Myocardial infarction

A heart attack or acute myocardial infarction (MI) occurs when one of the arteries
that supplies the heart muscle becomes blocked. Blockage may be caused by
spasm of the artery or by atherosclerosis with acute clot formation. The blockage
results in damaged tissue and a permanent loss of contraction of this portion of the
heart muscle.
Myocardial infarction (MI) is the irreversible
necrosis of heart muscle secondary to prolonged
ischemia. This usually results from an imbalance
of oxygen supply and demand.
CLASSIFICATION
1. Transmural: :(Q wave infarction) : most
infartcts are transmural involve the full
thickness of ventricular wall in the distribution
of single coronary artery.
These infracts are caused by ch atherosclerosis,
acute plaque changes b y occlusive thrombi and
less commonly thromboemboli or vasospasm.
2. Subendocardial: these infarcts involve inner one
third to one half of ventricular wall as subendo
cardial zone is less perfused area of myocardial
zone. The infarcts are caused by hypoperfusion
of myocardium and not by coronary occlusion.
These occur in hypotensive shock, and by typical
ECG findings these are so called non Q wave infar
Less common causes of MI:
o vasculitis PAN and kawasaki disease.
o Cocain use
o Embolization of plaque material
o Thrombosis syndrome
PATHOGENESIS:
Occlusion is typically seen in the proximal 2 cm of the
left anterior descending and left circumflex arteries
and in the proximal and distal thirds of the right
coronary artery.
o Rupture of the lipid-rich atheromatous plaque,
intraplaque hemorrhage, and

intraluminal thrombus
are three pathological hallmarks most commonly

recognized in the infarct-related coronary artery at
the site of acute

myocardial infarction.
o Role of the platelet-derived mediators (e.g. TXA2,
serotonin, ADP, & PDGF that promote thrombosis
and vasoconstriction occur.


o Diminished availability of those natural
endogenous substances that inhibit

platelet
aggregation, such as EDRF, tissue plasminogen
activator, and PGI2.

o Vasospsm is stimulated by mediators release
from platelets.
o Tissue factor activates the coagulation pathway.
o Thrombus occlude the lumen of vessel.
o Ischemia with out detection of coronary
thrombosis due to vaculitis

These serial sections of a coronary artery demonstrate grossly the
appearance of lumenal narrowing with atherosclerosis.
Grossly :Before 6 to 12 hours: No visible lesion is
seen.
By 18 to 24 hours: Infarct area becomes pale to
cyanotic & swollen.
In the first week: The infarct area becomes
progressively more sharply defined, yellow and
softened.
By the 7

to 10 days, circumference of the infarct
area becomes hyperemic, and progressively
expands.
By the 6 weeks, fibrous scar is well established.

myocardial infarction
(2) of the tip of the
anterior wall of
the heart (an
apical infarct)
after occlusion (1)
of a branch of the
left coronary
artery(LCA, right
coronar
Ohr 2hr
24hr
This is an acute myocardial infarction in the septum. After several days,
there is a yellowish center with necrosis and inflammation surrounded
by a hyperemic border.
This is an acute myocardial infarction of the anterior left ventricular free wall and
septum in cross section. Note that the infarction is nearly transmural. There is a
yellowish center with necrosis and inflammation surrounded by a hyperemic borde
When the infarction is 3 to 5 days old, the necrosis and inflammation are most
extensive, and the myocardium is the softest, so that transmural infarctions may be
complicated by rupture. A papillary muscle may rupture as well to produce sudden
valvular insufficiency. Rupture through the septum results in a left-to-right shunt
and right heart failure.
Remote myocardial infarction (weeks to years)
Time from Onset Gross Morphologic Finding
18 - 24 Hours Pallor of myocardium
24 - 72 Hours Pallor with some hyperemia
3 - 7 Days
Hyperemic border with central
yellowing
10 - 21 Days
Maximally yellow and soft
with vascular margins
7 weeks White fibrosis
Gross morphologic changes evolve over time as follows:
This is normal myocardium. There are cross striations and central nuclei. Pale pink
intercalated disks are also present.
Microscopic features:
Within 1 hour of ischemic injury, there is intercellular
edema and wavy fibers may be present at the
periphery of the infarct. These are noncontrctile dead
fibers, stretched by the adjacent viable contracting
myocytes
Electron microscopy shows reversible changes
(swelling of mitochondria & endoplasmic reticulum and
relaxation of myofibrils).
Histochemically, there is loss of oxidative enzyme & fall
of glycogen.
In 12 to 72 hours, there is infiltration of neutrophils
with progressive coagulative necrosis of myocytes.
Dead myocytes become hypereosinophilic with loss of
nuclei.



