Biochemical markers in

myocardial infarction
DR. ASHWINI NARAYANKAR
WHAT IS MYOCARDIAL INFARCTION?
Coronary heart disease (CHD)

• Atherosclerosis affecting the

coronary arteries

Acute coronary syndrome (ACS)

• CHD can lead to thrombotic
occlusion of coronary
blood flow

Myocardial infarction (MI)

• ACS with frank necrosis of
any amount of myocardium
 ANGINA PECTORIS • Once the diameter of a coronary artery is reduced to less than 10%– 20% of
its original size

EXERTIONAL ANGINA • When demand for oxygen increases, particularly during exercise.

ACUTE CORONARY • More rapid reduction in blood flow can occur when plaque stimulates
formation of a thrombus in a coronary artery.
SYNDROME

MYOCARDIAL INFARCTION • When a thrombus completely cuts off blood flow, the supplied muscle will
develop irreversible ischemic damage.

UNSTABLE ANGINA • When the blockage is not complete, irreversible muscle damage may be
avoided, but the patient will experience severe angina, even at rest.

CORONARY HEART • The broad spectrum of heart disease resulting from impaired coronary blood
flow .
DISEASE
Myocardial ischemia results from the
reduction of coronary blood flow to an
extent that leads to insufficiency of
oxygen supply to myocardial tissue

When this ischemia is prolonged &

irreversible, myocardial cell death &
necrosis occurs.
MIs can be categorized based on characteristic
changes on the electrocardiogram (ECG).
• ST elevation MIs (STEMIs) More severe MIs, generally involving
trans- mural damage to the myocardium, typically cause the rapid
appearance of ST segment elevations and the later appearance of Q
waves.
• MIs without these changes (non–Q wave MIs, or non ST elevation
MIs [NSTEMIs]Typically involve lesser degrees of muscle damage,
possibly only to the sub endocardium

But any ACS event carries serious risk for possibly lethal
arrhythmias and for future events.
• Damage to a sizable quantity of cardiac muscle carries the additional risk
of compromising the heart’s ability to pump blood, leading to the clinical
syndrome of Heart failure (HF)
Biochemical Changes in Acute Myocardial
Infarction (Mechanism of release of
myocardial markers)
Ischemia to myocardial
muscles (with low O2 supply)

Anaerobic glycolysis

Increased accumulation of
lactate

Decrease in pH

Activate lysosomal enzymes

Disintegration of myocardial
proteins

Cell death & necrosis

Release of intracellular
Clinical contents to blood ECG changes
manifestations BIOMARKERS
 DIAGNOSTIC CRITERIA FOR MI
According to the European Society of Cardiology (ESC)/American College of
Cardiology (AAC), Third universal definition of MI (2012) following criteria
satisfies the diagnosis of MI:

1.Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least
one value above the 99 t h percentile of the upper reference limit (URL) together with
evidence of myocardial ischemia with at least one of the following:
• Ischemic symptoms;
• Development of pathologic Q waves on the ECG;
• ECG changes indicative of new ischemia (ST segment elevation or
depression or LBBB); or
• Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality.

2. Pathologic findings of an acute MI.

A Biomarker Is Defined As A Measurable Substance Or Parameter That Is
An Indicator Of An Underlying Biological Or Pathological Process.

Therefore, Depending On The Underlying Process That We Are Referring

To, The Cardiac Markers Can Be Classified As
Markers Of Necrosis, Markers Of Ischemia And Markers Of Inflammation
CHARACTERISICS OF AN IDEAL BIOMARKER
• Specific
High myocardium/serum ratio
Not present in non-cardiac tissue, even pathologically
Differentiation of cardiac toxicity (acute versus chronic, necrosis,
hypertrophy, rhythm)
• Sensitive
Zero baseline
Marker of ‘early’, reversible cardiotoxicity
Immediate release with injury
• Predictive
Long half life in blood- gives indication of
reversibility
Release proportionate to extent of injury
• Robust
Rapid, simple, accurate and inexpensive
detection in all relevant species
• Bridge pre-clinical and clinical
PATHOPHYSIOLOGICAL INTERDEPENDENCE OF BIOCHEMICAL MARKERS FOR THE EVALUATION OF CARDIAC DISEASE

