Unit 5: Cardiac Markers & MCI

Cardiac Markers & MCI
Dr. Elham Sharif,PhD
Assistant professorof BiomedicalSciences
College of Health Sciences
Qatar University
Tel: 00974-4403-4788
Email: e.sharif@qu.edu.qa

OBJECTIVES
• After attending a lecture on cardiac markers, the students will:
• Identify/Explain the origin of six general symptoms of cardiac disease. (TL1)
• Identify/Discuss the aetiology and physiologic effects of the following cardiac conditions: Congenital
heart disease, Hypertensive heart disease, Infectious heart diseases, Coronary heart disease,
Congestive heart failure. (TL1)
• Identify nine risk factors for coronary heart disease. (TL1)
• Identify/List six features of an ideal cardiac marker. (TL1)
• Identify/List and briefly describe three novel markers of inflammation currently under investigation.
(TL1)
• Identify/Compare and contrast the specificity and sensitivity of the most commonly used serum
cardiac markers. (TL3)
• Assess the clinical utility of the various cardiac markers to assess myocardial
• infarction. (TL3)
• Identify/Analyze the role of the clinical laboratory in the assessment of a patient with cardiac disease.
(TL1)
• Assess the usefulness of point-of-care cardiac markers and the role of the clinical laboratory in the
use of these methods. (TL3)
• Interpret the biochemical data used in the investigation and diagnosis of disease, when given
problem based case studies. (TL3)
10/23/17 Dr Elham Sharif 3

Terminology
• Electrocardiogram (ECG) - tracing of electrical activity of the
heart.
• Myocardium: heart muscle
• Coronary arteries: three major blood vessels supplying blood and
oxygen to the heart muscles
• Angina: chest pain due to inadequate supply of oxygen to heart
muscle.
• Plaque; accumulated deposits of fat and other substances in the
blood vessels causing roughened and narrowed interior surface.
• Pectoris: chest
10/23/17 4Dr Elham Sharif

Pathologic Conditions of the Heart
• Cardiovascular Disease (CVD)
o Timely & accurate diagnosis made difficult by lack of tests
o Conditions highlighted in this chapter:
• Congestive heart failure
• Acute coronary syndromes (acute
myocardial infarction)
• Hypertensive heart disease.
• Infective heart disease.

Cardiovascular Disease (CVD)
7 classic symptoms
• Dyspnea: shortness of breath, due to diminished cardiac function.
• Chest pain: angina pectoris—pain from heart
• Palpitations: awareness of one’s own heartbeat, extra heartbeats.
• Syncope: fainting, disturbance in heat rhythm.
• Edema: swelling of tissue due to retention of water or lymph, due to
diminished cardiac function.
• Cyanosis: bluish discolorationof skin (pulmonary insufficiency)
• Fatigue: overall feeling of weariness or lack of energy, due to lack of
sleep
10/23/17Dr Elham Sharif 7
Pathologic Conditions of the Heart (cont’d)

Congenital Cardiovascular Defects
o Abnormalities arising from abnormal formation of heart or its
major blood vessels
o Signs & symptoms: cyanosis, pulmonary hypertension, clubbing
of fingers, embolism, reduced growth, syncope
o Associated factors
• Maternal rubella infection
• Maternal alcohol abuse
• Drug treatment & radiation
• Genetic & chromosomal abnormalities

Congenital Cardiovascular Defects (cont’d)
o Ventricular septal defects (most common): “hole” in heart: ‫عيوب‬
‫البطيني‬ ‫الحاجز‬(‫شيوعا‬ ‫األكثر‬" : )‫الثقب‬"‫القلب‬ ‫في‬
o Tetralogy of Fallot ‫فالو‬ ‫رباعية‬
o Transposition of great arteries ‫الكبيرة‬ ‫الشرايين‬ ‫انعكاس‬
o Atrioventricular septal defects ‫أذيني‬ ‫الجيبي‬ ‫الحاجز‬ ‫عيوب‬
o Coarctation of aorta ‫األبهر‬ ‫تضيق‬
o Hypoplastic left heart syndrome ‫القلب‬ ‫تصنع‬ ‫نقص‬ ‫متالزمة‬ ‫من‬ ‫بقي‬

Heart Failure
o Results from any structural or functional cardiac disorder
that impairs ability of ventricle to fill with or eject blood
o When left side of heart cannot pump:
• Excess fluid fills lungs
• Pulmonary edema & reduced output of blood to
systemic circulation
o When right side of heart cannot pump:
• Excess fluid in systemic circulation & generalized
edema
o Common causes: coronary artery disease,
cardiomyopathies, inflammatory heart disease, valvular
disease, arrhythmias, congenital cardiovascular failure

