Cardiac Function Tests.ppt

Cardiac Function Tests
Heart disease
Symptoms of heart disease
Congenital heart disease
Congestive heart failure
Acute coronary syndrome
Hypertensive heart disease
Infective heart disease
Diagnosis of heart disease
Laboratory diagnosis of AMI
Enzymes, cardiac proteins.
Markers of inflammation and coagulation
Markers of congestive heart failure
Other markers
The role of the lab in monitoring heart disease

Heart disease is the primary cause of illness and death
in the United States
50 000 000 patients have hypertension; 7600 000 patients suffer a
myocardial infarction each year; 4900 000 patients have been diagnosed
with congestive heart failure.
Patients of heart disease usually asymptomatic until late stage of the
disease.
Improved detection of heart disease  can save lives
Blood tests have been used to detect substances that are present in the
blood that indicate either disease or a future risk of the development of a
disease
Blood tests detect substances that normally are not present or measure
substances that, when elevated above normal levels, indicate disease
 selection of appropriate cardiac markers that provide the most effective
and clinically useful indicators of myocardial function is critical

Symptoms of heart disease
Patients with cardiac disease are often asymptomatic until a relatively late
stage in their condition.
The most frequent symptoms manifested in heart disease are dyspnea
Dyspnea:
 Dyspnea is a difficulty in breathing.
 It can be a result of cardiac or respiratory disease and is a normal
response during exercise in healthy individuals.
 Dyspnea as a result of cardiac disease may occur only on exercise or can
be present at rest in advanced disease.
Cyanosis:
 a bluish discoloration of the skin
 Result of dyspnea and is caused by an increased amount of
nonoxygenated hemoglobin in the blood.

Angina pectoris:
 is the most common symptom associated with ischemic heart disease.
 It is a gripping or crushing, central chest pain that may be felt around or
deep within the chest.
 The pain may radiate to the neck or jaw,
 It is typically worsened by exercise and relieved by rest.
 The pain is most often caused by a lack of oxygen to the myocardium as
a result of inadequate coronary blood flow
Palpitation:
 A palpitation may be an increased awareness of a normal heartbeat
or the sensation of a slow, rapid, or irregular heart rate.

Syncope:
 Partial or complete loss of consciousness with interruption of awareness
of oneself and ones surroundings.
 It is temporary and there is spontaneous recovery.
 The most common syncopal attacks are vasovagal in nature (simple
faints) and not a result of serious disease.
 Without warning, the patient falls to the ground with a slow or absent
pulse and, after a few seconds, the patient recovers consciousness
Fatigue:
 is a common, but nonspecific, cardiac symptom.
 Lethargy (Abnormal drowsiness) is associated with heart failure,
persistent cardiac arrhythmia, It may be a result of both poor cerebral
and peripheral perfusion and poor oxygenation of blood.

Edema:
 Retained fluid accumulates in the feet and ankles of patients
 The edema associated with heart disease is often absent in the morning
because the fluid is reabsorbed when lying down, but becomes
progressively worse during the day.
Unusual symptoms
 A cough may be the primary complaint in some patients with pulmonary
congestion.
 Nocturia (is the need to get up during the night in order to urinate, thus
interrupting sleep) is also common in patients with congestive heart
failure .
 Anorexia, abdominal fullness, right upper quadrant tenderness, and
weight loss are seen in patients with advanced heart failure but are rare
in mild or early heart disease.

Congenital Heart disease
Congenital heart defects are important cause cardiac disease and occur in
about 8% of live births. There is an overall male predominance, although
some specific lesions occur more frequently in females, and it is a common
cause of death in the first year of life
Congenital heart disease includes:
 Valvular defects that interfere with the normal blood flow
 Septal defects that allow mixing of oxygenated blood from the
pulmonary circulation with unoxygenated blood from the systemic
circulation,
 Shunts, abnormalities in position or shape of the aorta or
pulmonary arteries,
 Tetralogy of Fallot
 or a combination of these conditions. Many variations and
degrees of severity are possible.

