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Creatine Kinase and

Myocardial Infarction

Just a little trivia...

Myocardial Infarction
Heart Attack
Prolonged ischemia
Atherosclerosis is primarily responsible
Plaque rupture and erosion, platelet activation
and aggregation, coagulation pathway
activation and endothelial vasoconstriction
occur.

Non-modifiable Risk Factors


Age
Sex
Family History of premature coronary
heart disease

Modifiable Risk Factors

Smoking or tobacco use


Diabetes Mellitus
Hypertension
Hypercholesterolemia
Dyslipidemia
Obesity
Sedentary lifestyle
Psychosocial stress

Other causes

Coronary artery emboli


Coronary trauma
Drug use
Hyperthyroidism
Severe anemia

MI: Signs
Early changes in infarction (minutes to
days)
1. Drop in tissue oxygen levels
2. Rapid conversion from aerobic to anaerobic
metabolism
3. Accumulation of lactic acid and reduction in pH
4. Impairment of transmembrane Na-K-ATPase due to
impaired ATP production
5. Acute inflammatory response with infiltration of
neutrophils leading to further tissue damage

Late changes in infarction (days to weeks)


1. Resorption of irreversibly injured/dead
myocytes by macrophages
2. Fibrous tissue deposition and scarring
3. Ventricular remodeling
Infarct expansion
Remodeling of non-infarcted ventricle

MI: Symptoms

1. Chest pain/discomfort
2. Tachycardia
3. Dyspnea
4. Diaphoresis
5. Nausea/vomiting

PATHOPHYSIOLOGY OF MI
Lack of Blood Supply & O2 to the Myocardium
|
Anaerobic Metabolism
|
Lactic Acid Production
|
Acidosis
|
Conduction System Disorders
Dysrhythmias
Reduced Cardiac Contractility& Cardiac Output

MI: Changes in ECG

Diagnostic procedures

ECG
Chest x-ray
Echocardiogram
Angiogram (coronary catheterization)
Exercise stress test
CT scan or MRI
Blood tests cardiac enzymes

Cardiac Enzymes
Creatine Kinase
4-6 hours
Peak after 24 hours
Increased level may be
due to damage to other
kinds of cells

Troponin
2-6 hours
Peak 12-26 hours
Mre reliable indicator of
heart muscle damage

Creatine Kinase
Found in brain, skeletal muscles, and
heart.
Elevated levels heart attack, heart
muscle and skeletal muscle damage
3 different forms:
CK-MM skeletal muscles and heart
CK-MB mainly in the heart
CK-BB brain

CK-MB: elevated levels after heart attack.


Troponin- a more specific test to confirm
presence of heart attack
Trauma and conditions that damage
skeletal muscles may increase levels
Normal values:
Males 52-336 U/L
Female 38-176 U/L

CREATINE KINASE
ADP + creatine phosphate ATP + creatine
3 isozymes
CK1=BB
brain

CK2=MB
heart

CK3=MM
skeletal muscle

2 polypeptides
B subunits
M subunits

Diagnosis of Myocardial Infarction in


relation to creatine kinase

Appearance of CK2(MB) in plasma


Troponin T
Troponin I

Highly sensitive damage and specific for


cardiac tissue damage

Following injury to the myocardium, such as


occurs in acute MI, CK is released from the
damaged myocardial cells.
A rise in the CK activity can be found 4 to 8
hours after an infarction.
CK activity reaches a maximum after 12 to
24 hours and then falls back to the normal
range after 3 to 4 days.

Cycle

Treatment

Myocardial infarction

Treatment options
The immediate goal for MI is to restore
normal coronary blood flow to vessels and
salvage myocardium.
There are variety of medical and medicinal
therapies to treat an MI.

Drug therapy
goals of drug therapy are:
to break up or prevent blood clots
prevent platelets from gathering and
sticking to the plaque
stabilize the plaque
prevent further ischemia.

Drug therapy
ASPIRIN and other ANTIPLATELET
DRUGS
-to prevent blood clotting that may worsen
the heart attack
-antiplatelet drug called clopidogrel (Plavix
) is also usually given as soon as
possible. This works in a different way to
aspirin and adds to the action of reducing
platelet stickiness.

DRUG THERAPY
NITROGLYCERINE
principal action is vasodilatation
PAIN RELIEF
A strong pain killer like morphine given by
injection into a vein will ease the pain.