Acute Coronary Syndromes
Acute Myocardial infarction AMS/MI
o The word infarction comes from the Latin word infarcire, meaning “to
plug up or cram.” It refers to the clogging of the artery and crushing.
o Continuum of events: angina, reversible tissue injury, unstable angina,
myocardial infarction, extensive tissue necrosis
o Symptoms: chest pain, referred pain, nausea, vomiting, dyspnea,
diaphoresis, light-headedness
o Major cause: atherosclerosis (thickening & hardening of artery walls by
plaque deposits in lining of arteries)
o Results of atherosclerosis: narrowing of arteries, plaque disruption,
thrombus formation
o Predisposing factors: age, sex, family history, dyslipidemia, smoking,
hypertension, sedentary lifestyle, diabetes mellitus

ACUTE MYOCARDIAL INFARCTION
• The heart muscle, or myocardium, receives its blood flow from
three coronary arteries.
• If blood flow from the coronary arteries to the heart muscle
(myocardium) is restricted, not enough oxygen reaches the
heart.
• This is termed ischemia, it can cause chest pain or angina.
• If blood flow to a portion of the heart muscle is stopped entirely,
it can cause cell death, necrosis, and heart attack, or acute
myocardial infarction (AMI).
• The precipitating event that leads to blocking of blood flow is a
clot or dislodged plaque particle that prevents blood flow to
tissue.
Explanation

If cellular damage occur
• Troponin leaks from the heart tissue and is released into
the bloodstream.
• Damage to heart muscle fibers releases CK-MB into the
bloodstream as well.
• Other constituents released by damaged heart cells
include lactate dehydrogenase isoenzyme 1 (LD1),
aspartate transaminase (AST), and electrolytes.
Explanation

Hypertensive Heart Disease
o Heart diseases caused by direct or indirect effects of elevated
blood pressure (BP) (hypertension)
o Includes:
• left ventricular hypertrophy, coronary artery disease,
cardiac arrhythmias, & congestive heart failure
o The higher the BP, the greater the risk of heart attack, stroke,
& kidney diseases.
o Classes of hypertension:
1) normal, 2) prehypertension, 3) stage 1, & 4) stage 2
o Symptoms may include dizziness, headaches, palpitations,
restlessness, nervousness, tinnitus.

Infective Heart Disease
o Heart diseases caused by infectious agents :Chlamydia
trachomatis, Mycobacterium tuberculosis, Streptococcus pneumoniae,
Influenza, Adenovirus
o Rheumatic heart disease
• A serious complication of rheumatic fever
• Thought to result from an autoimmune response
o Infective endocarditis
• An infection of endocardial surface of heart caused by several
microorganisms & fungi
o Pericarditis
• Inflammation of pericardium from infection or autoimmune disorder

cardiac profile
• 1. Upon arrival to the emergency department, a cardiac
profile would be ordered to establish baseline values.
• Then the cardiac profile would be ordered for several samplings
in 3- to 8-hour intervals over a 12- to 24-hour period.
• Frequently blood is drawn every 3 hours for analysis during the
first 12-hour period.
• Laboratory testing used to assess AMI includes cardiac troponin
T or I, CK-MB, and sometimes myoglobin.
• In many institutions, once the cardiac troponin appears
elevated, additional sampling and testing is halted and the
elevated cardiac troponin is considered diagnostic for AMI.
update

CASE 1: CHEST PAIN

Case 1: Chest Pain
10/23/17 22
A 63 year old male was brought to the emergency department
after complaining of severe chest pain that had lasted for two
hours. He had been mowing his lawn when the pain developed,
and he became concerned when the pain did not subside after
he stopped the activity. He had no previous history of heart
disease. On presentation he was moderately overweight, dia-
phoretic, and in obvious discomfort. He described his chest
pain as “beginning in the center of my chest, then my arms,
neck, and jaw began to ache too.”
Diagnostic procedures were performed.
Dr Elham Sharif

Questions
• What is the most important consideration in the triage of
this patient?
• What tests should be ordered?

