Chapter 50

ST-Elevation Myocardial Infarction: Pathology,

Pathophysiology, and Clinic Features

Vinod Patel
University of South Florida
 The pathological diagnosis of myocardial infarction (MI)
requires evidence of myocyte cell death as a consequence of
prolonged ischemia.

 The clinical diagnosis of MI requires an integrated assessment

of the history with some combination of indirect evidence of
myocardial necrosis using biochemical, electrocardiographic,
and imaging modalities.
 Typical rise and/or fall of biochemical markers of myocardial
necrosis with at least one of the following:
• a) Ischemic symptoms
• b) Development of pathologic Q waves in the ECG
• c) ECG changes indicative of ischemia (ST segment
elevation or depression)
• d) Imaging evidence of new loss of viable myocardium or
new regional wall motion abnormality.
Pathologic findings of an acute myocardial infarction.
 Criteria for Healing or Healed Myocardial Infarction.
Any one of the following criteria satisfies the diagnosis for
healing or healed myocardial infarction:
• 1. Development of new pathological Q waves in serial
ECGs. The patient may or may not remember previous
symptoms. Biochemical markers of myocardial necrosis
may have normalized depending on the length of time that
has passed since the infarction developed.
• 2. Pathological findings of a healed or healing infarction.
 In the United States, nearly 1 million patients a year suffer
from an acute MI.
 More than 1 million patients with suspected acute MI are
admitted yearly to coronary care units in the United States.
 Of particular concern from a global perspective are
projections that the burden of disease in developing countries
will become similar to those now afflicting developed
countries.
 Drop in mortality appears to result from a fall in the incidence
of STEMI (replaced in part by an increase in the rate of
unstable angina/non-ST-segment elevation MI and a fall in the
case fatality rate once STEMI has occurred).
 The short-term mortality rate of patients with STEMI in
randomized trials is in the range of 6.5 to 7.5 %, whereas
observational data bases suggest 5 to 20%
 Clinical trial data from studies of fibrinolysis show that the
elderly (75 years old or older) continue to suffer a mortality
rate four times that of younger patients.
 Variation has also been observed in the treatment patterns of
certain population subgroups with STEMI, notably women
and blacks.
 Table 50.1
 Causes of MI without coronary atherosclerosis

Arteritis
• Luetic
• Granulomatous (Takayasu disease)
• Polyarteritis nodosa
• Mucocutaneous lymph node (Kawasaki) syndrome
• Disseminated lupus erythematosus
• Rheumatoid spondylitis
• Ankylosing spondylitis
 Trauma to coronary arteries
• Laceration
• Thrombosis
• Iatrogenic
• Radiation (radiation therapy for neoplasia)
 Coronary mural thickening with metabolic disease or intimal
proliferative disease
• Mucopolysaccharidoses (Hurler disease)
• Homocystinuria
• Fabry disease
• Amyloidosis
• Juvenile intimal sclerosis (idiopathic arterial calcification
of infancy)
• Intimal hyperplasia associated with contraceptive steroids
or with the postpartum period
• Pseudoxanthoma elasticum
• Coronary fibrosis caused by radiation therapy
 Luminal narrowing by other mechanisms
• Spasm of coronary arteries (Prinzmetal angina with normal
coronary arteries)
• Spasm after nitroglycerin withdrawal
• Dissection of the aorta
• Dissection of the coronary artery
 Emboli to Coronary Arteries
• Infective endocarditis
• Nonbacterial thrombotic endocarditis
• Prolapse of mitral valve Mural thrombus from left atrium,
left ventricle, or pulmonary veins
• Prosthetic valve emboli
• Cardiac myxoma
• Associated with cardiopulmonary bypass surgery and
coronary arteriography
• Paradoxical emboli
• Papillary fibroelastoma of the aortic valve (fixed embolus)

• Thrombi from intracardiac catheters or guidewires

 Congenital Coronary Artery Anomalies
• Anomalous origin of left coronary from pulmonary artery
• Left coronary artery from anterior sinus of Valsalva
• Coronary arteriovenous and arteriocameral fistulas
• Coronary artery aneurysms
 Myocardial Oxygen Demand-Supply Disproportion
• Aortic stenosis
• Incomplete differentiation of the aortic valve
• Aortic insufficiency
• Carbon monoxide poisoning
• Thyrotoxicosis
• Prolonged hypotension
• Takotsubo cardiomyopathy
 Hematological (in situ Thrombosis)
• Polycythemia vera
• Thrombocytosis
• Disseminated intravascular coagulation
• Hypercoagulability, thrombosis, thrombocytopenic purpura
 Miscellaneous
• Cocaine abuse
• Myocardial contusion
• Myocardial infarction with normal coronary arteries
• Complication of cardiac catheterization
 PLAQUE