. CRP, C-reactive protein;

sCD40L, soluble CD40
ligand; MPO
myeloperoxidase; PAPP-
A, pregnancy-
associated plasma
protein A; FFAu free
fatty acids unbound to
albumin; IMA,
ischaemia-modified
albumin; CK-MB, creatin
kinase isoenzyme MB;
BNP, B-type natriuretic
peptide; Nt-pro-BNP, N-
terminal fragment of pro-
BNP.
LABORATORY TESTS IN CARDIAC DISEASE
MARKERS OF CARDIAC TISSUE DAMAGE

CARDIOVASCULAR RISK FACTORS MARKERS

GENETIC ANALYSIS FOR CANDIDATE GENES OR RISK FACTORS

Eg MTHFR, LPL, IPF1
HISTORY OF CARDIAC BIOMARKERS
1954 • SGOT (AST)
1955 • LDH
1960 • CPK
1972 • CPK ISOFORMS BY ELECTROPHORESIS
1975 • CK-MB BY IMMUNOINHIBITION
1975 • MYOGLOBIN
1985 • CK-MB MASS IMMUNOASSAY
1989 • TROPONIN-T
1992 • TROPONIN-I
Markers of cardiac necrosis have come a long way since 1950s. Some of
the markers used in the past are no longer in use today

Current Cardiac Markers

Cardiac Markers of the Past
• CK-MB
• Total CK Activity

• Myoglobin • Aspartate Aminotransferase Activity

• CKMB Isoforms • Lactate Dehydrogenase Activity

• Troponin I and T • LD1/LD2 Ratio

 CARDIAC MUSCLE CELL

Size and subcellular distribution of myocardial proteins determines time

course of biomarker appearance in the general circulation
The appearance of these markers in the blood stream
and their measurable life in the blood following ischemia
depends on :

 Intracellular location
cytosol vs the structurally bound
 Molecular weight
larger diffuse at a slower rate than the smaller
 Rate of elimination
smaller rapidly as compared to larger
 Blood flow in the necrotic region
the release of structurally bound proteins are independent of the blood flow in
the infarcted region.
 Protein Elevations in Serum after MI

Time After Infarction: 1st Time After Infarction: Peak Duration of Elevation
Serum Protein Elevation (hours) Elevation (hours) (days)

AST/SGOT 2-4 2-4 3(~2-3xnormal only)

LDH 2-4 6-9 1
CK
4-6 18-36 3(~2-3xnormal only)

CKMB 2-4 24 3(~2-3xnormal only)

Myoglobin 2-3 6-9 1

Depends on extent of
Troponin I & T 4-6 24-36 damage(Trop I 7-10/ Trop T
10-14)
Transaminases have not endured as cardiac
markers because of abundance in liver,
skeletal muscle, and other tissues.

So they were soon superseded for cardiac

diagnosis by two other enzymes, lactate
dehydrogenase (LD) and creatine kinase (CK)
 LACTATE DEHYDROGENASE

Zinc containing Tetramer of two LD1 is relatively Patients with MI

enzyme active subunits, abundant in exhibit a
NADH can be H (heart) and M cardiac muscle, characteristic
easily monitored (muscle),134 kDa. whereas LD5 is pattern of
at 340 nm. more abundant in “flipped” LD,
Five isoenzymes . where the normal
skeletal muscle.
finding LD2 > LD1
is reversed.
The prolonged elevation makes it a good marker for those
patients admitted to the hospital after several days of MI.

However, its use is discouraged due to its non-specificity as its

increased levels are found in progressive muscular dystrophy,
myoglobinuria, leukemia, pernicious anemia, megaloblastic and
hemolytic anemia, renal disease and in generalized carcinoma .
 Catalyses the CK 1 (BB), CK2 In skeletal In the normal
conversion of (MB), and muscle, CKMB heart, an average
creatine to CK3 (MM). accounts for 0% of 15%–20% of
phosphocreatine CKMT- to 1 % of the total the CK is CKMB.
degrading ATP to Mitochondrial CK in type 1
ADP fibres and 2%–
Dimer 40kDa 6% of CK in type
2 fibres.
 CK-MB

HIGH SPECIFICITY FOR CARDIAC TISSUE

BEGINS TO RISE 4-6 HOURS OF INFARCTION

PEAKS AT ABOUT 12 HOURS

RETURNS TO BASELINE AT 24-36 HOURS

There are two forms of CK-MB:
CK-MB2 is the form recently released from tissue and is distinguished by the presence of a C-terminal lysine.
CK-MB1 is the form present in the circulation for a sufficient period of time for cleavage of the C-terminal lysine
by carboxypeptidase.
The two forms are resolved by a specialized piece of electrophoretic equipment. The finding of a considerable
fraction of recently released CK-MB2 is diagnostic for MI. CK-MB2 isoform is elevated as early as myoglobin and
is more specific. However, the need for specialized electrophoretic equipment is a disadvantage.
The key finding in myocardial infarction is an elevation of
CKMB to greater than 10 ng/mL, approximately 6-48 h
after the onset of chest pain.