Chest pain
• One of the most common reasons for seeking medical
attention
• Characteristics of cardiogenic chest pain (angina)
– induced by exercise
– described as “pressure”
– radiates to extremities
– MI not relieved by rest or vasodilatory drugs
• Only 25% of patients presenting with chest pain as the
primary complaint will ultimately be diagnosed as MI
(specificity=25%; sensitivity=80%)

Diagnosis of Heart Disease
Laboratory Diagnosis of Myocardial Infarction
o Myocardial infarction (MI): myocardial necrosis due
to prolonged ischemia
o Categorized by size of infarct
• Microscopic (focal necrosis)
• Small (<10% of left ventricular myocardium)
• Moderate (10–30% of left ventricular myocardium)
• Large (>30% of left ventricular myocardium)
o Diagnosis based on clinical symptoms,
electrocardiographic (ECG) changes, & rise/fall of
sensitive biochemical markers

Electro cardiogram ECG
• The ECG (or EKG) produces another form of objective information.
• The ECG tracings represent electrical current as it passes through
heart muscle, causing contractions in the upper and lower chambers.
• Each lead of the ECG represents a tracing of the electrical current as
it passes through a different plane of the heart.
• Cardiac damage, such as that caused by an AMI, produces areas of
dead cells within the muscle.
• Electrical current will not pass through these areas, and the tracing of
the area will show abnormalities

Normal Electrocardiogram
10/23/17 27
P
Q
R
S
T
U
Dr Elham Sharif

ECG changes in myocardial infarction
10/23/17 28
S
P
R
T
Q
S-T elevation
Dr Elham Sharif

Diagnostic value of ECG
• ECG changes depend on the location and severity of
myocardial necrosis
• 100% specific: almost 100% of patients with characteristic
Q-wave and S-T segment changes are diagnosed with
myocardial infarction.
• 50%  sensitive: as many as 50% of myocardial infarctions
do not produce characteristic ECG changes.
• ECG may be insensitive for detecting prognostically
significant ischemia

Ck
LD
AST
Enzyme markers

Creatine kinase
• CK is a cytosolic enzyme involved with the transfer of
energy in muscle metabolism.
• CK is a dimer composed of two subunits, B (brain) and
M (muscle), resulting in three cytosolic isoenzymes:
• CK-MM (CK-3), CK-MB (CK-2), and CK-BB (CK-1)

Creatine Kinase (CK)
10/23/17 32
Phosphocreatine
ADP
HK
Glucose Glucose-6-phosphate
NADPH
=340 nm
NADP+
GPD
6-Phosphogluconate
Oliver and Rosalki method (1967)
Creatine
CK
ADP ATP
Mg++
Dr Elham Sharif
Creatine Kinase (CK)

Tissue specificities of CK isoenzymes
Tissue
CK-1
(BB)
CK-2
(MB)
CK-3
(MM)
Skeletal muscle 0% 1% 99%
Cardiac muscle 1% 20% 79%
Brain 97% 3% 0%

Measurement of CK isoenzymes
• Electrophoresis (not used anymore)
• Immunoinhibition/precipitation
• Most modern methods use two-site (“sandwich”)
heterogeneous immunoassay
– Measures CK-MB mass, rather than activity

CK MB isoenzyme
• Rises within 4-6 hours after the onset of chest pain, peaks at 12-24 hours, and
returns to normal levels within 2-3 days.
• CK-MB activity assays is replaced by CK-MB mass assays:
o It measure the protein conc. rather than catalytic activity.
o Using mass assays reduces the analytical interference that lead to FP
test.
o It has higher clinical sensitivity of CK-MB.
o CK-MB mass assays can detect an increased amount of serum CK-MB
about 1 hour earlier than activity-based assays.
o Calculation of a relative index (CK-MB mass assay/total CK × 100) may
be used as an indicator of MI.
o The relative index allows the distinction between increased total CK due to
myocardial damage and that due to skeletal or neural damage:
• A relative index exceeding 3 is indicative of AMI.

Sensitivity/specificity of CK-MB
• >90% sensitive and specific for MI if measured within 7-18
hours.
• CK is a relatively small enzyme (MW = 86K), so it is filtered
and cleared by the kidneys; levels return to normal after 2-3
days.
• Sensitivity is poor when total CK is very high, and specificity
is poor when total CK is low.
• Presence of macro-CK results in false elevations

Lactate dehydrogenase (LD)
• LD activity is measured by monitoring absorbance at  = 340
nm (NADH)
• Total LD activity has poor specificity
40
Pyruvate Lactate
LD
NAD+NADH
Enzyme markers
10/23/17Dr Elham Sharif

LD isoenzyme Tissues
LD-1 Heart (60%), RBC, Kidney
LD-2 Heart (30%), RBC, Kidney
LD-3 Brain, Kidney
LD-4 Liver, Skeletal muscle, Brain, Kidney
LD-5 Liver, Skeletal muscle, Kidney
– Five isoenzymes, composed of combinations of H (heart) and M (muscle)
subunits.
–An increase in LD isoenzyme activity can indicate leakage from cells due to
cellular injury.