The etiology of congenital cardiac disease
 The etiology of congenital cardiac disease is often unknown
 However, most defects appear to be multifactorial and reflect a
combination of both genetic and environmental influences
 The rubella virus, the causative agent of German measles, Infection of the
mother during the first 3 months of pregnancy is associated with a high
incidence of congenital heart disease in the baby.
 Fetal alcohol syndrome is often associated with heart defects, as alcohol
affects the fetal heart by directly interfering with its development.
 Chromosomal abnormalities are associated with several developmental
syndromes, many of which include heart disease, the best-known example
is Down syndrome

Congenital Cardiac Disease
 The symptoms of congenital heart disease may be
• Evident at birth or during early infancy,
• Or they may not become evident until later in life.
 Signs and symptoms common to many congenital heart
diseases include cyanosis, pulmonary hypertension,
clubbing of fingers, embolism or thrombus formation,
reduced growth, or syncope

 The most common congenital cardiac lesions are:
 Ventricular septal defect (VSD):
 Commonly known as a hole the heart, is the most common
congenital cardiac malformation.
In this condition, blood flows through the septal defect from the
left ventricle to the right ventricle  causing less blood to be
pumped from the left ventricle and reducing output to the systemic
circulation.
More blood enters the pulmonary circulation  which overloads and
irreversibly damages the pulmonary vessels, causing pulmonary
hypertension.
Some small VSDs will close spontaneously but others should be
repaired surgically before the development of sever pulmonary
hypertension

The most common congenital cardiac lesions are:
 Atrial septal defects (ASD) are often first diagnosed in adulthood.
 This abnormality causes left-to-right shunting of blood between the
atria.
Pulmonary hypertension and atrial arrhythmia are common when the
patient is older than age 30 years, but most children with this condition
are asymptomatic.
A significant ASD should be surgically repaired as soon as possible
after diagnosis
 Coarctation of the aorta: is a narrowing of the aorta
 Congenital valve problems may be classified as stenosis (narrowing of a
valve that restricts the forward flow of blood) or valvular incompetence (a
valve that fails to close completely, allowing blood to leak backward

Tetralogy of Fallot
Tetralogy of Fallot is the most common cyanotic congenital heart abnormality in
children. It is a combination of four defects:
* Pulmonary valve stenosis is a narrowing of the pulmonary valve and the area
below the valve. This slows the flow of blood from the right side of the heart to
the lungs. The heart must pump harder to push blood to the lungs where the blood
picks up oxygen.
*Ventricular septal defect (VSD) is a hole in the wall that separates the lower
chambers (ventricles) of the heart.
* Overriding aorta is a defect in the position of the large artery (aorta) that
takes red (oxygen-rich blood) to the body. In a normal heart the aorta attaches to
the left ventricle. In tetralogy of Fallot, the aorta sits between the left and right
ventricles, over the VSD. This causes mixing of red and blue (oxygen-poor) blood.
* Right ventricular hypertrophy is the thickening of the right lower chamber of
the heart (ventricle). Unlike other muscles in your body, when the heart thickens it
does not work well. The heart has to pump harder to move blood through the
narrowed pulmonary valve and the area below

The most common congenital cardiac lesions are:
 Tetralogy of Fallot

Congestive heart failure
Congestive heart failure results when the heart is unable to pump blood
effectively.
 It is characterized by fluid accumulation, initially in the lungs and
subsequently throughout the body.
 When the heart is unable to pump efficiently, cardiac output decreases.
 When the left side of the heart fails  excess fluid accumulates in the
lungs, resulting in pulmonary edema  reduced output to the systemic
circulation  The kidneys respond to this decreased blood flow with
excessive fluid retention  making the heart failure worse.
 When the right side of the heart fails  excess fluid accumulates in
the systemic venous circulatory system and generalized edema results.
There is also diminished blood flow to the lungs and to the left side of
the heart, resulting in decreased cardiac output to the systemic
arterial circulation.

Congestive heart failure
Congestive heart failure may occur if the heart muscle is weak or if the heart is
stressed beyond its ability to react. The most common causes of congestive
heart failure: .

The most common causes of congestive heart failure:
Coronary artery disease:
is the most common cause of heart failure in the United
States.
Atherosclerosis of coronary arteries leads to ischemia
 a process that replaces active cardiac muscle with
fibrous tissue that does not function as cardiac muscle.
Obstruction of the cardiac vessels reduces blood flow
and forces the heart muscle into anaerobic metabolism,
producing waste products that can also damage the
tissue cells

Congestive heart failure:
Cardiomyopathies
 Result from an abnormality of the heart muscle.
 If the heart is unable to contract efficiently  the heart dilates
results in an enlarged heart with relatively thin cardiac walls.
 They are grouped as dilated cardiomyopathies, restrictive
cardiomyopathies, or hypertrophic cardiomyopathies
Arrhythmia:
 Malfunction of the cardiac conduction system, may also result in
congestive heart failure.
 Arrhythmia may be caused by ischemia, infarction, infilrates, electrolyte
imbalances, or chemical toxins