This is an early acute myocardial infarction. (<iday) Note the
prominent pink contraction bands.
1-2 daysThis is an early acute myocardial infarction. There is increasing loss of
cross striations, and some contraction bands are also seen, and the nuclei are
undergoing karyolysis. Some neutrophils are beginning to infiltrate the
myocardium.
1-2days This is an acute myocardial infarction. There is loss of cross
striations, and the nuclei are not present. There is extensive hemorrhage
here at the border of the infarction, which accounts for the grossly
apparent hyperemic border.
3-4 days This is an acute myocardial infarction of several days'
duration. There is a more extensive neutrophilic infiltrate along
with the prominent necrosis and hemorrhage.
Between 3 and 7 days after onset, dead myocytes begin to
disintegrate and are removed by macrophages and enzyme
proteolysis. There is proliferation of fibroblasts with formation of
granulation tissue, which progressively replaces necrotic tissue.
After 6 weeks, healing is complete by fibrosis.
Contraction band necrosis: Contraction band necrosis,
characterized by hypereosinophilic transverse bands of
precipitated myofibrils in dead myocytes is usually seen at the
edge of an infarct or with reperfusion (e.g. with thrombolytic
therapy).

Reperfusion of an infarct: Reperfusion of an infarct is also
associated with more hemorrhage, less acute inflammation, less
limitation of the acute inflammation to the periphery in the first
few days, reactive stromal cells, more macrophage infiltration
earlier and a more patchy distribution of necrosis, especially
around the periphery.



2-3 wks Toward the end of the first week, healing of the infarction becomes
more prominent, with capillaries, fibroblasts, and macrophages filled with
hemosiderin. The granulation tissue seen here is most prominent from 2 to
3 weeks following onset of infarction.
weeks years After a couple of weeks, healing is well under way, and there
is more extensive collagen deposition.
wks yrs The remote myocardial infarction is evidenced by a
collagenous scar seen here in a subendocardial location.
Time from Onset Microscopic Morphologic Finding
1 - 3 Hours Wavy myocardial fibers
2 - 3 Hours
Staining defect with tetrazolium or basic
fuchsin dye
4 - 12 Hours
Coagulation necrosis with loss of cross
striations, contraction bands, edema,
hemorrhage, and early neutrophilic infiltrate
18 - 24 Hours
Continuing coagulation necrosis, pyknosis of
nuclei, and marginal contraction bands
24 - 72 Hours
Total loss of nuclei and striations along with
heavy neutrophilic infiltrate
3 - 7 Days
Macrophage and mononuclear infiltration
begin, fibrovascular response begins
10 - 21 Days
Fibrovascular response with prominent
granulation tissue
7 Weeks Fibrosis
Microscopic morphologic changes evolve over time as follows:
Symptoms of a possible heart attack include chest pain and pain that radiates
down the shoulder and arm. Some people (the elderly, people with diabetes, and
women) may have little or no chest pain. Or, they may experience unusual
symptoms (shortness of breath, fatigue, weakness).
Women are more likely than men to have symptoms of nausea, vomiting, back or
jaw pain, and shortness of breath with chest pain.
Clinical features: Chest pain- 20-30% does not
cause chest pain, common in patients with
diabetes mellitus, hypertension, & in elderly
patients.
2. Nausea, diaphoresis and dyspnea.
Fate of the patient: hospitalized patients
(where angiography, echocardiography and
perfusion scintigraphy are available) usual fate
are:
i) About 25 % of patients dye of cardiogenic
shock or fatal arrythmia.
ii) Patients who survive the acute phase may
develop:

Congestive heart failure
- Cardiac arrythmia
- Left ventricular failure with pulmonary edema.
- Rupture of ventricular wall, interventricular
septum and papillary muscle
- Thromboembolism.
iii) 10-20% patients recover with no
complication.
iv) Early restoration of blood flow by
thrombolysis or balloon angioplasty provides
better prognosis.



Screening and Diagnosis
Stress
Test
Coronary
Angiography
Electro-
cardiogram
Diagnosis:It is based on symptoms,
electrocardiographic change and serum
elevation of myocardial enzymes (creatine
kinase-MB isoenzyme) or other proteins
(troponin I, troponin T or myoglobin), that
leak out of dead cells.
The classic EKG findings: ST segment
elevation, followed by T wave inversion and Q
waves, are associated with transmural
infarction. ST segment depression and T wave
inversion are associated with subendocardial
infarction.

