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Chapter 50 Chapter 50 ST-Elevation Myocardial ST-Elevation Myocardial Infarction: Pathology, Infarction: Pathology, Pathophysiology, Pathophysiology, and Clinic
Chapter 50 Chapter 50 ST-Elevation Myocardial ST-Elevation Myocardial Infarction: Pathology, Infarction: Pathology, Pathophysiology, Pathophysiology, and Clinic

Chapter 50

Chapter 50

ST-Elevation Myocardial

ST-Elevation Myocardial

Infarction: Pathology,

Infarction: Pathology,

Pathophysiology,

Pathophysiology,

and Clinic Features

and Clinic Features

Vinod Patel

Vinod Patel

University o

University of South Florida

f South Florida

 The The pat pathological prolonged prolonged isische chemmia. ia.  The The clini cliniccal diagnosis
The
The pat
pathological
prolonged
prolonged isische
chemmia.
ia.
The
The clini
cliniccal diagnosis
 The The pat pathological prolonged prolonged isische chemmia. ia.  The The clini cliniccal diagnosis

hological diagnosis of myocardial infarction (MI)

diagnosis of myocardial infarction (MI)

requires evidence of myocyte

requires evidence of myocyte

cell death as a consequence of

cell death as a consequence of

al diagnosis of MI

of MI

requires an integrated assessment

requires an integrated assessment

of the history with some combination of indirect evidence of

of the history with some combination of indirect evidence of

myocardial necrosis using bio

myocardial necrosis using biochemical, electrocardiographic,

chemical, electrocardiographic,

d imaging modalities.

anand imaging modalities.

 • • • •
 • • • • ischemia (ST segment ischemia (ST segment Typical rise and/or fall of

ischemia (ST segment

ischemia (ST segment

Typical rise and/or fall of biochemical markers of myocardial

Typical rise and/or fall of biochemical markers of myocardial

necrosis with at least one of the following:

necrosis with at least one

of the following:

  • a) a) Ischemic symptoms

Ischemic symptoms

  • b) b) Development of pathologic

Development of pathologic Q waves in the ECG

Q waves in the ECG

  • c) c) ECG changes indicative of

ECG changes indicative of

elevation or depression)

elevation or depression)

  • d) d) Imaging evidence

Imaging evidence

of

of

new loss of viable myocardium or

new loss of viable myocardium or

new regional wall motion

new regional wall motion abnormality.

abnormality.

Pathologic findings of an acute myocardial infarction.

Pathologic findings of

an acute myocardial infarction.

 Criteria for Healing or Healed Myocardial Infarction. Criteria for Healing or Healed Myocardial Infarction. Any
Criteria for Healing or Healed Myocardial Infarction.
Criteria for Healing or Healed Myocardial Infarction.
Any one of the following criteria satisfies the diagnosis for
Any one of the follow ing criteria satisfies the diagnosis for
healing or healed myocardial infarction:
healing or healed myocardial infarction:
1. Development of new pathological Q waves in serial
1. Development of new pathological Q waves in serial
ECGs. The patient may or may not remember previous
ECGs. The patient may or may not remember previous
symptoms. Biochemical marker s of myocardial necrosis
symptoms. Biochemical markers of myocardial necrosis
may have normalized depending on the length of time that
may have normalized depending on the length of time that
has passed since the infarction developed.
has passed since the infarction developed.
2. Pathological findings of a healed or healing infarction.
2. Pathological findings of a healed or healing infarction.
 from from anan acacuutete MMI.I.   Of particular concern Of particular concern cocoununtries tries..
from
from anan acacuutete MMI.I.
Of particular concern
Of particular concern
cocoununtries
tries..
ts in the United States. perspective are perspective are
ts in the United States.
perspective are
perspective are

In the United States, nearly 1 million patients a year suffer

In the United States, nearly 1

million patients a year suffer

More than 1 million patients

More than 1 million patients

with s

with suspected acute MI are

uspected acute MI are

admitted yearly to coronary care

admitted yearly to coronary care

uni

units in the United States.

from a global

from a global

projections that the burden of

projections that the burden of

disease in developing countries

disease in developing countries

will become similar to those now afflicting developed

will become similar to those

now afflicting developed

 unst unstaable case fatality rate once case fatality rate once  observational data bas 
unst unstaable
case fatality rate once
case fatality rate once
observational data bas
rate four times that of
rate four times that of
anandd bl blaacks cks..
the treatment patterns of
the treatment patterns of

6.5 to 7.5 %, whereas

Drop in mortality appears

Drop in mortality appears

to result

to result

from a fall in the incidence

from a fall in the incidence

of STEMI (replaced in part by an increase in the rate of

of STEMI (replaced in part by an increase in the rate of

ble angina/non-ST-segment elevation MI and a fall in the

angina/non-ST-segment elevation MI and a fall in the

STEMI

STEMI

has occurred).

has occurred).

The short-term mortality rate of patients with STEMI in

The short-term mortality rate

of patients with STEMI in

randomized trials is in the range of

randomized trials is in the range

of 6.5 to 7.5 %, whereas

observational data bases suggest

es s uggest

5 to 20%

5 to 20%

Clinical trial data from studies of fibrinolysis show that the

Clinical trial data from studies of fibrinolysis show that the

elderly (75 years old or

elderly (75 years old or

older)

older) continue to suffer a mortality

continue to suffer a mortality

younger patients.

younger patients.

Variation has also been

Variation has also been

observed in the treatment patterns of

observed in

certain population subgroups

certain population subgroups with STEMI, notably women

with STEMI, notably women

 TaTable ble 5050.1.1
 TaTable
ble 5050.1.1
Causes of MI without coronary atherosclerosis Causes of MI without coronary atherosclerosis  Arter Arteritis itis
Causes of MI without coronary atherosclerosis
Causes of MI without coronary atherosclerosis
Arter
Arteritis
itis
• LLuetic
uetic
Granulomatous (Takayasu diseas e)
Granulomatous (Takayasu disease)
Polyarteritis nodos a
Polyarteritis nodos a
Mucocutaneous lymph node (Kawasaki) syndrome
Mucocutaneous lymph node (Kawasaki) syndrome
Disseminated lupus erythematosus
Disseminated lupus erythematosus
Rheumatoid spondylitis
Rheumatoid spondylitis
Ankylosing spondylitis
Ankylosing spondylitis
Trauma to coronary arteries
Trauma to coronary arteries
• LLaceration
aceration
Thr
Thrombo
ombosis
sis
Iatrog
Iatrogeenic
nic
Radiation (radiation therapy for neoplasia)
Radiation (radiatio n therapy for neoplasia)
 Coronary mural thicken ing with metabolic disease or intimal Coronary mural thickening with metabolic disease
Coronary mural thicken ing with metabolic disease or intimal
Coronary mural thickening with metabolic disease or intimal
prolif proliferative erative dis diseeasasee
Mucopolysaccharidoses (Hurler disease)
Mucopolysaccharidoses (Hurler disease)
• Ho Hommocy ocystinu stinuria ria
• Fabry Fabry di disease sease
• Amy
Amyloidos
loidosisis
Juvenile intimal sclerosis (idiopathic arterial calcification
Juvenile intimal sclerosis (idi opathic arterial calcification
ofof infancy) infancy)
Intimal hyperplasia associated with contraceptive steroids
Intimal hyperplasia associated with contraceptive steroids
or with the postpartum period
or with the postpartum per iod
Pseudoxanthoma elasticum
Pseudoxanthoma elasticum
Coronary fibrosis caus ed by radiation therapy
Coronary fibrosis caused by radiation therapy
 • Spasm of coronary cocorronary onary ararteries teries)) • • •
Spasm of coronary
cocorronary
onary ararteries
teries))
 • Spasm of coronary cocorronary onary ararteries teries)) • • • Luminal narrowing by other

Luminal narrowing by other mechanisms

Luminal narrowing by other

mechanisms

Spasm of coronary arteries (Prinzmetal angina with normal

arteries (Prinzmetal angina with normal

Spasm after nitroglyce

Spasm after nitrogly

cerin

rin

withdrawal

withdrawal

Dissection of the aorta

Dissection of the aorta

Dissection of the coronary

Dissection of the coronary

artery

artery

 EEmmboli • • • • • CCard ardiac iac mmyyxxomomaa • • Paradoxical emboli Paradoxical
EEmmboli
CCard
ardiac
iac mmyyxxomomaa
Paradoxical emboli
Paradoxical emboli
 EEmmboli • • • • • CCard ardiac iac mmyyxxomomaa • • Paradoxical emboli Paradoxical

thrombus from left atrium,

boli ttoo CCororoonnaarry Arteries

y Arteries

Infective endocarditis

Infective endocarditis

Nonbacterial thrombotic endocarditis

Nonbacterial thrombotic endocarditis

Prolapse of mitral valve

Prolapse of mitral valve

Mural

Mural thrombus from left atrium,

left ventricle, or pulmonary veins

left ventricle, or pulmonary veins

Prosthetic valve emboli

Prosthetic valve emboli

Associated with cardiopulmonary bypass surgery and

Associated with cardiopulmonary bypass surgery and

coronary arteriography

coronary arteriograp

hy

Papillary fibroelastoma of

Papillary fibroelastoma of

the aortic valve (fixed embolus)

the aortic valve (fixed embolus)