 Release of chemokines by endothelial cells and increase

expression of adhesion proteins.
 Entry of WBC into the wall.
 T cells in the arterial wall produce cytokines which
stimulates endothelial cell proliferation and activate
microphages.
Events During Atherogenesis
 At autopsy, the atherosclerotic plaques of patients who died of
STEMI are composed of :
• 90% fibrous tissue of varying density and cellularity with
superimposed thrombus.
• 10% Calcium, lipid-laden foam cells, and extracellular
lipid.
• The atherosclerotic plaques generally more complex and
irregular than those in vessels not associated with STEMI.
• Coronary arterial thrombi are approximately 1cm in length
in most cases; adhere to the luminal surface of an artery;
and contain platelets, fibrin, erythrocytes, and leukocytes.
 The balance of synthetic and degradative activity of collagen,
the major structural component of the fibrous cap, account for
its mechanical strength and determines plaque stability and
prognosis.
 Statins -> stabalize plaques by their lipid lowering effect as
well as reduce plaque inflammation.
 2/3 of the plaques resulting in STEMI are caused by an
occlusion of 50% or less and 85% has occlusion of <70%
 The coronary distribution of STEMI is:
• LAD 40-50% RCA 30-40% Lcx 15-20%
 Vulnerable plaques
• Large area of foam cells and extracellular lipids
• Thin fibrous cap
• Few smooth muscle
• Clusters of inflammatory cells
 Role of acute plaque changes
• Rupture/fissuring: exposing the highly thrombogenic
plaque constituents.
• Erosion/ulceration: exposing the thrombogenic
subendothelial basement membrane to blood
• Hemorrhage into the atheroma, expending its volume.
 Plaque fissuring and disruption
• Overexpression of metalloproteinase enzymes such as
collagenase, gelatinase, and stromelysin
• Activated macrophages and mast cells abundant at the site.
• Stresses induced by intraluminal pressure, coronary
vasomotor tone, tachycardia (cyclic stretching and
compression), and disruption of nutrient vessels combine to
produce plaque disruption.
Junction of the fibrous cap and the adjacent normal plaque free
arterial segment is the location at which the blood flow-inducing
mechanical stresses within the plaque are highest and the fibrous
cap is thinnest.
 A number of key physiological variables such as systolic
blood pressure, heart rate, blood viscosity, endogenous tissue
plasminogen activator (t-PA) activity, plasminogen activator
inhibitor-1 (PAI-1) levels, plasma cortisol levels, and plasma
epinephrine levels exhibit circadian and seasonal variations
and increase at times of stress.
 Vasospasm is caused by:
• Circulating adrenergic agonists
• Locally released platelet contents
• Impaired secretion of endothelial cell relaxing factors
relative to contracting factors.
• Mediators released from peri-vascular inflammatory cells.
 Exposed to subendothelial collagen and necrotic plaque
contents, platelets undergo adhesion, aggregation, activation
and release of potent aggregators including TXA2, serotonin
and PF 3 -4
 Activation of extrinsic pathway.

http://www.youtube.com/watch?v=41h8OhRHAw0
 RIGHT VENTRICULAR INFARCTION.
• Approximately 50% of patients with inferior infarction
have some involvement of the right ventricle
• RV occurs less commonly than would be anticipated from
the frequency of atherosclerotic lesions involving the RCA.
 This discrepancy can probably be explained by the