• LD isoenzymes begin to leak out of dying heart muscle cells and
are detectable in the serum by 36 hours following a heart attack.
• Normal LD isoenzyme patterns show that LD2 is greater than LD1.
• The appearance of more LD1 than LD2, also called the
“flipped pattern,” is typical of cardiac muscle damage
– but is nonspecific since it also is associated with red blood cell
hemolysis or megaloblastic anemias.
• The flipped pattern, in which LD1>LD2, lasts up to 3 to 4 days
after the heart attack.
• LD levels rise at slow rate so they are not useful for early
detection or treatment of the disease.
• But, will remain in the bloodstream for 4-7 days after an AMI,
enabling clinicians to detect post-AMI conditions in patients who
have had mild heart attacks and did not seek diagnosis until
several days after the suspected illness
4210/23/17Dr Elham Sharif

LD isoenzyme electrophoresis (normal)
10/23/17 43
LD-1
LD-2
LD-3
LD-4
LD-5
LD-2 > LD-1 > LD-3 > LD-4 > LD-5
Cathode (-) Anode (+)
Dr Elham Sharif

LD isoenzyme electrophoresis (abnormal)
10/23/17 44
LD-1
LD-2
LD-3
LD-4
LD-5
LD-1 > LD-2 (flipped pattern)
Cathode (-) Anode (+)
Dr Elham Sharif

FIND THE DIFFERENCE?

Direct measurement of LD-1
• Electrophoresis is time-consuming and only semi-
quantitative
• Antibodies to the M subunit can be used to precipitate
LD-2, 3, 4, and 5, leaving only LD-1
o Method can be automated
o Normal LD-1/LDtotal ratio is less than 40%

Sensitivity and specificity of LD-1
• Sensitivity and specificity of the LD 1:2 “flip”, are 90+% within 24
hours of MI, but. . .
o May be normal for 12 or more hours after symptoms appear
(peak in 72-144 hours)
o May not detect minor infarctions
• Elevations persist for up to 10 days
• Even slight hemolysis can cause non-diagnostic elevations in
LD-1

• In order for these biomarkers to be more specific indicators of
AMI, they were analyzed together several times a day over a
period of 1 week.
• Analysis of isoenzymes of CK and LD also provided improved
specificity.
• The goal is to observe the peak and return to normal of these
enzymes in order to predict resolution of the heart attack or to
monitor for a second cardiac event

Cardiac proteins

• Cardiac troponins
o Troponin (I & T) is preferred marker.
o A complex of 3 proteins bound to thin filament of muscle
o Have high sensitivity & specificity for myocardial damage
• Myoglobin
o An oxygen-binding heme protein in cardiac/skeletal muscle
o Clinically useful for its early release from damaged muscle
• Myosin light chains (MLC)
o Not specific to cardiac injury; of limited clinical significance
o Combination of markersis recommended.

Myoglobin
• Low molecular weight protein (17,8 kilo-daltons)
• Myoglobin is an oxygen-binding heme protein that is present in
both cardiac and skeletal muscle.
• Myoglobin is a sensitive & early indicator marker of cardiac injury,
but non specific ….why?
• It is detected as early as 1 hour following AMI.
• Myoglobin, which is rapidly relaesaedfrom the necroticheart, undergoes
rapid renal clearance, theroforerenal RF can resultin increasemyoglobin
levels.
• Non-specific but sensitive marker--primarily used for negative
predictive value
o Because it is detected in pts with skeletal muscle disease,
trauma and RF.
update

Myoglobin cont’d
• Clinical significance
• 1) Increased in skeletal muscle injuries, muscular dystrophy, and
AMI
• 2) Myoglobin is released early in cases of AMI, rising in 1-3 hours
and peaking in 5-12 hours, and returns to normal in 18-30 hours.
o However, it is not tissue specific. It is better used as a negative
predictor in the first 2-4 hours following chest pain.
• Test methodology
• 1) Quantified by immunoassay
o Usually measured by sandwich, nephelometric, turbidimetric, or
fluorescence immunoassay.
• 2) Reference ranges: Male, 30-90 ng/mL; female, <50 ng/mL
update