Thrombi from intracardiac

Thrombi from intracardiac catheters or guidewires

catheters or guidewires

 Congenital Coronary Artery Anom alies Congenital Coronary Artery Anomalies • Anomalous origin of left coronary
Congenital Coronary Artery Anom alies
Congenital Coronary Artery Anomalies
Anomalous origin of left coronary from pulmonary artery
Anomalous origin of left coronary from pulmonary artery
Left coronary arter y from anterior sinus of Valsalva
Left coronary artery from anterior sinus of Valsalva
Coronary arteriovenous and arteriocameral fistulas
Coronary arteriovenous and arteriocameral fistulas
Coronary artery aneurysms
Coronary artery aneurysms
Myocardial Oxygen Demand- Supply Disproportion
Myocardial Oxygen Demand-Supply Disproportion
Ao
Aorrtictic sstenosis
tenosis
Incomplete differentiation of the aortic valve
Incomplete differentiation of the aortic valve
Aortic insufficiency
Aortic insufficiency
Carbon monoxide poisoning
Carbon monoxide poisoning
Thy
Thyrotoxi
rotoxiccososisis
Prolonged hypotension
Prolonged hypotension
Takotsubo cardiomyopathy
Takotsubo cardiomyopathy
 Hematological (in situ Thrombosis) Hematological (in situ Th rombosis) • Polycythemia vera Polycythemia vera •
Hematological (in situ Thrombosis)
Hematological (in situ Th rombosis)
Polycythemia vera
Polycythemia vera
Thr
Thrombo
omboccyytos
tosisis
Disseminated intravascular coagulation
Disseminated intravascular coagulation
Hypercoagulability, thrombosis, thrombocytopenic purpura
Hypercoagulability, thrombosis , thrombocytopenic purpura
Mi
Miscellaneous
scellaneous
• CCocaine
ocaine abuse
abuse
Myocardial contusion
Myocardial contusion
Myocardial infarction with normal coronary arteries
Myocardial infarction with normal coronary arteries
Complication of cardiac catheterization
Complication of cardiac catheterization
PLAQUE PLA QUE  Release of chemokines by endothelial cells and increase Release of chemokines by
PLAQUE
PLA QUE
Release of chemokines by endothelial cells and increase
Release of chemokines by endothelial cells and increase
expression of adhesion proteins.
expression of adhesion proteins.
Entry of WBC into the wall.
Entry of WBC into the wall.
T cells in the arterial wall produce cytokines which
T cells in the arterial wall produce cytokines which
stimulates endothelial cell proliferation and activate
stimulates endothelial cell pr oliferation and activate
mmicrophage icrophagess..
Events During Atherogenesis Events During A th e rogenesis
Events During Atherogenesis
Events During A th e rogenesis
 STEMI are composed STEMI are composed • 90% fibrous tissue 90% fibrous tissue • lipid.
STEMI are composed
STEMI are composed
90% fibrous tissue
90% fibrous tissue
lipid.
lipid.
and contain platele
 STEMI are composed STEMI are composed • 90% fibrous tissue 90% fibrous tissue • lipid.

cells, and extracellular

cells, and extracellular

throcytes, and leukocytes.

At autopsy, the atherosclerotic plaques of patients who died of

At autopsy, the atherosclerotic plaques of patients who died of

of :

of :

of varying

of varying density and cellularity with

density and cellularity with

superimposed thrombus.

superimposed thrombus.

10% Calcium, lipid-laden foam

10% Calcium, lipid-laden foam

The atherosclerotic plaques generally more complex and

The atherosclerotic plaques gen

erally more complex and

irregular than those in

irregular than those in

vessels not associated with STEMI.

vessels not associated with STEMI.

Coronary arterial thr

Coronary arterial thrombi are

ombi are

approximately 1cm in length

approximately 1cm in length

in most cases; adhere to the luminal surface of an artery;

in most cases; adhere to the luminal surface of an artery;

and contain platelets, fibrin, erythrocytes, and leukocytes.

ts, fibrin, ery

 The balance of synthetic and degradative activity of collagen, The balance of synthetic and degradative
The balance of synthetic and degradative activity of collagen,
The balance of synthetic and degradative activity of collagen,
the major structural component of the fibrous cap, account for
the major structural component of the fibrous cap, account for
itsits mmeechanical
chanical ststrength and determines plaque stability and
rength and determines plaque stability and
prognos prognosisis..
Statins -> stabalize plaques by their lipid lowering effect as
Statins -> stabalize plaques by their lipid lowering effect as
well as reduce plaque inflammation.
well as reduce plaque inflammation.
2/3 of the plaques resulting in STEMI are caused by an
2/3 of the plaques resulting in STEMI are caused by an
occlusion of 50% or less and 85% has occlusion of <70%
occlusion of 50% or less and 85% has occlusion of <70%
The coronary distribution of STEMI is:
The coronary distribution of STEMI is:
LAD 40-50%
LAD 40-50%
RCA 30-40%
RCA 30-40%
Lcx 15-20%
Lcx 15-20%
Vulne
Vulnerrable
able plaques
plaques
• LLarge area of foam cells and extracellular lipids
arge area of foam cel ls and extr acellular lipids
• Thin Thin ffibrous ibrous cap cap
Few smooth muscle
Few smooth muscle
Clusters of inflammatory cells
Clusters of inflammatory cells
 Role of acute plaque changes Role of acute plaque changes • Rupture/fissuring: exposing the highly
Role of acute plaque changes
Role of acute plaque changes
Rupture/fissuring: exposing the highly thrombogenic
Rupture/fissuring: exposing the highly thrombogenic
plaque plaque ccononstit stitueuennts. ts.
Erosion/ulceration: exposing the thrombogenic
Erosion/ulceration: exposing the thrombogenic
subendothelial basement membrane to blood
subendothelial basement membrane to blood
Hemorrhage into the atheroma, expending its volume.
Hemorrhage into the atheroma, expending its volume.
Plaque fissuring and disruption
Plaque fissuring and disruption
Overexpression of metalloproteinase enzymes such as
Overexpression of metalloproteinase enzymes such as
collagenase, gelatinase, and stromelysin
collagenase, gelatinase, and stromelysin
Activated macrophages and mast cells abundant at the site.
Activated macrophages and mas t cells abundant at the site.
Stresses induced by intraluminal pressure, coronary
Stresses induced by intraluminal pressure, coronary
vasomotor tone, tac hycardia (cyclic stretching and
vasomotor tone, tachycardia (cyclic stretching and
compression), and disruption of nutrient vessels combine to
compression), and disruption of nutrient vessels combine to
produce plaque disruption.
produce plaque disruption.
Junction of the fibrous cap and the adjacent normal plaque free Junction of the fibrous cap
Junction of the fibrous cap and the adjacent normal plaque free
Junction of the fibrous cap and the adjacent normal plaque free
arterial segment is the location at which the blood flow-inducing
arterial segment is the location at which the blood flow-inducing
mechanical stresses within the plaque are highest and the fibrous
mechanical stresses within t he plaque are highest and the fibrous
cap cap isis tthinnest hinnest..
 A number of key physiologic al variables such as systolic A number of key phy
A number of key physiologic al variables such as systolic
A number of key phy siologi cal variables such as systolic
blood pressure, heart rate, blood viscosity, endogenous tissue
blood pressure, heart rate, blood viscosity, endogenous tissue
plasminogen activator (t-PA ) activity, plasminogen activator
plasminogen activator (t- PA) activity, plasminogen activator
inhibitor-1 (PAI-1) levels, plasma cortisol levels, and plasma
inhibitor-1 (PAI-1) levels, plasma cortisol levels, and plasma
epinephrine levels exhibit circadian and seasonal variations
epinephrine levels exhibit circadian and seasonal variations
and increase at times of stress.
and increase at times of stress.
Vasospasm is caused by:
Vasospasm is caused by:
Circulating adrenergic agonists
Circulating adrenergic agonists
Locally released platelet contents
Locally released platelet contents
Im paired secretion of endothelial cell relaxing factors
Impaired secretion of endothelial cell relaxing factors
relative to contracting factors.
relative to contracting factors.
Mediators released from peri -vascular inflammatory cells.
Mediators released from peri-vascular inflammatory cells.
 anandd PPFF 33 -4-4 
anandd PPFF 33 -4-4
 anandd PPFF 33 -4-4  Exposed to subendothelial collagen and necrotic plaque Exposed to subendothelial

Exposed to subendothelial collagen and necrotic plaque

Exposed to subendothelial collagen and necrotic plaque

contents, platelets undergo adhesion, aggregation, activation

contents, platelets undergo adhesion, aggregation, activation

and release of potent aggr

and release of potent aggregators including TXA2, serotonin

egators including TXA2, serotonin

Activation of extrinsic pathway.

Activation of extrinsic pathway.

http://www.youtube.com/watch?v=41h8OhRHAw0

http://www.youtube.com/wa

tch?v=41h8OhRHAw0

 • •   that that ofof ththee left left  cavity cavity
that
that ofof ththee left
left
cavity
cavity
esions involving the RCA.
esions involving the RCA.

with inferior infarction

with inferior infarction

l lesions involving the RCA.

allows the chamber to

allows the chamber to

RIGHT VENTRICULAR INFARCTION.