 Clinical indications of congestive heart failure range from
mild symptoms that appear only on effort to the most
advanced conditions in which the heart is unable to function
without external support.
 Congestive heart failure is readily detectable if it involves a
patient with myocardial infarction, angina, pulmonary
problems, or arrhythmia
 Congestive heart failure is most commonly investigated
because of dyspnea, edema, cough, or angina.
 Other symptoms, as exercise intolerance, fatigue, and
weakness, are common

Acute Coronary Syndrome
Coronary heart disease is caused by a lack of nutrients and oxygen
reaching the heart muscle and resulting in myocardial ischemia.
Ischemia is a reduced blood supply to one area of the heart and is often
a result of atherosclerosis, thrombosis, spasms, or embolisms but may
also be a result of anemia, carboxyhemoglobinemia, or hypotension, which
causes reduced blood flow to the heart. Increased demand for oxygen
and nutrients as a result of extreme exercise.
Ischemic heart disease involves a progression of pathologic conditions
that includes erosion and rupture of coronary artery plaques, activation
of platelets, and thrombi.
This progression is termed Acute coronary syndrome and ranges from
unstable angina to extensive tissue necrosis in acute myocardial
infarction.

Coronary artery disease
Ischemia is the result of abnormal coronary
arteries, usually caused by an obstruction in
arteries. Atherosclerosis is a thickening and
hardening of the artery walls caused by
deposits of cholesterol-lipid-calcium plaque in
the lining of the arteries

Risk factors for development of arterial plaques:
Age: Atherosclerosis may develop in early life but becomes a more significant risk
factor with increasing age.
Sex: Men tend to be more affected by atherosclerosis than premenopausal women of
comparable age. After menopause, the difference tends to disappear.
Family history: Atherosclerosis is often found in members of the same family. Some
conditions are directly inherited, such as familial hypercholesterolemia and familial
combined hyperlipidemia.
Hyperlipidemia: An increased serum cholesterol concentration has been shown to have a
strong association with atherosclerosis. High level of LDL, low level of HDL
increases the risk
Smoking: There is a direct relationship between number of cigarettes smoked and the
risk of coronary artery disease
Hypertension: Both systolic and diastolic hypertensionis associated with increased risk
for atherosclerosis
Sedentary lifestyle: Regular exercise has shown some protection against the
development of heart disease
Diabetes mellitus: Because of the strong relationship between diabetes and vascular
disease
Response to stress. Aggressive, ambitious, compulsive persons have almost twice the
risk for coronary disease as persons who do not express these characteristics

Presentation of coronary heart disease
Consequences of Ischemia
Regardless of the etiology of the ischemia, there are three general results of
cardiac ischemia: congestive heart failure, angina pectoris, and myocardial
infarction.

 Results when there is reduced oxygen supply to the cardiac muscle,
causing it to fail to pump the blood efficiently.
Angina pectoris:
 is a symptom of inadequate perfusion of the heart muscle, resulting in
chest pain.
 Typical angina pectoris occurs with increased physical effort or stress
and usually rapidly resolves with rest.
 In patients with coronary artery disease, the narrowed cardiac vessels
do not allow for increased blood flow into the cardiac muscle at times of
additional physical or emotional stress  causing the pain

Myocardial infarction, or heart attack,
 Occurs when blood flow to an area of the cardiac muscle is suddenly
blocked
 This leads to ischemia and death of myocardial tissue.
 The heart tissue becomes in inflamed and necrotic at the point of
obstruction and is followed by the release of cellular enzymes and
proteins into the blood.
 The damaged area of the heart quickly loses its ability to contract and
conduct electrical impulses and oxygen supplies are depleted.
 This type of damage is irreversible and the area of necrosis is
eventually replaced by fibrous scar tissue.
 The severity of damage from a myocardial infarction varies greatly and
is primarily related to the size and location of the infarct

Hypertensive heart disease
 Hypertension is defined by the World Health Organization as systolic
pressure greater than 160 mm Hg and diastolic pressure greater than 95
mm Hg. It is one of the most common cardiovascular diseases,
 Blood pressure is determined by peripheral resistance if it is increased 
results in heart disease  because it increases the workload of the left
ventricle  eventually resulting in hypertrophy and dilation.
  The increase in size of the left ventricle causes the mitral valve to allow
circulation of blood into the left atrium that  with time, results in
dilatation and increased pressure in the left atrium  this increased
pressure is transferred to the pulmonary circulation and  affects the
right side of the heart.
 Another complicating factor in this process is that hypertension is also
associated with an increased prevalence of atherosclerosis, further
increasing risk for heart disease

Infective heart disease
 Infectious agents continue to be implicated in a variety of heart
diseases
 The most common infectious diseases involving the heart are rheumatic
heart disease, infectious endocarditis, and pericarditis
 Rheumatic fever is an inflammatory disease of children and young adults
that occurs as a result of complications from infection with group A
streptococci
 Rheumatic fever is not caused by a direct infection or toxin but because
of the antibodies against the streptococcal antigens cross-react with
similar antigens found in the heart and initiate a cell-mediated immune
response involving macro phages and lymphocytes.