CKMB is not cardiac specific, as about 1 % of the CK

found in skeletal muscle tissue is CKMB. The lack of
specificity of CKMB for cardiac tissue has led the use of
the CK index (“relative index")

CK Index = CKMB mass (ng/mL) / Total CK activity (U/L)

X 100
 Creatine kinase isoenzyme MB assay by electrophoresis. The activity of the
isoenzyme bands quantitated by scanning fluorometry. Total CK activity was
used for calculation of CK-MB level.

 CKMB < 10 ng/mL and an index < 2.5 is considered normal

 CKMB > 10 ng/mL and an index > 2.5 suggests cardiac damage
 CKMB > 10 ng/mL and an index < 2.5 suggests skeletal muscle damage
 False positives of CKMB

Myocarditis Shock Coronary insuffiency

Polymyositis Cardiac surgery Other myopathy
Muscle trauma Surgery Dermatomyositis
Muscular dystrophies Severe angina Drug-induced rhabdomyoloysis
Malignant hyperthermia Idopathic (rare)

It is advisable that during the first 24 hours at least three samples be drawn for in order to
pinpoint the peak of the elevation of CKMB. Demonstration of the peak (rise and fall) within
48 hours increases the specificity of the test since it occurs in MI but not in muscle disease in
which values plateau. An elevation of CKMB above 10 ng/mL with an elevated CK index
indicates myocardial infarction with very high specificity.
ERBA CHEM-7 CLINICAL CHEMISTRY ANALYSER
 CK MB (NAC act.) KIT
Diagnostic reagent for quantitative in vitro
determination of Creatine Kinase MB in human
serum and plasma. 400ul 100ul
 IMMUNOINHIBITION / MODIFIED IFCC METHOD
CK-M fractions inhibited by an anti CK-M antibody present in the
reagent.

Then the activity of the CK-B fraction is measured by the CK (NAC

act.) method

The CK-MB activity is obtained by multiplying the CK-B activity by

two.

Indication of MI is based on the following

factors:
Total CK (male) : >195 U/L at 37°C
(female) : >170 U/L at 37°C
CK-MB : > 24 U/L at 37°C
 CARDIAC TROPONIN
Thin filament of striated muscle.

The three individual proteins are tropomyosin binding subunit (TnT, 37 kDa), inhibitory subunit (TnI, 24
kDa), and calcium binding subunit (TnC, 18 kDa).
The Ca++ trigger for muscle contraction is transmitted via the Tn complex, which causes a
conformational change in another thin filament component, tropomyosin, allowing interaction between
actin and myosin to proceed.
• With the best assays in wide use at present, which have
detection limits around 0.01 ng/mL, many healthy individuals
have undetectable levels, so the normal range is not well
defined.
• The 99th percentile of the healthy population is around 0.04
ng/mL, depending on the assay. Levels above this threshold are
almost certainly indicative of myocyte damage but possibly
reveal a much lesser amount of damage than was detectable
with earlier cardiac markers such as CKMB.
PRINCIPLE
The Troponin T Test Device (Whole Blood/Serum/Plasma) is a qualitative, membrane based immunoassay for
the detection of cTnT in whole blood, serum or plasma. The membrane is pre-coated with capture reagent on
the test line region of the test. During testing, the whole blood, serum or plasma specimen reacts with the
particle coated with anti-cTnT antibodies. The mixture migrates upward on the membrane
chromatographically by capillary action to react with capture reagent on the membrane and generate a
colored line. The presence of this colored line in the test line region indicates a positive result, while its
absence indicates a negative result. To serve as a procedural control, a colored line will always appear in the
control line region indicating that proper volume of specimen has been added and membrane wicking has
occurred.
 REFERENCE RANGE
Cardiac Markers
Marker Reference Range
Cardiac troponin I (cTnI) <0.07 ng/mL *
Cardiac troponin T (cTnT) < 0.1 ng/mL *
Creatine kinase MB isoenzyme (CKMB) <10 ng/mL
<170 ng/mL (>25% increase over 90 min. suggests
Myoglobin
AMI)