RIGHT VENTRICULAR INFARCTION.

Approximately 50%

Approximately 50%

of patients

of patients

have some involvement of the right ventricle

have some involvement o

f the right ventricle

RV occurs less commonly

RV occurs less commonly

than would be anticipated from

than

would be anticipated from

the frequency of atherosclerotic

the frequency of atherosclerotic

This discrepancy

This discrepancy

can probably be explained by the

can probably be explained by the

lower oxygen demands

lower oxygen demands

Inter-coronary collateral system of the RV is richer than

Inter-coronary collateral system of the RV is richer than

The thinness of the

The thinness of the

RV wall

RV wall

derive some nutrition from the blood within the RV

derive some nutrition from the blood within the RV

 ATRIAL ATRIAL IINFA NFARCTI RCTIOON. N.  This can be seen in up to 10%
ATRIAL
ATRIAL IINFA
NFARCTI
RCTIOON.
N.
This can be seen in up to 10% of patients with STEMI if PR-
This can be seen in up to 10% of patients with STEMI if PR-
segment displacement is used as the criterion for atrial
segment displacement is used as the criterion for atrial
infarction infarction..
Although isolated atrial infarction is observed in 3.5% of
Although isolated atrial infarction is observed in 3.5% of
autopsies of patients with ST EMI, it often occurs in
autopsies of patients with STEM I, it often occurs in
conjunction with ventricular infarction.
conjunction with ventricular infarction.
Occurs more frequently in the atrial appendages
Occurs more frequently in the atrial appendages
(Rt > Lt) explained by higher oxygen content of left atrial
(Rt > Lt) explained by higher oxygen content of left atrial
blood. blood.
It has also been linked to reduced s ecretion of atrial natriuretic
It has also been linked to reduced s e cretion of atrial natriuretic
peptide and a low cardiac output syndrome when right
peptide and a low cardiac output syndrome when right
ventricular infarction coexists
ventricular infarction coexists .
 No plaque disruption in about 10% of cases. No plaque disruption in about 10% of
No plaque disruption in about 10% of cases.
No plaque disruption in about 10% of cases.
Many of these cases are caus ed by coronary artery spasm
Many of these cases are caused by coronary artery spasm
and/or thrombosis, perhaps with underlying endothelial
and/or thrombosis, perhaps with underlying endothelial
dysfunction or small plaques in apparent on coronary
dysfunction or small plaques in apparent on coronary
anangi giography. ography.
MI with angiographically normal coronary vessels.
MI with angiographically normal coronary vessels.
Yo
Younungg
Often have a history of cigarette smoking
Often have a history of cigarette smoking
(Takotsubo cardiomyopathy) catecholamine-mediated
(Takotsubo cardiomyopathy) catecholamine-mediated
myocardial stunning and microvascular dysfunction play
myocardial stunning and microvascular dysfunction play
imimportant portant rroles. oles.
 Transmural versus subendocardial infraction Transmural versus subendocardial infraction  Mos Mostt MMIsIs are are trans
Transmural versus subendocardial infraction
Transmural versus subendocardial infraction
Mos
Mostt MMIsIs are
are trans
transmmural
ural
Subendocardial infarct constitutes an area limited to inner 1/3
Subendocardial infarct constitutes an area limited to inner 1/3
oror ½. ½.
Plaque disruption -> thrombus-> lysis before necrosis
Plaque disruption -> thrombus-> lysis before necrosis
extends across maj or thickness.
extends across maj or thickness.
Chronic occlusion + prolonged severe reduction in
Chronic occlusion + prolonged severe reduction in
systemic blood pre ssure.
systemic blood pressure.
 Ana Anaerob erobicic gglycolys lycolysisis  Inadequate production of high-energy phosphates and Inadequate production of
Ana
Anaerob
erobicic gglycolys
lycolysisis
Inadequate production of high-energy phosphates and
Inadequate production of high-energy phosphates and
accumulation of potentially noxious breakdown products (such
accumulation of potentially noxious breakdown products (such
asas lactic lactic acid) acid)
Str
Striking loss of contractility occurs with in 60 seconds.
iking loss of contractility occurs with in 60 seconds.
Ultrasturctural evidence of irrevers ible myocyte injury.
Ultrasturctural evidence of irrevers ible myocyte injury.
CCell
ell dedeath:
ath:
Coagulation necrosis
Coagulation necrosis
Ap
Apot
otosis
osis
 Prior to cell death there is a period during which the ischemic Prior to cell
Prior to cell death there is a period during which the ischemic
Prior to cell death there is a period during which the ischemic
m yocyte is viable, but vulnerable to further injury if blood
myocyte is viable, but vulnerable to further injury if blood
flow is restored (ie, reperfusi on injury). During this period, the
flow is restored (ie, reperfusion injury). During this period, the
reintroduction of oxygen and energy into an abnormal cellular
reintroduction of oxygen and energy into an abnormal cellular
environment triggers addi tional events that produce further
environment triggers additional events that produce further
mmyocyte yocyte damdamagage. e.
Reperfusion injury refers to myocardial, vascular, or
Reperfusion injury refers to myocardial, vascular, or
electrophysiological dysfunction that is induced by the
electrophysiological dysfunc tion that is induced by the
restoration of blood flow to previously ischemic tissue.
restoration of blood flow to previously ischemic tissue.
Manifes
Manifestations
tations include:
include:
• RReperfusion arrhythmias
eperfusion arrhythmias
Endothelial cell damage leadi ng to microvascular
Endothelial cell damage leading to microvascular
dys dysfunction function
Myocardial stunning
Myocardial stunning
Myocyte death/ infarction
Myocyte death/ infarction
 following: following: • mi mitochondria tochondria • • • • Platelet Platelet activation activation •
following:
following:
mi
mitochondria
tochondria
• Platelet
Platelet activation
activation
membranes, including nstriction
membranes, including
nstriction

Factors that contribute to reperfusion injury include the

Factors that contribute to reperfusion injury include the

Damage to cellular and organelle

Damage to cellular and organelle membranes, including

Myocyte hypercontrac

Myocyte hypercontr

acture

ture

Free radical formation

Free radical formation

Aggregation of leukocytes

Aggregation of leukocytes

and inflammatory mediators

and inflammatory mediators

Complement activation

Complement activation

Activation of the pro-apoptotic signaling cascade

Activation of the pro-apoptotic

signaling cascade

Endothelium damage and

Endothelium damage and

vasoconstriction

vas oco

Time Gross Feattures Light Microscopy 0-30 None None mins ½- 4 hr None Waviness of fibers
Time
Gross Feattures
Light Microscopy
0-30
None
None
mins
½- 4 hr
None
Waviness of fibers at borders
4-12 hr
Occ dark mottling
Coagulation necrosis, edema,
hemorrhage
12-24 hr
Dark mottling
Ongoing necrosis, Contraction
band, WBC infiltrate
1-3 days
Mottling with yello-
WBC infiltrate
tan infarct center
3-7 days
Hyperemic border,
Dis integration of myofibers, early
central yellow-tan
phagocytosis of dead cells by
softening
macrophages at infract border
7-10 Maximally yello- Phagocytosis in process and days tan and soft, with formation of fibrovascular depressed
7-10
Maximally yello-
Phagocytosis in process and
days
tan and soft, with
formation of fibrovascular
depressed red-tan
granulation tissue at margins
margins
10-14
Red-gray depressed
Well established granulation
days
infarct borders
tiss ue with new blood vessels
and collagen deposition
2-8 wk
Gray-white scar,
Increased collagen deposition
progressive from
with decreased cellularity
border toward core
of infarct
>2
Scarring complete
Dense collagenous scar
months
Time Gross Feattures Ele ctron Microscopy 0- ½ hr None Relaxation of myofibrils, glycog en loss,
Time
Gross Feattures
Ele ctron Microscopy
0- ½ hr
None
Relaxation of myofibrils,
glycog en loss, mitochondrial
swelling.
½- 4 hr
None
Sarcolemmal disruption
 • of the luminal cros of the luminal cros one or more major one or
of the luminal cros
of the luminal cros
one or more major
one or more major

Chronic hypoxia, as

Chronic hypoxia, as

 • of the luminal cros of the luminal cros one or more major one or

is particularly well

is particularly well

The coronary collateral

The coronary collateral

circulation

circulation

developed in patients with

developed in patients with

Coronary occlusive disease, especially with the reduction

Coronary occlusive disease, especially with the reduction

s-sectional

s-sectional

area by more than 75% in

area by more than 75% in

ves sels

ves sels

occurs in cases of severe anemia,

occurs in cases of severe anemia,

chronic obstructive pulmonary disease, and cyanotic

chronic obstructive pulmonary disease, and cyanotic

congenital heart disease

congenital heart disease

Left ventricular hypertrophy.

Left ventricular hypertrophy.