The laboratory diagnosis of myocardial infarction:
1) This has been based on elevation of creatine
phosphokinase (CPK), with an MB fraction >5% of
the total CPK or a relative index >3 (if the MB The
elevation of CPK begins around 8 hours after the
onset of infarction, peaks around 18 hours and
ends around 48 hours .
2) The late diagnosis of myocardial infarction can
be based on elevation of lactate dehydrogenase
(LDH), with an LDH-1 fraction >40% of the total
LDH or LDH-1/LDH-2 ratio >1, because this peaks
around 5 days.
3) Recently, the early and late diagnosis of
acute myocardial infarction has been based on
elevated serum levels of cardiac troponin. This
elevation begins around 4 hours after the onset
of infarction and lasts longer than LDH; this test
has a sensitivity similar to CPK-MB fraction and
better than LDH.
For the diagnosis of acute myocardial infarction
even earlier than detectable by troponin levels,
myoglobin can be tested.
Elevated levels of myoglobin can be detected
around 2 hours after the onset of infarction, but
this has only about 60% specificity for the heart.
A new type of test being evaluated for the
diagnosis of acute myocardial infarction is CPK
MB isoform assay, which has a 96% sensitivity
and 93% specificity for infarction within 6 hours
of onset of chest pain.


The combination of CPK MB and troponin testing
can have even higher sensitivity and is used for
the purpose of "ruling out" myocardial
infarction.


Complications: It depends on the size , location
duration of the lesion.
With in minutes to 3 days of onset:
1. Arrythmias :75-95% i) ventricular fibrillation ; ii)
block of A-V bundles and its branches causing
acute heart failure.
2. Cardiogenic shock 10-15%(usually in large
infarct) causing acute heart failure.
3. Thrombotic complication- 15-40% mural
thrombus over infarct area or Atrial thrombus,
causing embolism to brain, kidney etc.
4. Rupture of heart.

3-14 days:
Large infarct: There is softening of dead muscle
(myomalacia cordis) leading to rupture &
death.
Site of rupture is ventricular wall, papillary
muscle & interventricular septum.
5. Acute fibrinous or hemorrhagic pericarditis -
over infarct area.
After weeks or months:
6. Chronic heart failure
7. Cardiac aneurysm, which may rupture
producing hemopericardium and death.


Myocardial Rupture

Myocardial aneurysm with
thrombosis inside.

Rupture (at the arrow) into the pericardial sac can produce a life-
threatening cardiac tamponade, as seen here. The septum may also
rupture.
Rupture of papillary muscle..mitral incompetence.
Left ventricular aneurysm
containing mural thrombus
A complication of infarction is aneurysm
formation, which is the bulge seen here in
the left ventricular wall. Note the very thin
white wall of the aneurysm toward the apex.

The myocytes here are hypertrophied, marked by the large, dark nuclei, and
there is interstitial fibrosis. This is an example of cardiomyopathy. In this case,
long-standing, severe occlusive atherosclerosis led to "ischemic" cardiomyopathy.
6- Dresslers syndrome
Is complication of transmural MI
-an autoimmune disorder resulting from
damage of the myocardium
-antibodies developed against protein release
from necrotic myocardial cells
-autoimmune pericarditis, pericardial friction
rub and pleurisy.

Blood tests: used to evaluate kidney and thyroid
function as well as to check cholesterol levels and the
presence of anemia.
Chest X-ray: shows the size of heart and whether
there is fluid build up around the heart and lungs.
Echocardiogram: shows a graphic outline of the
hearts movement
Ejection fraction (EF): determines how well heart
pumps with each beat.

Other Tests
R/ Revascularization procedures
1) Stenting
a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the
artery
the balloon is then inflated and causes the stent to
expand until it fits the inner wall of the vessel,
conforming to contours as needed
the balloon is then deflated and drawn back
The stent stays in place permanently, holding the
vessel open and improving the flow of blood.
2) Angioplasty
a balloon catheter is passed through the guiding catheter to the area
near the narrowing. A guide wire inside the balloon catheter is then
advanced through the artery until the tip is beyond the narrowing.
the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
balloon is inflated, compressing the plaque against the artery wall
once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.
3) Bypass surgery
healthy blood vessel is removed from leg, arm or chest
blood vessel is used to create new blood flow path in
your heart
the bypass graft enables blood to reach your heart
by flowing
around (bypassing) the
blocked portion of the
diseased artery. The
increased blood flow
reduces angina and
the risk of heart attack.
Get regular medical checkups.
Control your blood pressure.
Check your cholesterol.
Dont smoke.
Exercise regularly.
Maintain a healthy weight.
Eat a heart-healthy diet.
Manage stress.