*As assays become more sensitive and specific the

reference range for troponins continues to
decrease. Values greater than 99th percentile of
the upper reference limit (greater than 99th
percent of the normal population) should be
considered abnormal.
 OTHER MARKERS

MYOGLOBIN

Myoglobin is a heme containing protein that binds oxygen within cardiac

and skeletal muscle; only a single form is common to both muscle types.
• Molecular weight of only 18 kDa, myoglobin apparently leaks from damaged cells more
rapidly than other proteins.
• Peaks about 6 hours after MI and returns to baseline after 24 hours. Although myoglobin
may offer some advantage in early detection of myocardial damage, its value is limited by
its lack of specificity.
Carbonic Anhydrase III
• Present in skeletal but not in cardiac muscle, “negative” cardiac marker. It is released from
damaged muscle at a fairly fixed ratio to myoglobin. Thus myoglobin is a more specific indicator of
myocardial damage when its ratio to CA III is also elevated

Heart Fatty Acid–Binding Protein

• Heart fatty acid–binding protein (HFABP) is a low molecular weight (15 kDa)
protein that is a relatively early marker of myocardial damage, with kinetics
similar to that of myoglobin.
• It is not cardiac specific. However, the ratio of myoglobin to HFABP is
much lower in heart than in skeletal muscle and may have diagnostic
applicability.
 BRAIN NATRIURETIC PEPTIDE AND NTproBNP
• Released from cardiac tissue in response to ventricular wall stress in the absence of necrosis and
preceding angina and ST-segment changes.
• Elevations in the natriuretic proteins are merely an indication of hemodynamic stress, and fluid
overload states, and are not specific for heart disease.
• The higher concentrations of BNP and NT-proBNP are associated with a higher risk of death or heart
failure independently of other prognostic variables, including the left ventricular ejection fraction.
• The plasma concentration of BNP rises quickly, peaking at about 24h after infarction and its level and
duration of elevation corresponds to the likelihood of future adverse cardiac events.

Marker Reference Range

BNP (77-108) <100 pg/mL
NT-pro-BNP (1-76) if less than 75 years old <125 pg/mL
NT-pro-BNP (1-76) if greater than 75 years old 450 pg/mL
PROPOSED BIOCHEMICAL MARKERS FOR EARLY
DETECTION OF MYOCARDIAL INJURY IN BLOOD
Markers of cardiac ischaemia
• Unbound free fatty acids
• Ischaemia-modified albumin
• Glycogen phosphorylase BB

Markers of inflammation and plaque instability

• C-reactive protein
• Soluble CD40 ligand
• Myeloperoxidase
• Pregnancy-associated plasma protein A
 UNBOUND FREE FATTY ACID
• During hypoxia and ischemia, nonesterified fatty acids/FFAs
have been associated with an increased incidence of
ventricular dysrhythmias and death in patients with AMI
 ISCHEMIA-MODIFIED ALBUMIN

Ischemia modified albumin (IMA) is a unique type of cardiac marker (FDA approved in
2003) that is not a protein released from damaged myocytes. Rather, the test detects
a variant form of albumin,which is a marker seen in association with ischaemia

• The variant is measured by a spectrophotometry.

• it detects ischemia before irreversible cell damage occurs.
• The change in albumin appears to occur within minutes of ischemia and lasts for about 6 hours.
Assay has been reported to be positive within minutes of ischemia, peaking within 6h,
and remains elevated for up to 12h, thus allowing detection before the development of
myocardial necrosis [as evidenced by normal levels of creatinine kinase isoenzyme (CK-
MB), troponin and, myoglobin].

The albumin cobalt binding test has been approved by the FDA for use as a rule-out
marker for acute myocardial ischemia. The optimum cut-off for IMA, for ruling out ACS,
is 85kU/l and the higher values of 100kU/l or more can be used for risk stratification.

It is also found to be elevated in most patients with cirrhosis, bacterial and viral
infections, advanced cancers, stroke (brain ischemia), and end-stage renal disease.
Sensitivities that ranged from 71 to 98%, and specificities of 45–65%, with a NPV of 90–
97% for ACS. Thus, the main limitation of IMA at the present time is its low specificity.
 GLYCOGEN PHOSPHORYLASE BB
Glycogen phosphorylase (GP)catalyses the first step in glycogenolysis in which glycogen is converted to glucose1-phosphate,
utilizing inorganic phosphate.