 
 
 
 
 
 
 
 

LV

 
 
 
 
 
 
 

Four abnorm

Four

abnormal

al contr

 
 
 

1. DDyyssssynyncchrhrony

1.

ony

 
 

2. HHyypokinesi

2.

pokinesiss

 
 

3. AAkkinesis

3.

inesis

 
 

4.

inesis

4. DDyyskskinesis

 
 

 
 

accompanies dysfunct

 
 

 
 
 
 
 

recovery often occurs

recovery often occurs

 
 

 
 
 
 
 

following following STSTEEMMII

 
 
 
 
 
 
 
 
 
al myocardium initially
al myocardium initially

region.

LV systolic function

systolic function

contracactitionon patterns develop in sequence:

patterns

develop in sequence:

Hyperkinesis of the remai

Hyperkinesis of the remaining norm

ning normal myocardium initially

accompanies dysfunction

ion

of the infarcting segment.

of the infarcting segment.

Increased motion of the

Increased motion of the

non-infarcted region subsides within 2

non-infarcted region subsides within 2

weeks of infarction, during which time some degree of

weeks of infarction, during which time some degree of

in the infarct

in the infarct region.

The degree to which end-systolic volume increases is perhaps

The degree to which end-systolic volume increases is perhaps

the most powerful hemodynamic

the most powerful hemodynamic predictor of mortality

predictor of mortality

IsIschemi chemiaa at at dis distance: tance: contractile function in
IsIschemi
chemiaa at
at dis
distance:
tance:
contractile function in
zones zones
zones
zones

of the ventricle and loss of

of the ventricle and loss of

Patients with STEMI often also

Patients with STEMI often also

show

show

reduced myocardial

reduced myocardial

contractile function in non-infarcted

non-infarcted

This may result from previous obstruction of the coronary artery

This may result from previous obstruction of the coronary artery

supplying the non-infarcted region

supplying the non-infarcted region

collaterals from the freshly occluded infarct related vessel

collaterals from the freshly occluded infarct related vessel

 Infar Infarcctt extens extension: ion:  As necrotic myocytes slip pas t each other, the
Infar
Infarcctt extens
extension:
ion:
As necrotic myocytes slip pas t each other, the infarct zone
As necrotic myocytes slip pas t each other, the infarct zone
thins and elongates, especially in patients with large anterior
thins and elongates, especially in patients with large anterior
infarcts, leading to infarct expansion.
infarcts, leading to infarct expansion.
Ve
Vent
ntricular
ricular Dilatati
Dilatation:
on:
As
As the
the ventri
ventriccllee ddiilates
lates dur
during the first few hours to days after
ing the first few hours to days after
infarction , regional and global wall stress increases according
infarction, regional and global wall stress increases according
to Laplace's law. In some patients a vicious cycle of dilation
to Laplace's law. In some patients a vicious cycle of dilation
begetting further dilation ens ues. The degree of ventricular
begetting further dilation ensues. T he degree of ventricular
dilation, which depends closely on infarct size, patency of the
dilation, which depends closely on infarct size, patency of the
infarct-related artery, and activation of the renin-angiotensin-
infarct-related artery, and activation of the renin-angiotensin-
aldosterone system (RAAS), can be favorably modified by
aldosterone system (RAAS), can be favorably modified by
inhibitors of this system, even in the absence of symptomatic
inhibitors of this system, even in the absence of symptomatic
left left ventri ventricucullaarr dys dysfunction. function.
 Increasi ng stiffness in the infarcted zone of myocardium Increasing stiffness in the infarcted zone
Increasi ng stiffness in the infarcted zone of myocardium
Increasing stiffness in the infarcted zone of myocardium
imimproves left ventricular function because it prevents
proves left ventricular function because it prevents
paradoxical systolic wall motion (dyskinesia).
paradoxical systolic wall motion (dyskinesia).
When the abnormally contracting s egment exceeds 15%, the
When the abnormally contracting s e gment exceeds 15%, the
ejection fraction may decline and elevations of left ventricular
ejection fraction may decline and elevations of left ventricular
end-diastolic pressure and vol ume occur.
end-diastolic pressure and volume occur.
Clinical heart failure accompanies areas of abnormal
Clinical heart failure accompanies areas of abnormal
contraction exceeding 2 5%.
contraction exceeding 2 5%.
Cardiogenic shock, often fatal, accompanies loss of more than
Cardiogenic shock, often fatal, accompanies loss of more than
40% of the left ventricular myocardium.
40% of the left ventricular myocardium.
 end-diastolic pressure. end-diastolic pressure. 
end-diastolic pressure.
end-diastolic pressure.
 end-diastolic pressure. end-diastolic pressure.  and an initial rise in LV and an initial rise

and an initial rise in LV

and an initial rise in LV

These alterations associate with a decrease in the peak rate of

These alterations associ

ate with a decrease in the peak rate of

decline in LV pressure [peak

decline in LV pressure [peak (-)dP/dt], an increase in the time

(-)dP/dt], an increase in the time

constant of the fall in LV pre

constant of the fall in LV

pressure,

sure,

Over several weeks, end-diastolic volume increases and

Over several weeks, end-diastolic volume increases and

diastolic pressure begins to fall toward normal.

diastolic pressure begins to fall toward normal.

 AA mmararkekedd depression of left ventricular stroke volume depression of left ventricular stroke volume ultim
AA mmararkekedd depression of left ventricular stroke volume
depression of left ventricular stroke volume
ultim ately lowers aortic pressure and reduces coronary
ultimately lowers aortic pressure and reduces coronary
perfusion pressure; this condition may intensify myocardial
perfusion pressure; this cond ition may intensify myocardial
ischemia and thereby initiate a vicious circle. Systemic
ischemia and thereby initiate a vicious circle. Systemic
inflammation secondary to the infarction process leads to the
inflammation secondary to the infarction process leads to the
release of cytokines that contribute to vasodilation and a fall in
release of cytokines that contribute to vasodilation and a fall in
systemic vascular resistance.
systemic vascular resistance.
The inability of the left ventricle to empty normally also leads
The inability of the left ventricle to empty normally also leads
to an increased preload; that is, it dilates the well-perfused,
to an increased preload; that is, it dilates the well-perfused,
normally functioning portion of the left ventricle.
normally functioning portion of the left ventricle.
   antiatherogenic antiatherogenic  arrhy arrhythmthmias ias..
antiatherogenic
antiatherogenic
arrhy
arrhythmthmias
ias..
function + direct
function + direct

development of ventricular

EFFECTS OF TREATMENT

EFFECTS OF TREATMENT

Glucocorticosteroids and NSAID can cause scar

Glucocorticosteroids and NSAID can cause scar

thinning and greater infarct expansion,

thinning and greater infarct expansion,

RAAS inhibitors

RAAS inhibitors

attenuate ventricular enlargement +

attenuate ventricular enlargement +

attenuation of endothelial dysfunction + direct

attenuation of endothelial

dys

effects.

effects.

Inhibition of aldosterone action reduces collagen

Inhibition of aldosterone action reduces collagen

deposition and decreases the

deposition and decreases t

he development of ventricular

 PUL PULMMOONARY NARY • • • functional residual functional residual • REDUCTION OF OXOXYGE YGEN.
PUL
PULMMOONARY
NARY
functional residual
functional residual
• REDUCTION OF
OXOXYGE
YGEN.
N.

extravascular water.

extravascular water.

organ systems organ systems —total lung capacity, residual volume, as well residual volume, as well increases
organ systems
organ systems
—total lung capacity,
residual volume, as well
residual volume, as well
increases in pulmonary
increases in pulmonary

Pathophysiology

Pathophysiology

of other

of other

An inverse relationship exists

An inverse relationship exists between arterial oxygen

between arterial oxygen

tension and pulmonary artery

tension and pulmonary artery

diastolic pressure

diastolic pressure

widespread closure of

widespread closure of

small, dependent airways during the

small, dependent airways during the

first 3 days after STEMI.

first 3 days after STEMI.

Virtually all lung volume

Virtually all lung volume

indices—total lung capacity,

indices

capacity, and

capacity, and

as vital capacity—fall

as vital capacity—fall

during

during

STEMI. These reductions

STEMI. These reductions

cocorrrelate relate with with ththee elevations elevations ofof left- left-sisidededd ffilli illinngg prpress essures ures

and are most probably

and are most probably

caused by

caused by

REDUCTION OF AFFINITY OF HEMOGLOBIN FOR

AFFINITY OF HEMOGLOBIN FOR

Increase 2,3 DPG -> Increase in P50

Increase 2,3 DPG -> Increase in P50

18 percent increase

18 percent increase

in oxy

in

oxygen release from

gen release from

oxyhemoglobin in patients with cardiogenic shock.

oxyhemoglobin in patients with cardiogenic shock.

 PANCREAS. free fatty acids for contributing to the
PANCREAS.
free fatty acids for
contributing to the
ular failure, abnormalities the sympathetic nervous
ular failure, abnormalities
the sympathetic nervous

myocardium by permitting

• Glucose appears to be

favorable energy source than

a more

the

ischemic

ATP generation by anaerobic

glycolysis.

• Hyperglycemia and impaired

glucose tolerance are

common in patients with STEMI.

• As a consequence of splanchnic

vasoconstriction

accompanying severe left

ventric

in insulin secretion occur.

• In addition, increased activity of

system with augmented circulating catecholamines inhibits

insulin secretion and augments glycogenolysis, also

elevation of blood sugar.