Treatment to restore blood flow in the


blocked coronary artery
The part of the heart muscle without blood
and oxygen supply does not die
immediately.
If blood flow is restored within a few hours,
much of the heart muscle that would have
been damaged permanently will survive.

Emergency angioplasty
In this procedure a tiny wire with a balloon at the
end is put into a large artery in the groin or arm.
It is then passed up to the heart and into the
blocked section of a coronary artery using special
x-ray guidance.
The balloon is blown up inside the blocked part of
the artery to open it wide again.
A metal device (stent) may be left in the widened
section of the artery

BETABLOCKERS
Beta-blockers (eg Metoprolol, Seloken
)block the action of certain hormones
such as adrenaline.
Beta-blockers have some pro- tective effect
on the heart muscle, lower the blood
pressure and heart rate and they also help
to prevent abnormal heart rhythms from
developing.

TREATMENT AFTER A MI
Aspirin ((Trombyl ): to reduce the stickiness of
platelets in the blood which helps to prevent blood
clots forming.
Clopidogrel (Plavix ): in addition to aspirin,
especially after angioplasty with stenting.
Treatment duration: 6-12 months depending on
stent type.
A beta-blocker (Metoprolol/Seloken ): to slow the
heart rate, lower blood pressure and to reduce the
chance of abnormal heart rhythms developing.

An ACE inhibitor or angiotensin converting


enzyme-inhibitor (Ramipril/Triatec): ACE
inhibitors have a number of actions
including lowering the blood pressure,
reducing the risk of structural changes in
the damaged heart muscle and having a
protective effect concerning future events.

A statin drug (Simvastatin ): to lower the


level of cholesterol and other blood lipids
in your blood. This helps to prevent the
build-up of atheroma and therefore
reduces the risk in the future.

Medical procedures
CORONARY ANGIOPLASTY
BYPASS SURGERY

CORONARY ANGIOPLASTY
Plaque is made up of
extra cholesterol,
calcium, and other
substances that float in
blood. Over time,
plaque can build up on
the inside walls of the
coronary arteries and
block the blood flow. A
procedure called
angioplasty can open
up a blocked artery.

CORONARY ANGIOPLASTY
An angioplasty is done using a
thin, soft tube called a catheter.
The catheter is guided into the
blood vessels of the heart. First,
your doctor inserts the catheter
into a blood vessel in the groin,
arm, or wrist. A very thin guide wire
is inside the catheter. Your doctor
carefully guides the catheter
through blood vessels into the
blocked portion of the coronary
artery. Your doctor watches the
movement of the catheter in the
blood vessels on an X-ray screen.

CORONARY ANGIOPLASTY
After the catheter reaches
the blocked artery, your
doctor will move the guide
wire farther into the
blocked portion. A small
balloon is slid along the
guide wire into the blocked
artery. In most cases, a
small, expandable stent is
placed in the artery with
the balloon.

CORONARY ANGIOPLASTY
The small balloon is
inflated. The balloon may
stay inflated for a short
time. The pressure from
the inflated balloon
presses the plaque
against the wall of the
artery, creating more room
for blood to flow. The
inflated balloon also
expands the stent.

CORONARY ANGIOPLASTY
Next, the balloon is
deflated. But the stent
stays expanded. The stent
presses against the walls
of the artery and keeps the
artery open. Your doctor
removes the balloon, guide
wire, and catheter. The
stent remains in the blood
vessel, allowing the blood
to flow normally again.

CORONARY ANGIOPLASTY
After an
angioplasty, the
blocked artery is
opened up and
oxygen- and
nutrient-rich blood
flows more
normally into the
heart muscle.

CORONARY ARTERY BYPASS


Coronary artery
bypass grafting
(CABG) surgery
reroutes blood
around blocked
arteries,
increasing blood
flow to the heart
muscle tissue.

CORONARY ARTERY BYPASS


The surgeon
makes a vertical
incision in the skin
and muscle in the
middle of the
chest and then
cuts through the
breastbone
(sternum).

CORONARY ARTERY BYPASS


The surgeon
spreads the rib
cage with a
retractor to
expose the heart
and then cuts
through the lining
that protects the
heart
(pericardium).

CORONARY ARTERY BYPASS


To reroute blood flow
around the diseased
blood vessel,
surgeons typically
use a portion of the
saphenous vein in
the leg or an internal
mammary artery.