Temporal changes in myoglobin and CK-
MB

Cardiac Proteins- Troponins
10/23/17 54
• The preferred biomarkers for assessment of myocardial necrosis are
the cardiac troponins.
• The major function of troponins is to bind calcium and regulate muscle
contraction.
• Troponin is a complex of three proteins that bind to the thin filament
(actin) of cardiac and skeletal muscle:
1. Troponin C (calcium-binding component), binds to four Ca
ions, thus regulating contraction.
2. Troponin I (inhibitory component), inhibits the activity
actinomyosin ATPs.
3. Troponin T (tropomyosin-binding component).
Dr Elham Sharif

Troponin
10/23/17 55
Thick Filament
Myosin
Tropomyosin Actin
TnC
TnT (42 Kd)
TnI (23 Kd)
Dr Elham Sharif
Cardiac Proteins- Troponins cont’d

• Following injury to skeletal or heart muscle cells, the troponin
complex and free troponin subunits are released into the
bloodstream.
• The troponins have high sensitivity and specificity for
myocardial damage.
• Troponins rise 4-10 hours after the onset of symptoms, peak
at 12-48 hours, and remain elevated for 4-14 days.
• TnT measurements are extremely useful in patients who do
not seek medical attention in the 2- to 3-day window when
CK-MB is elevated.
• Cardiac TnT begins to rise within a few hours after the onset
of chest pain, peaks at 2 days, and can remain elevated for 7-
10 days.

• Cardiac TnI is also helpful in monitoring patients after
reperfusion treatment.
• Cardiac TnI is cardiac specific due to the presence of an
additional amino acid residue on the amino-terminal end.
• After an AMI, the TnI increases above the reference range
between 4 and 6 hours after chest pain onset, peaks at 12-
18 hours, and returns to within reference limits in about 6
days, depending on AMI.
• Recently, an ultrasensitive TnI assay (TnI-Ultra) has been
developed that offers a more sensitive assay for the
detection of TnI and the detection of myocardial injury
earlier than the current assays.

Troponins cont.
• During the process of muscle necrosis, troponins I and T
are released from the dying muscle fibers into the
bloodstream.
• Increases in the concentration of troponins I and T above
the reference levels in serum indicate heart muscle fiber
damage and necrosis.
• Serum troponins generally are not elevated with angina or
early stages of decreased blood flow before actual muscle
fiber death.

Clinical significance
• 1) cTnT or cTnl (cardiac troponin T or cardiac troponin I) is
used as an AMI indicator because of specificity and early rise
in serum concentration following AMI.
• 2) In cases of AMI:
o cTnT increases in 3—4 hours following infarction, peaks in
10-24 hours, and returns to normal in 10-14 days.
o cTnl increases in 3-6 hours following infarction, peaks in
14-20 hours, and returns to normal in 5-10 days.

10/23/17 60
•Troponins released from heart muscle remain in the bloodstream from 1
to 14 days after onset of AMI, making them the preferred marker for
detection of an AMI.
• Troponins, as cardiac markers, appear to have many advantages
over CKMB primarilydue to their:
•quick release following heart muscle damage.
• longevity in the bloodstream following the heart attack.
•TnI is not found in detectable amounts in the serum of patients
with:
• multiple injuries
•strenuous exercise
•renal failure
•acute or chronic skeletal muscle disease.
Dr Elham Sharif

Tissue specificity of Troponin subunits
• Troponin C is the same in all muscle tissue
• Troponins I and T have cardiac-specific forms, cTnI and cTnT
• Circulating concentrations of cTnI and cTnT are very low
normally.
• cTnI and cTnT remain elevated for several days in MI
• Hence, Troponins would seem to have the specificity of
CK-MB (or better), and the long-term sensitivity of LD-1
Methods used for detection of troponins are
immunochemical (ELISA, MEIA, CIA, ECIA)

WHO has a Myocardial Infarction?
• A clinical history of ischemic-type chest
discomfort
• Changes on serially obtained ECG tracings
• A rise and fall in serum cardiac markers
10/23/17 64
A patient presenting with any two of the following:
Source JACC 28;1996:1328-428
Dr Elham Sharif

Sensitivity/Specificity of WHO Criteria

What Cardiac Markers do Labs Offer?