 • • • •
an increase in myocardial
an increase in myocardial

ADRENAL MEDULLA.

ADRENAL MEDULLA.

The plasma and urinary catecholamine levels peak during

The plasma and urinary catecholamine levels peak during

the

the first 24 hours with

the first 24 hours with

the greatest rise in plasma

greatest rise in plasma

catecholamine secretion occurring during the first hour.

catecholamine secretion occurring during the first hour.

Serious arrhythmias

Serious arrhythmias

and result in

and result i

n an increase in myocardial

oxygen consumption, both

oxygen consumption, both directly and indirectly, as a

directly and indirectly, as a

consequence of catecholamine-induced elevation of

consequence of catecholamine-induced elevation of

circulating free fatty

circulating free fatty

acids.

acids.

Circulating catecholamines enhance platelet aggregation

Circulating catecholamines enhance platelet aggregation

Hyper catecholamine state

Hyper catecholamine state

is a foundation for beta-

is

a foundation for beta-

adrenergic receptor blocker regimens in the acute phase.

adrenergic receptor blocker regimens in the acute phase.

 ALDOSTERONE SY • myocardial vessels myocardial • anandd aldo aldostero res resppecti ectivvel ely. y.
ALDOSTERONE SY
myocardial vessels
myocardial
anandd aldo aldostero
res resppecti ectivvel ely. y.

vessels.

.

 ALDOSTERONE SY • myocardial vessels myocardial • anandd aldo aldostero res resppecti ectivvel ely. y.

ACTIVATION OF THE RENIN-ANGIOTENSIN-

ACTIVATION OF THE RENIN-ANGIOTENSIN-

ALDOSTERONE SYSTEM.

STEM.

Both locally and systemically generated angiotensin II can

Both locally and systemically generated angiotensin II can

stimulate the production of various growth factors, such as

stimulate the production of various growth factors, such as

platelet-derived growth factor and transforming growth

platelet-derived growth factor and transforming growth

factor-beta, that promote compensatory hypertrophy in the

factor-beta, that promote compensatory hypertrophy in the

as

as

noninfarcted m yocardium,

noninfarcted myocardium,

well as control the structure

well as control the structure

and tone of the infarct-related coronary and other

and tone of the infarct-related coronary and other

Angiotensin II also causes

Angiotensin II also causes

release of endothelin, PAI-1,

release of endothelin, PAI-1,

steronne, which may cause vasoconstriction,

e, which m

ay cause vasoconstriction,

impaired fibrinolysis, and increased sodium retention,

impaired fibrinolysis, and increased sodium retention,

 • ketosteroids, as we •
ketosteroids, as we

ADRENAL CORTEX.

ADRENAL CORTEX.

ketosteroids, as well

patients with STEMI.

patients with STEMI.

 • ketosteroids, as we • ADRENAL CORTEX. ADRENAL CORTEX. ketosteroids, as well patients with STEMI.

Plasma and urinary 17-hydroxycorticosteroids and

Plasma and urinary 17-hydroxycorticosteroids and

ll

as aldosterone, rise markedly in

as aldosterone, rise markedly in

The magnitude of the elevation

The magnitude of the elevation

of cortisol correlates with

of cortisol correlates with

infarct size and mortality.

infarct size and mortality.

 • • • ababnonormrmaallities ities •
ababnonormrmaallities
ities

Released early after

Released early after

Originate both from

Originate both from

increased risk of cardiac-
increased risk of cardiac-

NATRIURETIC PEPTIDES

NATRIURETIC PEPTIDES

STEMI, peaking at about 16 hours.

STEMI, peaking at about 16 hours.

the infarcted myocardium, as well as

the infarcted myocardium, as well as

viable noninfarcted myocardium

viable noninfarcted myocardium

Correlates with infarct

Correlates with infarct size and

size and

regional wall motion

regional wall motion

Conversely, patients

Conversely, patients

with

with

persistently elevated levels at 3

persistently elevated levels at 3

to 4 weeks after STEMI have

to 4 weeks after STEMI have

an increased risk of cardiac-

an

related mortality over the

related mortality over the

ensuing 5 to 10 years.

ensuing 5 to 10 years.

 THYRO THYROIIDD GLA GLAND. ND. • Transient decrease Transient decrease infarct. infarct. •
THYRO
THYROIIDD GLA
GLAND.
ND.
Transient decrease
Transient decrease
infarct.
infarct.
the third day after the the third day after the
the third day after the
the third day after the

SH) levels.

SH) levels.

in serum tri-iodothyronine (T3) levels, a

in serum tri-iodothyronine (T3) levels, a

fall that is most marked on about

fall that is most marked on about

Variable cha nges or

Variable changes or

no change in thyroxine (T4) and

no change in thyroxine (T4) and

thyroid-stimulating hormone (T

thyroid-stimulating ho

rmone

 RRENENALAL FUNC FUNCTTION ION • Prerenal azotemia and acute r enal failure can complicate Prerenal
 RRENENALAL FUNC FUNCTTION ION
Prerenal azotemia and acute r enal failure can complicate
Prerenal azotemia and acute renal failure can complicate
cacarrdiogenic diogenic shock. shock.
Increase in circulating atrial natriuretic peptide play a role
Increase in circulating atrial natriuretic peptide play a role
in the hypotension that accompanies right ventricular
in the hypotension that accompanies right ventricular
infarction infarction..
 PLPLATATLLETS: ETS:
Circulating platelets are hyper-aggregable in patients with
Circulating platelets are hyper-aggregable in patients with
STEMI. Platelets from STEMI patients have an increased
STEMI. Platelets from STEMI patients have an increased
propensity for aggregation locally in the area of a disrupted
propensity for aggregation locally in the area of a disrupted
plaque and also release vasoactive substances.
plaque and also release vasoa ctive substances.
 HEMOSTATIC • • • • capable of altering capable of altering
HEMOSTATIC
capable of altering
capable of altering

Platelet factor 4 and

Platelet factor 4 and

increased during the

increased during the

Interpretation of the

Interpretation of the

thrombosis and is thrombosis and is
thrombosis and is
thrombosis and is

of platelet and coagulation

of platelet and coagulation

HEMOSTATIC MARKERS

MARKERS.

Elevated serum fibrinogen

Elevated serum fibrinogen

degradation products

degradation products

beta-thromboglobulin

beta-thromboglobulin

Fibrinopeptide A, a protein released from fibrin by

Fibrinopeptide A, a protein released from fibrin by

thrombin, is a marker of ongoing g

thrombin, is a marker of ongoin

early hours of STEMI.

early

hours of STEMI.

coagulation tests may be complicated

coagulation tests may be complicated

by elevated blood levels of catecholamines, concomitant

by elevated blood levels of catecholamines, concomitant

shock, and/or pulmonary embolism, conditions that are all

shock, and/or pulmonary

embolism, conditions that are all

various tests

various tests

function and use of antithrombotic agents.

function and use of antithrombotic agents.

 LLEUEUKOCY KOCYTTEES. S. • cocorronary onary ararteries teries.. •
LLEUEUKOCY
KOCYTTEES.
S.
cocorronary
onary ararteries
teries..
 LLEUEUKOCY KOCYTTEES. S. • cocorronary onary ararteries teries.. • Leukocytosis usually accompanies STEMI in proportion

Leukocytosis usually accompanies STEMI in proportion to

Leukocytosis usually accompanies STEMI in proportion to

the magnitude of the

the magnitude of the necr

necrotic

otic

process, elevated

process, elevated

glucocorticoid levels, and possibly inflammation in the

glucocorticoid levels, and possibly inflammation in the

The magnitude of elevation of the leukocyte count

The magnitude of elevation of the leukocyte count

associates with in-hospital

associates with in-hospital

mortality after STEMI.

mortality after STEMI.

 • •

BLOOD VISCOSITY.

BLOOD VISCOSITY.

 • • BLOOD VISCOSITY. BLOOD VISCOSITY. Increase in blood viscosity is Increase in blood viscosity

Increase in blood viscosity is

Increase in blood viscosity is

due to hemoconcentration in

due to hemoconcentration in

the first few days after

the first few days after infarction.

infarction.

Elevated serum concentrations of alpha2-globulin and

Elevated serum concentrat

ions of alpha2-globulin and

fibrinogen, components of the acute phase response to

fibrinogen, components of the acute phase response to

tissue necrosis responsible

tissue necrosis responsible

for late increases.

for late increases.

 Predis Predispos posing ing Factors Factors:: • STSTEEMMI.I. • •
Predis
Predispos
posing
ing Factors
Factors::
STSTEEMMI.I.

, ,

URES hypotension (e.g., hypotension (e.g., s caused by vasospasm.
URES
hypotension (e.g.,
hypotension (e.g.,
s caused by vasospasm.

i caused by vasospasm.

CLINICAL

CLINICAL

FEAT

FEATURES

Heavy exercise (particularly in fatigued or habitually

Heavy exercise (particularly in fatigued or habitually

inactive patients) and emotional stress can precipitate

inactive patients) and emotional stress can precipitate

Noncardiac surgical

Noncardiac surgical

procedur

procedures

hemorrhagic or septic shock)

hemorrhagic or septic

shock)

and increased myocardial

and increased myocardial

oxygen demands caused by aortic stenosis, fever,

oxygen demands caused by aortic stenosis, fever,

tachycardia, and agitation can also be responsible for

tachycardia, and agitation can also be responsible for

myocardial necrosis.

myocardial necrosis.