Diagnosis of heart disease
Because of its dangerous consequences  great efforts have
been made to determine the best tools for the early and
accurate diagnosis of acute myocardial infarction (AMI).
WHO determined criteria for the diagnosis of AMI
History  acute, severe and prolonged chest pain
ECG
Serum cardiac markers  an initial rise and subsequent fall of
certain enzymes/proteins serum concentration
Single diagnostic laboratory test that quickly and
accurately assess cardiac function does not exist  A
combination of cardiac markers is required.
Research is going on to find a cardiac marker that would be
useful in evaluating many types of heart conditions.

Features required for an ideal marker
 The marker should be absolutely heart specific to allow reliable
diagnosis of myocardial damage in the presence of skeletal muscle
injury.
 The marker should be highly sensitive to detect even minor heart
damage.
 The marker should be able to differentiate reversible from irreversible
damage.
 In acute myocardial infarction, the marker should allow monitoring of
reperfusion therapy and estimation of infarct size and prognosis.
 The marker should be stable and the measurement rapid, easy to
perform, quantitative, and cost effective.
 The marker should not be detectable in patients who do not have
myocardial damage

Lab diagnosis of AMI
• Enzymes
 AST, LD are no longer used
 Creatinine kinase, CK-MB
• Cardiac proteins
 Myoglobin
 Troponin T and troponin I
 Cardiac myosin light chains

Lab diagnosis of AMI
Enzymes
AST
LD
 These enzymes were used as indicator for MI but they are
no longer used in diagnosis because of lack of specificity to
cardiac cells
 Although LD isoenzyme determinations increase specificity
for cardiac tissue, with the LDI and LD2 subfractions being
most indicative of cardiac involvement, the National
Academy of Clinical Biochemistry recommends that LD and
LD isoenzymes no longer have a role in diagnosis of cardiac
diseases

Creatine kinase (CK)
 Creatine kinase (CK) is a cytosolic enzyme involved in the
transfer of energy in muscle metabolism.
 It is a dimer comprised of two subunits (the B, or brain
form, and the M, or muscle form), resulting in three CK
isoenzymes.
 The CK-BB (CKl) isoenzyme is of brain origin and only found in
the blood if the blood-brain barrier has been breached.
 CK-MM (CK3) isoenzyme accounts for most of the CK activity
in skeletal muscle,
 whereas CK-MB (CK2) has the most specificity for cardiac
muscle, even though it accounts for only 3-20% of total CK
activity in the heart, it can be used as a marker of early AMl

CK-MB (CK-2)
 CK-MB is a valuable tool for the diagnosis of AMl because of its
relatively high specificity for cardiac injury.
 Extensive experience with CK-MB has established it as the gold
standard for other cardiac markers.
 It takes at least 4-6 hours from onset of chest pain before CK-
MB activities increase to significant levels in the blood.
 Peak levels occur at 12-24 hours, and serum activities usually
return to baseline levels with 2-3 days
 Although the specificity of CK-MB for heart tissue is greater
than 85%, it is also found in skeletal muscle and false-positive
results may be caused at clinical conditions such as muscle
disease and acute or chronic muscle injuries

CK-MB (CK-2)
 CK-MB activity assays have been increasingly replaced by CK-MB mass
assays that measure the protein concentration of CK-MB rather than
its catalytic activity.
 These laboratory procedures are based on immunoassay techniques
using monoclonal antibodies and have fewer interferences and higher
analytic sensitivity than activity-based assays.
 Mass assays can detect an increased concentration of serum CK-MB
about 1 hour earlier than activity-based methods
 To increase specificity of CK-MB for cardiac tissue, it has been
proposed that that a ratio (relative index) of CK-MB mass/CK activity
be calculated  If this ratio exceeds 3, it is indicative of AMI rather
than skeletal muscle damage
 CK isoforms may be effectively used as indicators of reperfusion after
thrombolytic therapy in patients with confirmed AMI