lower oxygen demands

 Inter-coronary collateral system of the RV is richer than

that of the left

 The thinness of the RV wall allows the chamber to

derive some nutrition from the blood within the RV

cavity
 ATRIAL INFARCTION.
 This can be seen in up to 10% of patients with STEMI if PR-
segment displacement is used as the criterion for atrial
infarction.
 Although isolated atrial infarction is observed in 3.5% of
autopsies of patients with STEMI, it often occurs in
conjunction with ventricular infarction.
 Occurs more frequently in the atrial appendages
(Rt > Lt) explained by higher oxygen content of left atrial
blood.
 It has also been linked to reduced secretion of atrial natriuretic
peptide and a low cardiac output syndrome when right
ventricular infarction coexists.
 No plaque disruption in about 10% of cases.
 Many of these cases are caused by coronary artery spasm
and/or thrombosis, perhaps with underlying endothelial
dysfunction or small plaques in apparent on coronary
angiography.
 MI with angiographically normal coronary vessels.
• Young
• Often have a history of cigarette smoking
 (Takotsubo cardiomyopathy) catecholamine-mediated
myocardial stunning and microvascular dysfunction play
important roles.
 Transmural versus subendocardial infraction
 Most MIs are transmural
 Subendocardial infarct constitutes an area limited to inner 1/3
or ½.
• Plaque disruption -> thrombus-> lysis before necrosis
extends across major thickness.
• Chronic occlusion + prolonged severe reduction in
systemic blood pressure.
 Anaerobic glycolysis
 Inadequate production of high-energy phosphates and
accumulation of potentially noxious breakdown products (such
as lactic acid)
 Striking loss of contractility occurs with in 60 seconds.
 Ultrasturctural evidence of irreversible myocyte injury.
 Cell death:
• Coagulation necrosis
• Apotosis
 Prior to cell death there is a period during which the ischemic
myocyte is viable, but vulnerable to further injury if blood
flow is restored (ie, reperfusion injury). During this period, the
reintroduction of oxygen and energy into an abnormal cellular
environment triggers additional events that produce further
myocyte damage.
 Reperfusion injury refers to myocardial, vascular, or
electrophysiological dysfunction that is induced by the
restoration of blood flow to previously ischemic tissue.
Manifestations include:
• Reperfusion arrhythmias
• Endothelial cell damage leading to microvascular
dysfunction
• Myocardial stunning
• Myocyte death/ infarction
 Factors that contribute to reperfusion injury include the
following:
• Damage to cellular and organelle membranes, including
mitochondria
• Myocyte hypercontracture
• Free radical formation
• Aggregation of leukocytes and inflammatory mediators
• Platelet activation
• Complement activation
• Activation of the pro-apoptotic signaling cascade
• Endothelium damage and vasoconstriction
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, Disintegration 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 red-tan granulation tissue at margins
margins
10-14 Red-gray depressed Well established granulation
days infarct borders tissue 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 Electron Microscopy
0- ½ hr None Relaxation of myofibrils,
glycogen loss, mitochondrial
swelling.
½- 4 hr None Sarcolemmal disruption
 The coronary collateral circulation is particularly well
developed in patients with
• Coronary occlusive disease, especially with the reduction
of the luminal cross-sectional area by more than 75% in
one or more major vessels
• Chronic hypoxia, as occurs in cases of severe anemia,
chronic obstructive pulmonary disease, and cyanotic
congenital heart disease
• Left ventricular hypertrophy.
 LV systolic function

 Four abnormal contraction patterns develop in sequence:

• 1. Dyssynchrony
• 2. Hypokinesis
• 3. Akinesis
• 4. Dyskinesis
 Hyperkinesis of the remaining normal myocardium initially
accompanies dysfunction of the infarcting segment.
 Increased motion of the non-infarcted region subsides within 2
weeks of infarction, during which time some degree of
recovery often occurs in the infarct region.
 The degree to which end-systolic volume increases is perhaps
the most powerful hemodynamic predictor of mortality
following STEMI
Ischemia at distance:
Patients with STEMI often also show reduced myocardial
contractile function in non-infarcted zones
This may result from previous obstruction of the coronary artery
supplying the non-infarcted region of the ventricle and loss of
collaterals from the freshly occluded infarct related vessel
 Infarct extension:
 As necrotic myocytes slip past each other, the infarct zone
thins and elongates, especially in patients with large anterior
infarcts, leading to infarct expansion.
 Ventricular Dilatation:
 As the ventricle dilates during the first few hours to days after
infarction, regional and global wall stress increases according
to Laplace's law. In some patients a vicious cycle of dilation
begetting further dilation ensues. The degree of ventricular
dilation, which depends closely on infarct size, patency of the
infarct-related artery, and activation of the renin-angiotensin-
aldosterone system (RAAS), can be favorably modified by
inhibitors of this system, even in the absence of symptomatic
left ventricular dysfunction.
 Increasing stiffness in the infarcted zone of myocardium
improves left ventricular function because it prevents
paradoxical systolic wall motion (dyskinesia).
 When the abnormally contracting segment exceeds 15%, the
ejection fraction may decline and elevations of left ventricular
end-diastolic pressure and volume occur.
 Clinical heart failure accompanies areas of abnormal
contraction exceeding 25%.
 Cardiogenic shock, often fatal, accompanies loss of more than
40% of the left ventricular myocardium.
 These alterations associate with a decrease in the peak rate of
decline in LV pressure [peak (-)dP/dt], an increase in the time
constant of the fall in LV pressure, and an initial rise in LV
end-diastolic pressure.
 Over several weeks, end-diastolic volume increases and
diastolic pressure begins to fall toward normal.
 A marked depression of left ventricular stroke volume
ultimately lowers aortic pressure and reduces coronary
perfusion pressure; this condition may intensify myocardial
ischemia and thereby initiate a vicious circle. Systemic
inflammation secondary to the infarction process leads to the
release of cytokines that contribute to vasodilation and a fall in
systemic vascular resistance.
 The inability of the left ventricle to empty normally also leads
to an increased preload; that is, it dilates the well-perfused,
normally functioning portion of the left ventricle.
 EFFECTS OF TREATMENT
 Glucocorticosteroids and NSAID can cause scar