Rarely, munition workers

Rarely, munition workers

exposed to high concentrations

exposed to high concentrations

of nitroglycerin develop MI when they are withdrawn from

of nitroglycerin develop MI when they are withdrawn from

this exposure, suggesting

this exposure, suggesting

that it is

that

 •
..
..

CIRCADIAN PERIODICITY.

CIRCADIAN PERIODICITY.

Peak incidence of events between 6 am and noon

Peak incidence of events between 6 am and noon

associated with rises

associated with rises

in plasma catecholamines and cortisol

in plasma catecholamines and cortisol

and increases in platelet aggregability..

and increases in platelet aggregability

• CCirircacaddiaiann peak is absent in patients receiving beta blocker

peak is absent in patients receiving beta blocker

or aspirin before their presentation with STEMI

or aspirin before their pres

entation with STEMI

 • • • • • EECGCG cchanges hanges • An Angi ginana • Infr Infracacttion/s
• EECGCG cchanges hanges
• An Angi ginana
• Infr Infracacttion/s ion/sccarar
 • • • • • EECGCG cchanges hanges • An Angi ginana • Infr Infracacttion/s

Ischemic cascade outlinin

Ischemic cascade outlining the Sequence of events:

g the Sequence of events:

Perfusion Abnormality

Perfusion Abnormality

Diastolic Dysfunction

Diastolic Dysfunction

Abnormal DTI/ Strain

Abnormal DTI/ Strain

(Systolic)

(Systolic)

Visibly Abnormal Wall Motion

Visibly Abnormal Wall Motion

 HIST HISTOORYRY   
HIST
HISTOORYRY
 HIST HISTOORYRY    PRODROMAL SYMPTOMS. PRODROMAL SYMPTOMS. A feeling of general malaise A

PRODROMAL SYMPTOMS.

PRODROMAL SYMPTOMS.

A feeling of general malaise

A feeling of general malaise

or frank exhaustion often

or frank exhaustion often

accompanies other symptoms

accompanies other symptoms

preceding STEMI.

preceding STEMI.

Women may present differently than men.

Women may present differently than men.

 NANATTURUREE OOFF THE • • •
NANATTURUREE OOFF THE
of angina with respect to of angina with respect to
of angina with respect to
of angina with respect to

THE PPAIN.

AIN.

The pain is prolonged,

The pain is prolonged,

usually lasting for more than 30

usually lasting for more than 30

minutes and frequently for

minutes and frequently for a number of hours.

a number of hours.

In patients with preexisting angina pectoris, the pain of

In patients with preexisting angina pectoris, the pain of

infarction usually resembles that

infarction usually resembles that

location. However, it is gener

location. However, it is generally much more severe, lasts

by

by

ally much more severe, lasts

longer, and is not relieved

longer, and is not relieved

rest and nitroglycerin.

rest and nitroglycerin.

Both angina pectoris

Both angina pectoris and the pain of STEMI are thought to

and the pain of STEMI are thought to

arise from nerve endings in ischemic or injured, but not

arise from nerve endings in ischemic or injured, but not

necrotic myocardium.

necrotic myocardium.

 GI GI SYM SYMPTOM PTOMS. S. • • symptoms include symptoms include imimpependnding ing doom.
GI
GI SYM
SYMPTOM
PTOMS.
S.
symptoms include
symptoms include
imimpependnding
ing doom.
doom.
presumably because of presumably because of phase of STEMI. Other phase of STEMI. Other
presumably because of
presumably because of
phase of STEMI. Other
phase of STEMI. Other

effects of opiates if used.

effects of opiates if used.

Nausea and vomiting may

Nausea and vomiting may

occur,

occur,

activation of the vagal

activation of the vagal

reflex or

reflex or

Occasionally, a patient complains of diarrhea or a violent

Occasionally, a patient complains of diarrhea or a violent

urge to defecate during the acute

urge to defecate during the acute

feelings of profound weakness,

feelings of profound weakness,

dizziness, palpitations, cold perspiration, and a sense of

dizziness, palpitations, cold perspiration, and a sense of

 SILE SILENTNT SSTEMI TEMI  ATYPICAL PRESENTATION ATYPICAL PRESENTATION • He Hearartt failur failuree •
SILE
SILENTNT SSTEMI
TEMI
ATYPICAL PRESENTATION
ATYPICAL PRESENTATION
He
Hearartt failur
failuree
Classic angina pectoris without a particularly severe or
Classic angina pectoris without a particularly severe or
prolonged prolonged epis episode ode
Atypical location of the pain
Atypical location of the p ain
Central nervous system manifestations, resembling those of
Central nervous system manifestations, resembling those of
stroke, secondary t o a sharp reduction in cardiac output in a
stroke, secondary to a sharp redu ction in cardiac output in a
patient with cerebral arteriosclerosis
patient with cerebral arteriosclerosis
Apprehension and nervousness
Apprehension and nervousness
Sudden mania or psychosis
Sudden mania or psychosis
• Syncope
Syncope
Ov
Overerwwhelm
helming
ing weakness
weakness
Acute indigestion and
Acute indigestion and
Peripheral embolization.
Peripheral embolization.
 GENERAL APPEARANCE. GENERAL APPEARANCE. • Cool and clammy Skin Cool and clammy Skin • Bluish
GENERAL APPEARANCE.
GENERAL APPEARANCE.
Cool and clammy Skin
Cool and clammy Skin
Bluish or mottled color over t he extremities
Bluish or mottled color over the extremities
Marked facial pallor with severe cyanosis of the lips and
Marked facial pallor with severe cyanosis of the lips and
nanaiill beds beds
De pending on the degree of cerebral perfusion, patient in
Depending on the degree of cerebral perfusion, patient in
shock may converse normally or may evidence confusion
shock may converse normally or may evidence confusion
anandd di disor sorientation ientation
HEHEARARTT RRATATEE..
Marked bradycardia to a rapid regular or irregular
Marked bradycardia to a rapid r egular or irregular
tachycardia, depending on the underlying rhythm and the
tachycardia, depen ding on the underlying rhythm and the
degree of left ventricular failure
degree of left ventricular failure
 BLOOD PRESSURE. BLOOD PRESSURE. • • • systolic blood pres the process can be the
BLOOD PRESSURE.
BLOOD PRESSURE.
systolic blood pres
the process can be
the process can be
mm Hg. Their mm Hg. Their
mm Hg. Their
mm Hg. Their

discharge.

levels of blood pressure,

levels of blood pressure,

may also transiently have

may also transiently have

HTN among previously normoten-sive patients presumably

HTN among previousl

y normoten-sive patients presumably

as a consequence of

as a consequence of

adrenergic discharge.

adrenergic

Normalization of BP in hypertensive patient after STEMI,

Normalization of BP in hypertensive patient after STEMI,

eventually regain their

eventually regain their elevated

elevated

generally 3 to 6 months after infarction.

generally 3 to 6 months after

infarction.

Bezold-Jarisch reflex activation

Bezold-Jarisch reflex activation

systolic blood pressure below 90

sure below 90

hypotension eventually resolves spontaneously, although

hypotension eventually resolves spontaneously, although

accelerated by intravenous atropine (0.5

accelerated by intravenous atropine (0.5

to 1 mg) and assumption of the Trendelenburg position.

to 1 mg) and assumption of the

Trendelenburg position.

 TEMPERATURE AND RESPIRATION. TEMPERATURE AND RESPIRATION. • Most patients with extensive STEMI develop fever, a
TEMPERATURE AND RESPIRATION.
TEMPERATURE AND RESPIRATION.
Most patients with extensive STEMI develop fever, a
Most patients with extensive STEMI develop fever, a
nonspecific response to tissue necrosis, within 24 to 48
nonspecific response to tis sue necrosis, within 24 to 48
hours of the onset of infarctio n.
hours of the onset of infarction.
Fever usually resolves by the fourth or fifth day after
Fever usually resolves by the fourth or fifth day after
infarction infarction..
JUGULAR VENOUS PULSE.
JUGULAR VENOUS PULSE.
Right ventricular infarction (whether or not it accompanies
Right ventricular infarction (whether or not it accompanies
left ventricular infarction) often results in marked jugular
left ventricular infarction) often results in marked jugular
venous distention and, when it is complicated by necrosis
venous distention and, when it is complicated by necrosis
or ischemia of right ventricular papillary muscles, tall
or ischemia of right ventricular papillary muscles, tall c-v
c-v
waves of tricuspid regurgitation are evident.
waves of tricuspid regurgitation are evident.
 CCARO AROTTIIDD PPUULSE LSE.. • • left-t left-to-r o-right ight shshuunt nt.. •
CCARO
AROTTIIDD PPUULSE
LSE..
left-t
left-to-r
o-right
ight shshuunt
nt..
stroke volume.
stroke volume.

ventricular septum with a

ventricular septum with a

left ventricular dysfunction.

left ventricular dysfunction.

A small pulse suggests a reduced

A small pulse suggests a reduced stroke volume.