Time profiles of cardiac markers after AMI

Cardiac Proteins
Several proteins may be monitored in suspected cases of AMI to give
significant diagnostic information
Myoglobin:
 an oxygen-binding heme protein that accounts for 5-10% of all
cytoplasim proteins
 It is rapidly released from striated muscles (both skeletal and
cardiac muscle) when damaged.
 Because of the abundance of myoglobin in cardiac and skeletal muscle
tissue, the upper reference limit of serum myoglobin directly reflects
the patient's muscle mass and, therefore, varies with gender, age, and
physical activity.
 However, because of its small size, myoglobin is rapidly cleared by the
kidneys, making it an unreliable long term marker of cardiac damage.

Myoglobin
 Myoglobin is significantly more sensitive than CK and CK-MB activities during
the first hours after chest pain onset
 It rises 1-4 hours
 Peaks 6-9 hours
 Returns to normal 18-24 hours
 If myoglobin concentration remains within the reference range 8 hours
after onset of chest pain, AMI can essentially be ruled out.
 CK-MB determinations are preferable over myoglobin in
 patients who are admitted later than 10-12 hours after chest pain onset
because the myoglobin concentration may have already returned to
reference ranges within that time frame
 patients with renal disease (renal failure) because myoglobin will be
consistently increased as a result of decreased clearance by the diseased
kidneys.
 Myoglobin can be used as an indicator of reinfarction
 A persistently normal concentration will rule out reinfarction in patients with
recurrent chest pain after AMI

Troponins
 Enzymes, electrolytes, and proteins are integrated to convert the
chemical energy of ATP to into mechanical work and allow the muscle
to contract
 Actomyosin, ATPase, calcium, aktin, myosin, and a complex of three
proteins known as troponin complex are major participants in muscle
contraction
 The three polypeptides of the troponin complex are troponin T,
troponin I, and troponin C.
 Troponin C is not heart specific.
 Unlike CK-MB, the serum troponins are not found in the serum of
healthy individuals.
 The cardiac troponins may be released in reversible ischemia as well
as irreversible myocardial necrosis.

TroponinT
Troponin T (TnT)
 Allows for both early and late diagnosis of AMI.
 Serum concentrations of TnT
 Begin to rise within a few hours of chest pain onset and
 Peak by day 2.
 A plateau lasting from 2 to 5 days
 The serum TnT concentration remains elevated beyond 7 days
before returning to reference values.
 The early appearance of TnT gives no better diagnostic information
than CK-MB or myoglobin concentrations within the first 4 hr, but the
sensitivity of TnT for myocardial infarct is 100% from 12 hours to 5
days after chest pain onset.
 Also, the degree of elevation of TnT after AMI is significant, often up
to a 200-fold increase over the upper limit of reference intervals

TroponinT
TnT concentrations are particularly useful for diagnosing myocardial
infarction in patients
 Who do not seek medical attention within the usual 2- to 3-day
window during which total CK and CK-MB are elevated
 It is also useful in the differential diagnosis of myocardial damage
in patients with cardiac symptoms as well as skeletal muscle injury
because the TnT results will clearly and specifically indicate the
extent of the cardiac damage
 Cardiac TnT also has value in monitoring patients after reperfusion
of an infarct-related coronary artery.
The degree of elevation of TnT on days 3-4 after AMI can also be used
as a practical and cost-effective estimate of myocardial infarct size

Troponin I
 Troponin I (TnI) is only found in the myocardium making it extremely
specific for cardiac disease.
 It is also found in much higher concentrations than CK-MB in cardiac muscle,
making it a sensitive indicator of cardiac injury.
 TnI is not found in detectable amounts in the serum of patients with
multiple injuries or athletes after strenuous exercise, in patients with
acute or chronic skeletal muscle disease, in patients with renal failure, or in
patients with elevated CK-MB, unless myocardial injuries are also present.
 TnI is a good biochemical assessment of cardiac injury in critically ill
patients, those with multiple organ failure, and situations in which CK/CK-MB
elevations may be difficult to interpret.
 Time profile
 Increases above the reference range 4 and 6 hours after the onset of
chest pain
 Peaks 12-18 hours
 Returns to reference values in about 6 days