thinning and greater infarct expansion,

 RAAS inhibitors attenuate ventricular enlargement +

attenuation of endothelial dysfunction + direct

antiatherogenic effects.
 Inhibition of aldosterone action reduces collagen

deposition and decreases the development of ventricular

arrhythmias.
 Pathophysiology of other organ systems
 PULMONARY
• An inverse relationship exists between arterial oxygen
tension and pulmonary artery diastolic pressure
• widespread closure of small, dependent airways during the
first 3 days after STEMI.
• Virtually all lung volume indices—total lung capacity,
functional residual capacity, and residual volume, as well
as vital capacity—fall during STEMI. These reductions
correlate with the elevations of left-sided filling pressures
and are most probably caused by increases in pulmonary
extravascular water.
• REDUCTION OF AFFINITY OF HEMOGLOBIN FOR
OXYGEN.
 Increase 2,3 DPG -> Increase in P50

 18 percent increase in oxygen release from

oxyhemoglobin in patients with cardiogenic shock.
 PANCREAS.
• Glucose appears to be a more favorable energy source than
free fatty acids for the ischemic myocardium by permitting
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 ventricular failure, abnormalities
in insulin secretion occur.
• In addition, increased activity of the sympathetic nervous
system with augmented circulating catecholamines inhibits
insulin secretion and augments glycogenolysis, also
contributing to the elevation of blood sugar.
 ADRENAL MEDULLA.
• The plasma and urinary catecholamine levels peak during
the first 24 hours with the greatest rise in plasma
catecholamine secretion occurring during the first hour.
• Serious arrhythmias and result in an increase in myocardial
oxygen consumption, both directly and indirectly, as a
consequence of catecholamine-induced elevation of
circulating free fatty acids.
• Circulating catecholamines enhance platelet aggregation
• Hyper catecholamine state is a foundation for beta-
adrenergic receptor blocker regimens in the acute phase.
 ACTIVATION OF THE RENIN-ANGIOTENSIN-
ALDOSTERONE SYSTEM.
• Both locally and systemically generated angiotensin II can
stimulate the production of various growth factors, such as
platelet-derived growth factor and transforming growth
factor-beta, that promote compensatory hypertrophy in the
noninfarcted myocardium, as well as control the structure
and tone of the infarct-related coronary and other
myocardial vessels.
• Angiotensin II also causes release of endothelin, PAI-1,
and aldosterone, which may cause vasoconstriction,
impaired fibrinolysis, and increased sodium retention,
respectively.
 ADRENAL CORTEX.
• Plasma and urinary 17-hydroxycorticosteroids and
ketosteroids, as well as aldosterone, rise markedly in
patients with STEMI.
• The magnitude of the elevation of cortisol correlates with
infarct size and mortality.
 NATRIURETIC PEPTIDES
• Released early after STEMI, peaking at about 16 hours.
• Originate both from the infarcted myocardium, as well as
viable noninfarcted myocardium
• Correlates with infarct size and regional wall motion
abnormalities
• Conversely, patients with persistently elevated levels at 3
to 4 weeks after STEMI have an increased risk of cardiac-
related mortality over the ensuing 5 to 10 years.
 THYROID GLAND.
• Transient decrease in serum tri-iodothyronine (T3) levels, a
fall that is most marked on about the third day after the
infarct.
• Variable changes or no change in thyroxine (T4) and
thyroid-stimulating hormone (TSH) levels.
 RENAL FUNCTION
• Prerenal azotemia and acute renal failure can complicate
cardiogenic shock.
• Increase in circulating atrial natriuretic peptide play a role
in the hypotension that accompanies right ventricular
infarction.
 PLATLETS:
• Circulating platelets are hyper-aggregable in patients with
STEMI. Platelets from STEMI patients have an increased
propensity for aggregation locally in the area of a disrupted
plaque and also release vasoactive substances.
 HEMOSTATIC MARKERS.
• Elevated serum fibrinogen degradation products
• Platelet factor 4 and beta-thromboglobulin
• Fibrinopeptide A, a protein released from fibrin by
thrombin, is a marker of ongoing thrombosis and is
increased during the early hours of STEMI.
• Interpretation of the coagulation tests may be complicated
by elevated blood levels of catecholamines, concomitant
shock, and/or pulmonary embolism, conditions that are all
capable of altering various tests of platelet and coagulation
function and use of antithrombotic agents.
 LEUKOCYTES.
• Leukocytosis usually accompanies STEMI in proportion to
the magnitude of the necrotic process, elevated
glucocorticoid levels, and possibly inflammation in the
coronary arteries.
• The magnitude of elevation of the leukocyte count
associates with in-hospital mortality after STEMI.
 BLOOD VISCOSITY.
• Increase in blood viscosity is due to hemoconcentration in
the first few days after infarction.
• Elevated serum concentrations of alpha2-globulin and
fibrinogen, components of the acute phase response to
tissue necrosis responsible for late increases.
 CLINICAL FEATURES