A sharp, brief upstroke is

A sharp, brief upstroke is

often observed in patients with

often

observed in patients with

mitral regurgitation or

mitral regurgitation or

ruptured

ruptured

Pulsus alternans reflects s

Pulsus alternans reflects severe

evere

 THE THE CHE CHESTST.. • •  Class I patients Class I patients  CCllass
THE
THE CHE
CHESTST..
Class I patients
Class I patients
 CCllass
not not have have aann SS3. 3.
and
 THE THE CHE CHESTST.. • •  Class I patients Class I patients  CCllass

Cough with hemoptysis, suggesting pulmonary embolism

Cough with hemoptysis, sugges

ting pulmonary embolism

with infarction, can also occur.

with infarction, can also occur.

Kilip classification (1967)

Kilip classification (1967)

free of rales and a third heart sound.

free of rales and a third heart sound.

are

are

ass IIII patients have rales but only to a mild to

patients have rales but only to a mild to

moderate degree (<50%50% of lung fields) and may or may

moderate degree

of lung fields) and may or may

Class III have rales

Class III have rales

in

in

more than half of each lung field

more than half of each lung field

and frequently have pulmonary edema.

frequently have pulmonary edema.

Class IV patients

Class IV patients

are in

are in cardiogenic shock.

cardiogenic shock.

 PAL PALPAT PATION. ION. • •
PAL
PALPAT
PATION.
ION.
 PAL PALPAT PATION. ION. • • third heart sound. Presystolic pulsation, synchronous with an audible

third heart sound.

Presystolic pulsation, synchronous with an audible fourth

Presystolic pulsation, synchronous with an audible fourth

heart sound, reflecting

heart sound, reflecting

a vigorous left atrial contraction

a vigorous left atrial contraction

fill ing a ventricle with

filling a ventricle with

reduced compliance.

reduced compliance.

In the presence of left ventricular systolic dysfunction, an

In the presence of left ventricular systolic dysfunction, an

the

outward movement of

outward movement of

the left ventricle can be palpated in

left ventricle can be palpated in

early diastole, coincident

early diastole, coincident

with a

with a third heart sound.

 HEHEARARTT SOUND SOUNDSS • Ventricular dysfun ction and/or prolongation of the P-R Ventricular dysfunction a
HEHEARARTT SOUND
SOUNDSS
Ventricular dysfun ction and/or prolongation of the P-R
Ventricular dysfunction a nd/or prolongation of the P-R
interval makes soft first heart sound
interval makes soft first heart sound
Patients with marked ventricular dysfunction and/or left
Patients with marked ventricular dysfunction and/or left
bundle branch block may hav e paradoxical splitting of the
bundle branch block may have paradoxical splitting of the
second second hea hearrtt ssound. ound.
AA ffourth
ourth heart
heart ssound
ound isis almalmost
ost uunniiveverrsall
sallyy pres
present
ent inin
patients in sinus rhythm.
patients in sinus rhythm.
A third heart sound may be caused not only by left
A third heart sound may be caused not only by left
ventricular failure but also by increased inflow into the left
ventricular failure but also by increased inflow into the left
ventricle, as occurs when mitral regurgitation or ventricular
ventricle, as occurs when mitral regurgitation or ventricular
septal defect complicates STEMI.
septal defect complicates STEMI.
 MURMURS MURMURS • • ster sternal nal border. border.
MURMURS
MURMURS
ster
sternal
nal border.
border.
muscle dysfunction, left muscle dysfunction, left regurgitation (caused by regurgitation (caused by
muscle dysfunction, left
muscle dysfunction, left
regurgitation (caused by
regurgitation (caused by

of pulmonary hypertension

Mitral valve apparatus

Mitral valve apparatus

(papillary

(papillary

ventricular dilation).

ventricular dilation).

The systolic murmur of tricuspid

The systolic murmur of tricuspid

right ventricular failure because

right ventricular failure because of pulmonary hypertension

and/or right ventricular infarction or by infarction of a right

and/or right ventricular infarction or by infarction of a right

ventricular papillary

ventricular papillary

muscle)

muscle)

also heard along the left

also heard along the left

 ABABDOMEN DOMEN.. • Particularly in an inferior location with diaphragmatic Particularly in an inferior location
ABABDOMEN
DOMEN..
Particularly in an inferior location with diaphragmatic
Particularly in an inferior location with diaphragmatic
irritation, the pain m ay be localized to the epigastrium or
irritation, the pain may be localized to the epigastrium or
the right upper quadrant.
the right upper quadrant.
R ight heart failure, characterized by hepatomegaly and a
Right heart failure, characterized by hepatomegaly and a
positive abdominojugular reflux.
positive abdominojugular reflux.
EEXTXTRREEMMITITIIEES.
S.
STEMI may have a history of int ermittent claudication and
STEMI may have a history of intermittent claudication and
demonstrate physical findings o f PVD.
demonstrate physical findings of PVD.
NENEURUROPSYCHIATRI
OPSYCHIATRICC FI
FINDNDIINGNGS.
S.
Except for the altered mental status that occurs in patients
Except for the altered mental status that occurs in patients
with STEMI who have a markedly reduced cardiac output
with STEMI who have a markedly reduced cardiac output
and cerebral hypoperfusion, the findings on neurological
and cerebral hypoperfusion, the findings on neurological
examination are normal unless the patient has suffered
examination are normal unless the patient has suffered
cerebral embolism secondary to a mural thrombus.
cerebral embolism secondary to a mural thrombus.
 • • the the blood. blood.
the
the blood.
blood.
 • • the the blood. blood. interstitium and ultimately interstitium and ultimately molecular weight, local

interstitium and ultimately

interstitium and ultimately

molecular weight, local

molecular weight, local

Laboratory Findings

Laboratory Findings

Serum Markers of Cardiac Damage

Serum Markers of Cardiac Damage

ST-segment elevation and

ST-segment elevation

and

Q waves are seen in only about

Q waves are seen in only about

half of MI cases on presentati

half of MI cases on presentation.

on.

Enzyme diffuse into

Enzyme diffuse into

the cardi

the cardiac

into the microvasculature

into the microvasculature

and lymphatics in the region of

and lymphatics in the region of

the infarct The rate of appearance of these macromolecules

the infarct The rate of

appearance of these macromolecules

in the peripheral circulation depends on several factors

in the peripheral circulation depends on several factors

including intracellular

including intracellular

location,

location,

blood and lymphatic

blood and lymphatic

flow,

flow,

and the rate of elimination from

and the rate of elimination from

 
 
 
 
 
 
 
 

CREATINE KINASE

CREATINE KINASE

 

 

 
 
 
 

MMMM and

and MB:

MB: Hea

Hearrtt

 

 
 

CCK-MK-MBB eelleevati vation. on.

 
 
 
 
 
 
 
 
 
tly MM) The MB m, uterus, and prostate.
tly MM) The MB
m, uterus, and prostate.

ISOENZYMES.

ISOE

NZYMES.

Three isoenzymes of CK exist (MM, BB, and MB).

Three isoenzymes of CK exist (MM, BB, and MB).

BB: Extracts of brain and

BB: Extracts of brain and

kidney

kidney

MB: Skeletal muscle (1

MB: Skeletal muscle (1

to 3%)(Mostly MM) The MB

to 3%)(Mos

isoenzymes of CK can also be pr

isoenzymes of CK can also be present in minor quantities in

esent in minor quantities in

the small i ntestine, tong

the small intestine, tongue, diaphra

ue, diaphragm, uterus, and prostate.

g

CK-MB mass/ CK activity (Relative index) of about 2.5 is

CK-MB mass/ CK activity (Relative index) of about 2.5 is

indicative of a myocardial rather

indicative of a myocardial rather

than a skeletal source of the

than a skeletal source of the

 MYOGL MYOGLOBOBIIN. N.  
MYOGL
MYOGLOBOBIIN.
N.

are

are

reached considerably reached considerably
reached considerably
reached considerably

This monomeric heme protein is

This monomeric heme protein is

released into the circulation

released into the circulation

from injured myocardial cells

from injured myocardial cells

and can be detected within a few

and can be detected within a few

hours after the onset of infarction.

hours after the onset of infarction.

Peak levels of serum myoglobin

Peak levels of serum myoglobin

earlier (1 to 4 hours) than

earlier (1 to 4 hours) than

peak values of serum CK.

peak values of serum CK.