CORONARY ARTERY BYPASS


Regardless of which
type of blood vessel
is used, oxygen-rich
blood from the aorta
is rerouted around
the blocked section
of the coronary
artery to feed the
heart muscle.

LIFESTYLE CHANGES
For some people, lifestyle changes may
be the only treatment needed.
Lifestyle changes include following:
a heart healthy diet
doing physical activity regularlY
maintaining a healthy weight
quitting smoking
reducing stress.

Weak diagnostic performance of


troponin, creatine kinase and
creatine kinase-MB to diagnose or
exclude myocardial infarction after
successful resuscitation

International Journal of Cardiology


February 2014

Background
Reports on the results of a retrospective
trial to evaluate troponin T, creatine kinase
and creatinine kinase-mb in patients with
successful cardiopulmonary resuscitation
to later invasive diagnosis f AMI by
comparing measured concentrations of
these cardiac markers to the results of
coronary angiography, the current gold
standard for AMI diagnosis.

Introduction
Sudden cardiac arrest is a frequent and leading
cause of death. Acute myocardial infarction is one
of the most frequent causes.
A standardized post-resuscitation care should be
administered t improve probability of survival.
Such as inducing therapeutic hypothermia.
Recent studies have shown that urgent
percutaneous coronary intervention (PCI) have
posed survival benefits after successful
resuscitation.

Current guidelines advocate the use of PCI in


all patients in whom coronary artery disease
and cardiac ischemia are suspected.
ECG- diagnostic hallmark of acute MI and
infarction.
Troponin T and I, creatine kinase and its
isoenzymes can be used to diagnose MI.
Some say: troponin and CK are good
diagnostic marker to detect AMI, while..
Others say: troponin and CK have weak
sensitivity and specificity for detecting AMI
after resuscitation.

Objective
The aim of the study is to evaluate the
diagnostic accuracy of the cardiac injury
markers troponin, creatine kinase and
creatine kinase-MB to diagnose or exclude
myocardial infarction after cardiac arrest.

Methods
226 patients who underwent diagnostic coronary
angiography after sudden cardiac arrest were
analyzed retrospectively (2001-2010).
Details on their angiography were also studied to
classify subjects into 2 categories: W/CAD and
NO CAD
Levels of troponin T, CK, and CK-MB were taken
on admission and 6hours, 24hours and 36hours
later. This data was compared with results of
angiography

Analysis of cardiac markers


CK UV assay : 170U/L for men and 145 U/L
for women
CK-MB UV assay: 24U/L
TNT immunologic assay : <0.05 ug/L

Summary
Cardiac markers cornerstone in dx of MI.
Study evaluated 3 main cardiac markers in
diagnosing MI that had been secured with
angiography after resuscitation.
Initial elevation above the cut-off for dx of
MI.
Patients with AMI had an increase in TNT
and CK levels peaking at 6-24hours after
the event

Moderate increase in CK-MB and weak


statistical significance in comparing levels
in AMI and non-AMI patients.
Hypoperfusion after subcritical stenosis
during CPR only mildly contributes to the
systemic elevated levels of TNT and CK.
Patients without any CAD also presented
elevted amount of cardiac markers,
indicating that cardiac arrest and/or CPR
may lead to release of cardiac enzymes
and proteins.

Previous studies have reported


reasonably good diagnostic performance
of cardiac injury marker to diagnose AMI
after resuscitation. These studies did not
use coronary angiography to diagnose
AMI but rather they employed ECG.
Previous studies that used angiography,
the gold standard in diagnosing AMI, the
cardiac enzymes had weak diagnostic
performance.

In line with this the researchers were not


able to produce favorable diagnostic
performance of TNT, CK and CK-MB to
diagnose AMI.
Even with high levels of the cardiac
markers, the sensitivity and specificity
were not favorable.

Results
AMI and non-AMI patients showed
increasing levels of troponin T and CK
after resuscitation.
AMI groups showed significantly higher
TNT and CK levels
ROC were calculated to determine
diagnostic precision of TNT, CK and CKMB
Results showed mediocre diagnostic
precision.

TNT
Sensitivity : 70.9%
Specificity : 61.2%

CK
Sensitivity : 62.5%
Specificity : 73.7%

CK-MB
Sensitivity : 58.8%
Specificity : 72.7%

Conclusion
Cardiac injury markers cant be used to
reliably diagnose or rule out AMI after
resuscitation.
Coronary angiography should be extended
to all patients without an alternative
diagnosis exxplaining the occurence of
cardiac arrest.

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