• Markers of Inflammation and Coagulation
Disorders
o High-sensitivity C-reactive protein
• An acute-phase protein produced by liver in response to injury, infection, &
inflammation
• Useful in its high predictive value for coronary artery disease
o Pregnancy-associated plasma protein A
• A zinc-binding protein found in high serum concentrations of women in
advanced stages of pregnancy
o Lipoprotein-associated phospholipase A2
• An enzyme associated with small dense LDL-C particles

• Markers of Congestive Heart Failure (CHF)
• Natriuretic Peptides:
• Polypeptide Hormones
• Tissue location and function a. Three forms: ANP, CNP, BNP
• Although effects are minimal, they function to promote excretion of sodium and
water by increasing the glomerular filtration rate and decreasing the tubular
reabsorption of sodium by the kidneys.
o B-type natriuretic peptide (BNP) & terminal fragment of its prohormone
(NT-proBNP)
• B-type (brain) natriuretic peptide (BNP) is synthesized in and secreted
from myocardial ventricles in response to ventricular volume expansion
and pressure overload.
• BNP causes dilation of blood vessels and promotes sodium and water
loss, thus reducing fluid load on the heart to improve cardiac function.

Natriuretic Peptides:
• Clinical significance:
• BNP increased in congestive heart failure (CHF)
• Work well in diagnosing heart failure & are of prognostic value in
patients with acute coronary syndrome
• Patients with levels <20 pmol/L are unlikely to have CHF; those with
results above this level have high probability of it.
• BNP quantified by fluorescence and chemiluminescence immunoassays
• Reference range: BNP < 100 pg/mL
• ProBNP assay measures N-terminal proBNP (NT-proBNP), which is
released when BNP is cleaved from precursor proBNP.
o NT-proBNP has a longer half-life than BNP.
o Measurement of NT-proBNP shows no interference from nesiritide
(human recombinant BNP) administration to treat CHF.
o NT-proBNP is measured by electrochemiluminescence.
UPDATE

High-sensitivity CRP (hs-CRP)
• C-reactive protein (CRP): ^-globulin that is an acute-phase reactant
• High-sensitivity CRP refers to the sensitivity of the assay to determine low
levels in serum.
o Used as a predictor for cardiovascular risk; increased levels seen in
inflammation, infection, stress, trauma, and AMI.
o Quantified by immunoassay; hs-CRPdetection limit 0.05 mg/L
• Reference ranges: Males, 0.3-8.6 mg/L; females, 0.2-9.1 mg/L
• Cardiovascular risk classification:
o Low risk <1.0 mg/L;
o average risk 1.0-3.0 mg/L;
o high risk >3.0 mg/L
UPDATE

Homocysteine
o Elevated levels cause damage to arterial walls that precedes formation of
plaques. It is an indicator of arterial inflammation.
o a. Immunoassay, fluorometric, chromatographic
• Reference range: 5-15 |xmol/L
UPDATE

• Patient-Focused Cardiac Tests
o Early diagnosis of MI results in less cardiac tissue damage, fewer
complications, shorter hospital stays, & faster recovery.
o Point-of-care (POC) testing for cardiac markers can reduce
turnaround time.
o Medical & technical issues to address when POC is used:
• Qualitative vs. quantitative test systems
• Panel of cardiac markers vs. discrete, single analyte results
• Determining diagnostic cut-off values for MI on POC results &
correlating those results with other results from lab

Diagnosis of Heart Disease (cont’d)
• Role of Laboratory in Monitoring Heart Disease
o Involves measuring effects of heart on other organs, such as lungs,
liver, & kidney
o Common lab tests for monitoring heart disease
• Arterial blood gases
• Serum electrolyte (sodium, potassium, chloride, calcium)
• AST, ALT, & ALP levels
• Lipid evaluation
• Highly sensitive thyroid-stimulating hormone assay
• Complete blood count & blood cultures

References
• Bishop., ML, Fody., E.P. Schoeff, LE , Clinical Chemistry:
Techniques, Principles, Correlations (Bishop, Clinical
Chemistry) ISBN: 978-0781790451, Publisher: Lippincott
Williams & Wilkins; Sixth Edition, 2010.
• Marshall, W.J., Bangert, S.K.; Clinical Chemistry 6th
edition, ISBN 0-7234-3328-3 -Publisher: Mosby, Release
date: 2008.
• Christenson, R.H., Gregory, L.C., Johnson, L.J. (2001).
APPLETON & LANGES OUTLINE REVIEW CLINICAL
CHEMISTRY, ISBN 0070318476, Publisher: McGraw Hill
Companies.
Dr Elham Sharif
7610/23/17

Unit 5: Cardiac Markers & MCI

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Unit 5: Cardiac Markers & MCI