l/m2/min

4 1 B Hyperdinamic
II pulmonary congestion
1 A Compensated
3

2.5 l/m2/
2
III isolated
sistemic IV cardiogenic shock
1
hypoperfusion
Pulmonary capillary wedge pressure

10 20 30 mmHg
 Clinical examination: symptoms
Ischemic pain:
Excruciating central chest or all anterior thorax
Irradiated to both shoulders, arms, (left shoulder and arm), neck, jaw, or
posterior thorax
Intense
Different description: constrictive, penetrating, central chest weight
Lasts > 30 min or repeated intense chest pain lasting more hours
Does not disappear at rest and GTN does not alleviate it
Accompanied by:
Adrenergic signs: profuse sweating, palpitations, anxiety
Shortness of breath, polypneic
Digestive symptoms: nausea, vomiting
dizziness, syncope
 Clinical examination: signs
Initial vegetative imbalance first hour:
either sympathetic NS pallor, cold sweats, polypnea, tacycardia
or parasympathetic NS in inferior MI hypotension, bradycardia, nausea
Heart rhythm:
tachycardic or bradicardic
Ventricular premature beats
Heart sounds:
soft S1
Gallop sounds: S4 +/- S3
Functional MR or MR due to mechanical complication
pericardial rub: 10-20% of pts: epicardial necrosis or extensive necrosis
BP:
Reactive HT due to sympathetic overstimulation
hypotension:
Vasodepressor reflex (Bezold Jarisch): coronary and systemic VDil due to
myocardial ischemia and coronary occlusion
inferior MI +/- RV infarction (low preload)
anterior MI with acute severe systolic LV dysfunction
 Diagnosis
Chest pain (variable, may lack in old people, DM)
Standard ECG
Elevated serum enzymes diagnostic for
myocardial necrosis

Other serum markers

Chest X-ray
Echocardiography
Coronary angiography to perform primary PCI
 ECG diagnosis in acute STEMI
Age and gender specific
New ST elevation at J point in 2 contiguous
leads
> 0.1 mV in all leads except V2-V3
In leads V2-V3 in men
> 0.2 mV > 40 years
> 0.25 mV < 40 years
In leads V2-V3 in women
> 0.15 mV in women
Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
 ECG diagnosis in acute NSTEMI

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
 ECG changes in acute STEMI

1. supra-acute MI: high symmetric T waves; 3. sub- acute MI: isoelectric ST,
monophasic QRS complex; Q waves; negative T waves;
first 4-6h form chest pain onset after 24-48h can be present
for a few weeks

2. Acute MI: persistent ST, 4. Chronic phase: Q waves;

new Q waves; positive T waves;
after 4-6 h can be maintained after 2-3 months form index event
in the first 24-48h

NB. ECG changes are significantly accelerated by reperfusion treatment

Classification of MI depending on admission ECG

Anatomy of Electrocardio- 30 day 1-year

Categories occlusion graphic pattern mortality (%) mortality (%)
ST V16, I, aVL and
1. Proximal left Proximal to first septal
anterior descending perforator
fascicular or bundle 19.6 25.6
branch block

Proximal to large
2. Mid-left anterior
descending
diagonal, but distal to ST V16, I, aVL 9.2 12.4
first septal perforator

3. Distal left anterior

Distal to large diagonal ST V14 or ST I,
descending or or of diagonal itself aVL, V56 6.8 10.2
diagonal
ST II, III, aVF and
4. Moderate to large any or all of the
inferior (posterior, Proximal RCA or left following:
lateral, right circumflex a. V1, V3R, V4R or 6.4 8.4
ventricular) b. V5V6 or
c. R > S in V1, V2
Distal RCA or left
5. Small inferior circumflex, branch ST II, III, aVF only 4.5 6.7
occlusion
 STEMI Topol 1:
anterolateral MI + RBB + LAHB
=
occluded proximal LAD

LVF or cardiogenic
shock are frequent
STEMI Topol 1: anterolateral MI + LAHB
STEMI Topol 2: anteroseptal MI
= occluded mid LAD

Cardiogenic shock is rare

LVF is possible; apical aneurysm

or intracardiac thrombus also

possible
 STEMI Topol 3:
high lateral MI =
occluded distal LAD
or diagonal vessel

Mechanical
complications
very rare
 STEMI Topol 4:
AMI postero-inf and RV
=
occluded proxymal RCA
or dominant Cx
Frequent mechanical complications
Complete AV block
STEMI Topol 5:
strictly inferior MI =
occluded distal RCA sau
distal dominant Cx