 Predisposing Factors:
• Heavy exercise (particularly in fatigued or habitually
inactive patients) and emotional stress can precipitate
STEMI.
• Noncardiac surgical procedures , hypotension (e.g.,
hemorrhagic or septic shock) and increased myocardial
oxygen demands caused by aortic stenosis, fever,
tachycardia, and agitation can also be responsible for
myocardial necrosis.
• Rarely, munition workers exposed to high concentrations
of nitroglycerin develop MI when they are withdrawn from
this exposure, suggesting that it is caused by vasospasm.
 CIRCADIAN PERIODICITY.
• Peak incidence of events between 6 am and noon
associated with rises in plasma catecholamines and cortisol
and increases in platelet aggregability .
• Circadian peak is absent in patients receiving beta blocker
or aspirin before their presentation with STEMI..
 Ischemic cascade outlining the Sequence of events:
• Perfusion Abnormality
• Diastolic Dysfunction
• Abnormal DTI/ Strain (Systolic)
• Visibly Abnormal Wall Motion
• ECG changes
• Angina
• Infraction/scar
 HISTORY
 PRODROMAL SYMPTOMS.
 A feeling of general malaise or frank exhaustion often
accompanies other symptoms preceding STEMI.
 Women may present differently than men.
 NATURE OF THE PAIN.
• The pain is prolonged, usually lasting for more than 30
minutes and frequently for a number of hours.
• In patients with preexisting angina pectoris, the pain of
infarction usually resembles that of angina with respect to
location. However, it is generally much more severe, lasts
longer, and is not relieved by rest and nitroglycerin.
• Both angina pectoris and the pain of STEMI are thought to
arise from nerve endings in ischemic or injured, but not
necrotic myocardium.
 GI SYMPTOMS.
• Nausea and vomiting may occur, presumably because of
activation of the vagal reflex or effects of opiates if used.
• Occasionally, a patient complains of diarrhea or a violent
urge to defecate during the acute phase of STEMI. Other
symptoms include feelings of profound weakness,
dizziness, palpitations, cold perspiration, and a sense of
impending doom.
 SILENT STEMI
 ATYPICAL PRESENTATION
• Heart failure
• Classic angina pectoris without a particularly severe or
prolonged episode
• Atypical location of the pain
• Central nervous system manifestations, resembling those of
stroke, secondary to a sharp reduction in cardiac output in a
patient with cerebral arteriosclerosis
• Apprehension and nervousness
• Sudden mania or psychosis
• Syncope
• Overwhelming weakness
• Acute indigestion and
• Peripheral embolization.
 GENERAL APPEARANCE.
• Cool and clammy Skin
• Bluish or mottled color over the extremities
• Marked facial pallor with severe cyanosis of the lips and
nail beds
• Depending on the degree of cerebral perfusion, patient in
shock may converse normally or may evidence confusion
and disorientation
 HEART RATE.
• Marked bradycardia to a rapid regular or irregular
tachycardia, depending on the underlying rhythm and the
degree of left ventricular failure
 BLOOD PRESSURE.
• HTN among previously normoten-sive patients presumably
as a consequence of adrenergic discharge.
• Normalization of BP in hypertensive patient after STEMI,
eventually regain their elevated levels of blood pressure,
generally 3 to 6 months after infarction.
• Bezold-Jarisch reflex activation may also transiently have
systolic blood pressure below 90 mm Hg. Their
hypotension eventually resolves spontaneously, although
the process can be accelerated by intravenous atropine (0.5
to 1 mg) and assumption of the Trendelenburg position.
 TEMPERATURE AND RESPIRATION.
• Most patients with extensive STEMI develop fever, a
nonspecific response to tissue necrosis, within 24 to 48
hours of the onset of infarction.
• Fever usually resolves by the fourth or fifth day after
infarction.
 JUGULAR VENOUS PULSE.
• Right ventricular infarction (whether or not it accompanies
left ventricular infarction) often results in marked jugular
venous distention and, when it is complicated by necrosis
or ischemia of right ventricular papillary muscles, tall c-v
waves of tricuspid regurgitation are evident.
 CAROTID PULSE.
• A small pulse suggests a reduced stroke volume.
• A sharp, brief upstroke is often observed in patients with
mitral regurgitation or ruptured ventricular septum with a
left-to-right shunt.
• Pulsus alternans reflects severe left ventricular dysfunction.
 THE CHEST.
• Cough with hemoptysis, suggesting pulmonary embolism
with infarction, can also occur.
• Kilip classification (1967)
 Class I patients are free of rales and a third heart sound.