DimerNof two identical subunits. Three different GP isoenzymes have been described in human tissues: GPLL (liver), GPMM
(muscle), and GPBB (brain). In the heart, GPBB is predominant.

In cardiomyocytes, GP is associated with glycogen and the sarcoplasmatic reticulum and forms a macromolecular complex.

GPBB levels increase between 1 and 4h from chest pain onset and return to the reference interval within 1–2 days after AMI onset

The accelerated GPBB release from cardiomyocytes after successful thrombolysis leads to a more rapid increase in GPBB, earlier and usually
also higher peak values. GPBB thus may be useful, along with other soluble myocardial proteins, for assessing the effectiveness of
thrombolytic therapy noninvasively. GPBB also increases, early on, in patients with UA and reversible ST-T alterations in the resting ECG at
hospital admission and could be useful for early risk stratification in these patients.
 C-REACTIVE PROTEIN (CRP)
protein found in serum or plasma at elevated levels during an inflammatory process. It is a sensitive marker of acute and
chronic inflammation and infection , short-term and long term morality risk not only for patients with acute and chronic
ischemic heart disease but also for those at risk for atherosclerosis.

Increases in CRP levels detected by assays with expanded sensitivity to very low levels of CRP, so-called high-sensitivity CRP
(hs-CRP), showed a strong correlation as an independent risk factor for future cardiac events.

New rapid tests for CRP at the ultrasensitive level have also been developed. Guidelines published by the Centers for
Disease Control/AHA indicate that based on results using standardized assays with precision to or below 0.3mg/l, cut points
of low risk (<1.0mg/l), average risk (1–3mg/l), and high risk (>3.0mg/l) be assigned to those patients with an intermediate
10-year CHD risk (10–20% Framingham Risk Score/Adult Treatment Panel III guidelines) [4].
hs-CRP predicts new coronary events in patients with ACS and unstable angina (UA), AMI, and risk of restenosis after
revascularization procedures, independent of troponin T [5]. The estimations that more than 30% of patients with severe
UA do not present with elevated hs-CRP levels along with its nonspecific nature pose a limitation to its use
 SOLUBLE CD40 LIGAND
The CD40 and CD40 ligand (CD40L) system is expressed on a variety of cell types including activated platelets, vascular endothelial
cells, vascular smooth muscle cells, monocytes, and macrophages.

After expression on the cell surface, CD40L is partly cleaved by proteases and subsequently released into the circulation as soluble
CD40L (sCD40L) that can be detected in serum and plasma.

The main source of circulating sCD40L is platelets . It also shows that the antiplatelet treatment using the glycoprotein IIb/IIIa
receptor antagonist abciximab is beneficial to patients with elevated sCD40L levels.

Several clinical studies have consistently reported that sCD40L is elevated in patients with ACS and that it provides prognostic
information with therapeutic implications independent of established cardiac markers.

Furthermore, patients with UA have higher plasma concentrations of sCD40L than healthy volunteers or those with stable angina,
and elevation of sCD40L in this setting indicates a higher risk for recurrent events.

The current standard for recurrent MI prediction by simultaneous assessment of sCD40L and cardiac troponin I (cTnI) yields
independent and complementary prognostic information, thus enabling more powerful prediction of adverse cardiac outcomes
 MYELOPEROXIDASE
Released from activated neutrophils, myeloperoxidase (MPO) is a leukocyte enzyme possessing powerful prooxidative and pro-
inflammatory properties that play important roles in the pathogenesis of destabilization of coronary artery disease (CAD).

MPO catalyzes the conversion of chloride and hydrogen peroxide to hypochlorite. It has been implicated in the
oxidation of lipids contained within LDL cholesterol and consumption of endothelial-derived nitrous oxide, thereby
reducing nitrous oxide bioavailability and impairing its vasodilating and anti-inflammatory properties.
The blood and leukocyte MPO activity is found to be higher in patients with CAD than angiographically verified normal individuals .
A recent study has shown an association of MPO levels with the risk of future CAD in an apparently healthy population . Thus, even
in the absence of myocardial necrosis and in negative cardiac troponin patients, baseline measurements of MPO significantly
enhance the identification of patients at risk.
New rapid tests for MPO levels have been developed and studies suggest that a value of more than 350mg/l is associated with a
considerably increased risk of heart attack .