Mechanical complications
are rare
hypotension: RV infarction
frequent vagal reactions
to look for V3R, V4R, V7-9
Other patterns of STEMI according to ECG
changes
Strict posterior AMI:
Occlusion of marginal or PL branches of the Cx
ST elevation strictly limited to posterior leads: V7-V9
mirror ST depression in precordial leads: V1-V3
Large symmetric R waves in precordial leads: V1-V3
No hemodynamic consequences; possible involvement the
lateral wall of LV or inferior RV
NON STEMI
Old terminology:
Sub-endocardial MI
Non-Q MI
Different ECG patterns:
Large negative T waves in
precordial leads
Persistent ST segment depression
Biphasic T waves
ECG changes are similar to those in
unstable angina, but are persistent
and are associated with diagnostic
increase of serum enzymes
 Serum markers of myocardial necrosis
Enzyme Normal Onset of Maximum Complete Other clinical
values increase resolution situations with
increase
Myoglobin 2-3 h 12 h 2 days Rhabdomyolysis

Total CK 25-90U 6-12 h 24 h 3 days Muscular disease, stroke,

renal, intestinal disease

5% of CK
CK-MB 6h 12-24 h 2-3 days Strenuous exercise, muscular
trauma, external DC shock,
intestinal disease, uterus.

TGO (ASAT) 0-35U 8-12 h 18-36 h 4-5 days Hepatic disease, CHF,
Muscular disease, stroke, infarct
renal

LDH 25-100U 24-48 h 3-4 zile 7-10-14 Hepatic disease, CHF,

days Renal disease, intestinal
disease, hemolytic anemia,
leukemia, cancer

LDH1 15-25% of
LDH
12-24 h 3-4 zile 7-10-14 Hematologic and renal disease

days

TnT & TnI Different 6h 24 h 3-4 days Many renal, cerebral,

assays cardiac conditions
 Bio-markers for diagnosis of myocardial
necrosis - infarction

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
 Elevation of serum troponin due
cardiomyocyte injury (including necrosis)

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
Dynamics of serum markers of myocardial
necrosis
Other blood samples with changes in AMI
Inflammatory Sdr : ESR, fibrinogen, C reactive protein, leukocytosis
Systemic pro-coagulant status: platelet aggregation and coagulation
Blood glucose:
High blood glucose due to adrenergic reaction of associated DM
25 - 50% of pts with AMI are diabetic or have altered OGTT
Total cholesterol , LDL HDL
Cholesterol is reduced in AMI; dyslipidemia should be correctly
assessed 6 weeks after AMI (pt already on high-dose statin)
serum K+ and Mg2+ (hypo favors ventricular arrhythmia)
Creatinine: renal dysfunction alters prognosis and interferes with
necessary medication (i.e. ACEI or sartans)
Assessment of other metabolic RF:
Hyperuricemia
homocysteine
 Chest X ray in AMI

Pulmonary oedema in AMI

 Imaging diagnosis of acute myocardial
infarction

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
Echocardiography in AMI
Allows assessment of systolic and diastolic
dysfunction:

systolic function remains stable after

day 5-7 post-MI

Allows assessment of the extent of

segmental wall motion anomalies

Helps diagnosis of mechanical

complications:

Rupture of the free wall or of IV

septum

Acute mitral regurgitation (papillary

rupture)

Demonstrates pericardial fluid

Coronary angiography and primary PCI in
AMI
 Diagnosis criteria of type 1 and type 2
acute myocardial infarction

Thygessen K et al. 3rd Universal Definition of Myocardial Infarction. Eur Heart J 2012;33:2551-67.
 Differential diagnosis of AMI
1. Other acute ischemic sdr with or without ST segment elevation:
Vasospastic angina
Unstable angina
2. Persistent ST segment elevation post MI (frozen ST segment), usually LV aneurysm
3. Other acute cardiac disease
Acute pericarditis, myocarditis
4. Hyperkalemia (large symmetric pointed T wave)
5. Digitalis toxicity for NSTEMI, concave ST segment depression
6. acute non ischemic LV failure (other causes of pulmonary edema)
7. extracardiac disease:
non cardiogenic pulmonary edema; acute pulmonary embolism
acute aortic dissection
Perforated peptic ulcer
acute mediastinitis spontaneous esophageal perforation
Gastro-esophageal reflux
Acute cholecystitis
Acute pancreatitis
Spontaneous pneumothorax
 ECG recording
showing
pseudo AMI
due to hyper K+

Wang K. NEJM 2004;351:593.

 Recommended readings
Harrisons Principles of Internal Medicine; 19th ed, 2015

Goldman-Cecil Medicine, (Cecil Textbook of Medicine), 25th

ed, 2015, chapter 72 and 73.

3rd universal definition of myocardial infarction:

Free full download at: http://www.escardio.org/Guidelines/Clinical-Practice-
Guidelines/Third-Universal-Definition-of-Myocardial-Infarction

Acute MI in patients presenting with ST-elevation:

Free full download at: http://www.escardio.org/Guidelines/Clinical-Practice-
Guidelines/Acute-Myocardial-Infarction-in-patients-presenting-with-ST-
segment-elevation-Ma