 Class II patients have rales but only to a mild to

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

not have an S3.
 Class III have rales in more than half of each lung field

and frequently have pulmonary edema.

 Class IV patients are in cardiogenic shock.
 PALPATION.
• Presystolic pulsation, synchronous with an audible fourth
heart sound, reflecting a vigorous left atrial contraction
filling a ventricle with reduced compliance.
• In the presence of left ventricular systolic dysfunction, an
outward movement of the left ventricle can be palpated in
early diastole, coincident with a third heart sound.
 HEART SOUNDS
• Ventricular dysfunction and/or prolongation of the P-R
interval makes soft first heart sound
• Patients with marked ventricular dysfunction and/or left
bundle branch block may have paradoxical splitting of the
second heart sound.
• A fourth heart sound is almost universally present in
patients in sinus rhythm.
• A third heart sound may be caused not only by left
ventricular failure but also by increased inflow into the left
ventricle, as occurs when mitral regurgitation or ventricular
septal defect complicates STEMI.
 MURMURS
• Mitral valve apparatus (papillary muscle dysfunction, left
ventricular dilation).
• The systolic murmur of tricuspid regurgitation (caused by
right ventricular failure because of pulmonary hypertension
and/or right ventricular infarction or by infarction of a right
ventricular papillary muscle) is also heard along the left
sternal border.
 ABDOMEN.
• Particularly in an inferior location with diaphragmatic
irritation, the pain may be localized to the epigastrium or
the right upper quadrant.
• Right heart failure, characterized by hepatomegaly and a
positive abdominojugular reflux.
 EXTREMITIES.
• STEMI may have a history of intermittent claudication and
demonstrate physical findings of PVD.
 NEUROPSYCHIATRIC FINDINGS.
• Except for the altered mental status that occurs in patients
with STEMI who have a markedly reduced cardiac output
and cerebral hypoperfusion, the findings on neurological
examination are normal unless the patient has suffered
cerebral embolism secondary to a mural thrombus.
 Laboratory Findings