MPO plays a role in the degradation of the fibrous cap, making it both a marker of inflammation (neutrophil activation) and plaque
instability (that precedes ACS). This property makes MPO a useful marker for short-term risk stratification.
• PAPP-A is released during plaque destabilization and appears to be a valuable indicator of UA and
AMI in patients lacking other indicators of necrosis.

• PAPP-A as a marker can detect plaque rupture before markers that indicate onset of MI and
myocardial necrosis. This capability for early determination of event risk makes PAPP-A a promising
novel cardiac biomarker with potential applications for CAD risk assessment, diagnosis, and
management.
 INTERLEUKIN-6
Interleukin-6 (IL-6) is a cytokine, a nonantibody protein, and intercellular mediator.

Cytokine IL-6 is produced by a variety of cells in the body; plasma concentrations reflect both the intensity of
plaque vulnerability to rupture and, following percutaneous coronary intervention, restenosis.

Cytokine IL-6 is involved in the pathogenesis of ACS and has the following effects: stimulating the linear
production of fibrinogen and CRP, stimulating the macrophage to produce tissue factor and MMPs, platelet
aggregation, adhesion molecules, tumor necrosis factor, and vascular smooth muscle cell proliferation.

Cytokine IL-6 predicts future MIs in healthy men and total mortality in the elderly. Elevation of circulating IL-6
is a strong and independent marker of increased mortality in acute coronary events.
This indicates high clinical sensitivity of cardiac biomarkers after 2-8 hours of clinical event

Several markers should no longer be used to evaluate cardiac disease like AST, total CK activity, LDH, LD
isoenzymes with exception of hydroxyl butyrate dehydrogenase (HBD), which is used to estimate infarct size.
HBD has sequence homology to H subunit of LDH, so can be considered as LD1.

In majority of patients’ blood should be obtained for testing at hospital admission (0 hours), at 6 to 9
hours, and again at 12 to 24 hours if the earlier specimens are normal and clinical event of suspicion is high.
For patient in need of early diagnosis a rapidly appearing biomarker like myoglobin has been suggested to
be added to serial cardiac troponin monitoring.

Cardiac troponin > CK-MB mass > CK-MB activity > CK. An adequate biomarker should show a rising or falling
pattern (at least one sample) when tested 6 hours apart (E.g. one at 0 hour and another at 6 hour) in the
setting of clinical ischemia and absence of non cardiac cause of biomarker elevation.
Markers of myocardial necrosis have been used for decades and have withstood the test
of time. Troponins remain the gold standard for diagnosing AMI but CK-MB suffices in its
absence. Myoglobin is the earliest (<1h) indicator of myocardial necrosis and has
excellent NPV. CK-MB isoforms are useful in detecting early AMI (2–4h), and rapid assays
are now available.

Markers for inflammation and plaque destabilization are nonspecific to cardiac disease
but have, time and again, proved to be useful adjuncts as diagnostic markers for ACS in
the ED when used in combination with TnI and brain natriuretic peptide (BNP). hs-CRP is
the most valuable among these and predicts new coronary events in such cardiac
patients independent of troponin T. Elevated PAPP-A levels identify patients with UA
even in the absence of elevations in cTn or hs-CRP levels. Although increased MPO has a
role superior to that of PAPP-A, CD40L, and cytokines, is still inferior to CRP
INFLAMMATION AND PLAQUE ISCHEMIA EARLY NECROSIS INTERMEDIATE/FATE NECROSIS HEART FAILURE
DESTABILIZATION

C- reactive protein (CRP) Ischemia modified albumin Myoglobin CKMB Brain natriuretic
Hs-CRP
peptide(BNP)
Myeloperoxidase Glycogen phosphorylase CKMB Cardiac troponin(cTn) Terminal fragment
enzyme BB (GPBB) cTnT of prohormone
Soluble CD-40L (sCD40L) Free fatty acids cTnI of BNP

Pregnancy associated plasma

Protein A

Interlukin-6
REFERENCES :

• Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined–a

consensus document of the Joint European Society of Cardiology/American College of
Cardiology Committee for the redefinition of myocardial infarction
• Cardiac biomarkers – the old and the new: a review Vikas Singh, Pedro Martinezclark,
Mario Pascual, Eric Scot Shaw and William W. O’Neill
• Biomarkers of acute myocardial infarction in the elderly: troponin and beyond Martin
G Rains,1 Charles A Laney,1 Alison L Bailey,1 and Charles L Campbell1,2