TTrroponin oponin  CARDIAC-SPECIFIC TROPONINS. CARDIAC-SPECIFIC TROPONINS.  The troponin complex c onsists of three subunits
TTrroponin
oponin
CARDIAC-SPECIFIC TROPONINS.
CARDIAC-SPECIFIC TROPONINS.
The troponin complex c onsists of three subunits that regulate
The troponin complex consists of three subunits that regulate
the calcium-mediated contractile process of striated muscle.
the calcium-mediated contractile process of striated muscle.
Troponin C, which binds Ca2 +;
Troponin C, which binds Ca2+;
Troponin I (TnI), which binds to actin and inhibits actin-
Troponin I (TnI), which binds to actin and inhibits actin-
myosin interactions; and
myosin interactions; and
Troponin T (TnT), which binds to tropomyosin, thereby
Troponin T (TnT), which binds to tropomyosin, thereby
attaching the troponin complex to the thin filament.
attaching the troponin complex to the thin filament.
 Approximately 6% of T nt and 2 to 3% of TnI is found in a
Approximately 6% of T nt and 2 to 3% of TnI is found in a
Approximately 6% of Tnt and 2 to 3% of TnI is found in a
cytos cytosolic olic pool. pool.
Although both TnT and T nI are pres ent in cardiac and skeletal
Although both TnT and TnI are present in cardiac and skeletal
muscle, they are encoded by different genes and their amino
muscle, they are encoded by different genes and their amino
acaciidd sequenc sequencee di differs ffers..
cTnT assays are produced by a single manufacturer, leading to
cTnT assays are produced by a single manufacturer, leading to
relative uniformity of cutoffs, where as several manufacturers
relative uniformity of cutoffs, whereas several manufacturers
produce produce cTnI cTnI asassay says.s.
When cardiac troponins are released from myocytes, there is a
When cardiac troponins are released from myocytes, there is a
mixture of free cTnT and free cTnI along with a complex of
mixture of free cTnT and free cTnI along with a complex of
the I-C-T components that is further degraded to a complex of
the I-C-T components that is further degraded to a complex of
I-CI-C and and free free cTcTnnTT
 SESERUM RUM LIPI LIPIDDSS  For patients admitted beyond 24 to 48 hours, more accurate
SESERUM
RUM LIPI
LIPIDDSS
For patients admitted beyond 24 to 48 hours, more accurate
For patients admitted beyond 24 to 48 hours, more accurate
determinations of serum lipid levels are obtained about 8
determinations of serum lipid levels are obtained about 8
weeks after the infarction has occurred.
weeks after the infarction has occurred.
HEMATOLOGICAL FINDINGS.
HEMATOLOGICAL FINDI NGS.
High WBC develops within 2 hours, reaches a peak 2 to 4
High WBC develops within 2 hours, reaches a peak 2 to 4
da ys after infarction, and returns to normal in 1 week;
days after infarction, an d returns to normal in 1 week;
ESR: is usually normal during the first day or two after
ESR: is usually normal during the first day or two after
infarction, even though fever and leukocytosis may be present.
infarction, even though fever and leukocytosis may be present.
An elevated CRP leve l appears to identify patients with worse
An elevated CRP leve l appears to identify patients with worse
angiographic appearance of the infarct artery and a greater
angiographic appearance of the infarct artery and a greater
likelihood of developing heart failure.
likelihood of developi ng heart failur e.
J-shaped relationship between baseline hemoglobin values and
J-shaped relationship between baseline hemoglobin values and
clinical events. 14 to 15gm/d l – 17gm/dl
clinical events. 14 to 15gm/dl – 17gm/dl
 have an increased inci artery artery..    Although precordial S necessary to ascertain
have an increased inci
artery artery..
Although precordial S
necessary to ascertain
necessary to ascertain

ababnonormrmaallityity isis prpreessent. ent.

ion ofof the the riright ght coronary coronary of the lateral, or inferior of the lateral,
ion ofof the
the riright
ght coronary
coronary
of the lateral, or inferior
of the lateral, or inferior
wall subendocardial
wall subendocardial

absence of pre-excitation or

absence of pre-excitation or

inferior or lateral Q waves

inferior or lateral Q waves

E KG

EKG

Patients with an abnormal R wave in V1 (0.04 second in

Patients with an abnormal R

wave in V1 (0.04 second in

duration and/or R/S ratio ≥1 in the

duration and/or R/S ratio ≥1

in the

right ventricular hypertrophy)

right ventricular hypertrophy) with

with

have an increased incidence of isolated occlusion of a

dominant LAD without

dominant LAD without

den

ce of isolated occlusion of a

collateral c

collateral circulation; such patients

irculation; such patients

have a lower ejection fraction, increased end-systolic volume,

have a lower ejection fraction, increased end-systolic volume,

an d higher complication rate

and higher complication rate

than patients with inferior

than patients with inferior

infarction because of isolated

infarction because of isolated

occlusion

occlus

Q-WAVE AND NON-Q-WAVE INFARCTION.

Q-WAVE AND NON-Q-WAVE INFARCTION.

E. E.

ISCHEMIA AT A DISTANC

ISCHEMIA AT A DISTANC

Although precordial ST-segment depression associates more

T-segm

ent depression associates more

comm only with extensive

commonly with extensive infarction

infarction

septal segments, rather than anterior

septal segments, rather than anterior

ischemia, imaging techniques

ischemia, imaging techniques

such

such

as echocardiography are

as echocardiography are

whether an anterior wall motion

whether an anterior wall motion

  ST-segment elevation ST-segment elevation vevent ntricular ricular iinfarction. nfarction. 
ST-segment elevation
ST-segment elevation
vevent
ntricular
ricular iinfarction.
nfarction.
in these leads.
in these leads.

E KG

EKG

RIGHT VENTRICULAR INFARCTION.

RIGHT VENTRICULAR INFARCTION.

in right

in right

precordial leads (V1, V3R-

precordial leads (V1, V3R-

V6R) is a relatively sensitive and specific sign of right

V6R) is a relatively sensitive and specific sign of right

A QS or QR pattern in leads V3R and/or V4R also suggests

A QS or QR pattern in leads

V3R and/or V4R also suggests

right ventricular myocardial necrosis but has less predictive

right ventricular myocardial necrosis but has less predictive

accuracy than ST-segment elevation

accuracy than ST-segment elevation in these leads.

 X-ray X-ray  eleva elevatteed. d.  resorb and the radiogr clea clearr ..
X-ray
X-ray
eleva elevatteed. d.
resorb and the radiogr
clea
clearr ..
pressure has become pressure has become pulmonary congestion to pulmonary congestion to
pressure has become
pressure has become
pulmonary congestion to
pulmonary congestion to

Imaging

Imaging

Up to 12 hours can elapse

Up to 12 hours can elapse be

before

fore pulmonary edema

pulmonary edema

accumulates after ventricular filling

accumulates after ventricular filling

The post-therapeutic phas

The post-therapeutic ph

ase lag represents a longer time

e lag represents a longer time

interval; up to 2 days are required for pulmonary edema to

interval; up to 2 days ar

e required for pulmonary edema to

resorb and the radiographic s

aphic signs of

igns of

 • • Ao Aorrtictic dis dissecti sectioon. n. • •
Ao
Aorrtictic dis
dissecti
sectioon.
n.
ventricular septal rupture, ventricular septal rupture,
ventricular septal rupture,
ventricular septal rupture,

ECHOCARDIOGRAPHY

ECHOCARDIOGRAPHY

Wall motion abnormality

Wall motion abnormality

Severity of mitral or

Severity of mitral or

tricuspid regurgitation

tricu

pid regurgitation

Identification of the site of acute

Identification of the

site of acute

quantification of shunt flow a

quantification of shunt flow across the resulting defect, and

cross the resulting defect, and

assessment of acute cardiac tam

assessment of acute cardiac tamponade are also possible.

ponade are also possible.

 • ecechocardi hocardioogrgraphy. aphy.  • the triad of clinical
ecechocardi
hocardioogrgraphy.
aphy.
the triad of clinical
findings, and serum findings, and serum
findings, and serum
findings, and serum

COMPUTED TOMOGRAPHY

COMPUTED TOMOGRAPHY

It probably is more sensitive for thrombus detection than is

It probably is more sensitive for thrombus detection than is

NUCLEAR IMAGING

NUCLEAR IMAGING

Cardiac radionuclide imaging for the diagnosis of MI

Cardiac radionuclide imag

ing for the diagnosis of MI

should be restricted to

should be restricted to

special limited situations in which

special limited situations in which

the triad of clinical history, ECG

history , ECG

marker measurements

marker measurements

is unavailable or unreliable.

is unavailable or unreliable.

ESTIMATION OF INFARCT SIZE ESTIMATION OF INFARCT SIZE  EELELECCTTROC ROCARARDI DIOOGRAPHY. GRAPHY. • A relationship
ESTIMATION OF INFARCT SIZE
ESTIMATION OF INFARCT SIZE
EELELECCTTROC
ROCARARDI
DIOOGRAPHY.
GRAPHY.
A relationship between the number of ECG leads showing
A relationship between the number of ECG leads showing
ST-segment elevation and mortality rate exists.
ST-segment elevation and mortality rate exists.
SERUM CARDIAC MARKERS.
SERUM CARDIAC MARKERS.
Clinically, the peak CK or CK-MB provides an
Clinically, the peak CK or CK-MB provides an
approximate estimate of infarct size and is widely used
approximate estimate of infar ct size and is widely used
prognos prognostically. tically.
Measuring a cardiac-specific troponin level several days
Measuring a cardiac-specific troponin level several days
after STEMI, even in cases of successful reperfusion, may
after STEMI, even in cases of successful reperfusion, may
provide a reliable estimate of infarct size because such late
provide a reliable estimate of infarct size because such late
troponin measurements reflect delayed release from the
troponin measurement s reflect delayed release from the
myofilament bound pool in damaged myocytes.
myofilament bound pool in damaged myocytes.


Thank

Thank

you you
you
you