 Serum Markers of Cardiac Damage

• ST-segment elevation and Q waves are seen in only about
half of MI cases on presentation.
• Enzyme diffuse into the cardiac interstitium and ultimately
into the microvasculature and lymphatics in the region of
the infarct The rate of appearance of these macromolecules
in the peripheral circulation depends on several factors
including intracellular location, molecular weight, local
blood and lymphatic flow, and the rate of elimination from
the blood.
 CREATINE KINASE ISOENZYMES.
 Three isoenzymes of CK exist (MM, BB, and MB).
 BB: Extracts of brain and kidney
 MB: Skeletal muscle (1 to 3%)(Mostly MM) The MB
isoenzymes of CK can also be present in minor quantities in
the small intestine, tongue, diaphragm, uterus, and prostate.
 MM and MB: Heart
 CK-MB mass/ CK activity (Relative index) of about 2.5 is
indicative of a myocardial rather than a skeletal source of the
CK-MB elevation.
 MYOGLOBIN.
 This monomeric heme protein is released into the circulation
from injured myocardial cells and can be detected within a few
hours after the onset of infarction.
 Peak levels of serum myoglobin are reached considerably
earlier (1 to 4 hours) than peak values of serum CK.
 Troponin

 CARDIAC-SPECIFIC TROPONINS.
 The troponin complex consists of three subunits that regulate
the calcium-mediated contractile process of striated muscle.
• Troponin C, which binds Ca2+;
• Troponin I (TnI), which binds to actin and inhibits actin-
myosin interactions; and
• Troponin T (TnT), which binds to tropomyosin, thereby
attaching the troponin complex to the thin filament.
 Approximately 6% of Tnt and 2 to 3% of TnI is found in a
cytosolic pool.
 Although both TnT and TnI are present in cardiac and skeletal
muscle, they are encoded by different genes and their amino
acid sequence differs.
 cTnT assays are produced by a single manufacturer, leading to
relative uniformity of cutoffs, whereas several manufacturers
produce cTnI assays.
 When cardiac troponins are released from myocytes, there is a
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
I-C and free cTnT
 SERUM LIPIDS
 For patients admitted beyond 24 to 48 hours, more accurate
determinations of serum lipid levels are obtained about 8
weeks after the infarction has occurred.
 HEMATOLOGICAL FINDINGS.
 High WBC develops within 2 hours, reaches a peak 2 to 4
days after infarction, and returns to normal in 1 week;
 ESR: is usually normal during the first day or two after
infarction, even though fever and leukocytosis may be present.
 An elevated CRP level appears to identify patients with worse
angiographic appearance of the infarct artery and a greater
likelihood of developing heart failure.
 J-shaped relationship between baseline hemoglobin values and
clinical events. 14 to 15gm/dl – 17gm/dl
 EKG
 Patients with an abnormal R wave in V1 (0.04 second in
duration and/or R/S ratio ≥1 in the absence of pre-excitation or
right ventricular hypertrophy) with inferior or lateral Q waves
have an increased incidence of isolated occlusion of a
dominant LAD without collateral circulation; such patients
have a lower ejection fraction, increased end-systolic volume,
and higher complication rate than patients with inferior
infarction because of isolated occlusion of the right coronary
artery.
 Q-WAVE AND NON-Q-WAVE INFARCTION.
 ISCHEMIA AT A DISTANCE.
 Although precordial ST-segment depression associates more
commonly with extensive infarction of the lateral, or inferior
septal segments, rather than anterior wall subendocardial
ischemia, imaging techniques such as echocardiography are
necessary to ascertain whether an anterior wall motion
abnormality is present.
 EKG

 RIGHT VENTRICULAR INFARCTION.

 ST-segment elevation in right precordial leads (V1, V3R-
V6R) is a relatively sensitive and specific sign of right
ventricular infarction.
 A QS or QR pattern in leads V3R and/or V4R also suggests
right ventricular myocardial necrosis but has less predictive
accuracy than ST-segment elevation in these leads.
 Imaging

 X-ray
 Up to 12 hours can elapse before pulmonary edema
accumulates after ventricular filling pressure has become
elevated.
 The post-therapeutic phase lag represents a longer time
interval; up to 2 days are required for pulmonary edema to
resorb and the radiographic signs of pulmonary congestion to
clear .
 ECHOCARDIOGRAPHY
• Wall motion abnormality
• Aortic dissection.
• Severity of mitral or tricuspid regurgitation
• Identification of the site of acute ventricular septal rupture,
quantification of shunt flow across the resulting defect, and
assessment of acute cardiac tamponade are also possible.
 COMPUTED TOMOGRAPHY
• It probably is more sensitive for thrombus detection than is
echocardiography.
 NUCLEAR IMAGING
• Cardiac radionuclide imaging for the diagnosis of MI
should be restricted to special limited situations in which
the triad of clinical history, ECG findings, and serum
marker measurements is unavailable or unreliable.
 ESTIMATION OF INFARCT SIZE

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