Markers of inflammation and coagulation disorders
 Studies have evaluated several acute phase proteins as potential
markers for cardiovascular risk assessment,
 There is evidence that C-reactive protein (CRP) is a reliable
predictor of acute coronary syndrome risk
 CRP is an acute phase reactant produced primarily by the liver.
 It is stimulated by interleukin-6 and increases rapidly with
inflammation.
 CRP is a sensitive marker for ongoing chronic inflammation that is
not affected by ischemic injury.
 It rises significantly in response to injury, infection, or other
inflammatory conditions
 is not present in appreciable amounts in healthy individuals.

hs-CRP
 Reliable, automated high sensitivity assays for CRP (hs-CRP) are exist that
allow detection of the small increases of CRP often seen in cardiac disease
 Epidemiologic data document a positive association between hs-CRP and the
prevalence of coronary artery disease.
 Elevated baseline levels of hs-CRP are correlated with higher risk of future
cardiovascular morbidity and mortality among those with and without
clinical evidence of vascular disease.
 hs-CRP also demonstrates prognostic capacity in those who do not yet have
a diagnosis of vascular disease
 The level of CRP has been shown to correlate with future risk as follows:
CRP level less than 1mg/L: lowest risk
CRP levels of 1 to 3mg/L: intermediate risk
CRP greater than 3mg/L: highest risk

Fibrinogen
Fibrinogen is a soluble glycoprotein produced in the liver and
involved in platelet aggregation and coagulation.
It is also an acute-phase protein produced in response to
inflammation.
A relationship has been established between elevated levels
of fibrinogen and risk of cardiovascular disease and may
serve as a marker of long-term prognosis.

D-Dimer
 D-Dimer is the end product of the ongoing process of thrombus
formation and dissolution that occurs at the site of active plaques in
acute coronary syndromes.
 Because this process precedes myocardial cell damage and release of
protein contents, it can be used for early detection.
 It remains elevated for days so it may be an easily detectable
physiologic marker of an unstable plaque even when the troponins or
CK-MB are not increased, potentially identifying high-risk patients
 D-Dimer lacks specificity for cardiac damage as it is increased in other
conditions that cause thrombosis.
 Elevations of D-Dimer have been shown to be useful in predicting
risk for future cardiac events.

Markers of congestive heart failure
 Brain-type, or B natriuretic peptide (BNP), is a peptide hormone secreted
primarily by the cardiac ventricles.
 It acts on the renal glomerulus to stimulate urinary excretion of sodium and
to increase urine flow without affecting the glomerular filtration rate,
blood pressure, or renal blood flow
 Plasma concentrations of BNP are increased in diseases characterized by an
expanded fluid volume (renal failure, hepatic cirrhosis with ascites, primary
aldosteronism, and congestive heart failure)
 Diagnosis of congestive heart failure (CHF) is difficult because of its
nonspecific symptoms, as well as the lack of a specific biochemical marker
Patients with a BNP < 20 pmol/L are unlikely to have CHF
Patients with BNP > 20 pmol/L have a high probability of CHF
 BNP may also be clinically relevant in determining the prognosis of patients,
especially those with a diagnosis of CHF or those who have experienced a
recent AMI

Other markers for AMI
 Glycogen phosphorylase isoenzyme BB (GPBB)
More sensitive than the other markers during the first 3-4 hours after
onset of chest pain
It is not specific for cardiac tissue
 Heart fatty acid-binding protein (H-FABP)
H-FABP content in skeletal muscle is only 10-30% of that found in cardiac
muscle, it is more sensitive than myoglobin
It increases rapidly within 2-4 hours, peaks within 5-10 hours and returns to
normal within 24-36 hours
The magnitude of the increase in plasma levels has a good correlation with
the size of the infarction
 Carbonic Anhydrase (CA) Isoenzyme III
CAIIl is not found in cardiac muscle and, therefore, can be used to
differentiate between skeletal muscle and cardiac muscle damage when
performed in conjunction with a more heart-specific analyte such as
myoglobin.

Other markers
Ischemia-modified albumin (IMA)
 IMA is produced when albumin comes into contact with ischemic tissue,
altering it and making it more resistant to binding metals
 IMA is produced continually during ischemia and rises within 2-3 hours
of an ischemic event
Homocysteine
 Homocysteine is a naturally occurring amino acid found in blood, which is
associated with vitamin B1, B6, and folic acid deficiency.
 An elevated homocysteine level is a potential risk factor for coronary
heart disease, cerebral vascular disease, carotid artery disease, and
peripheral vascular disease by promoting plaque formation.

Cardiac myosin light chains (MLC)
 Cardiac myosin light chains (MLC) are also involved with
muscle contractions.
 Recent research has determined that MLC is no more
specific for cardiac injury than CK-MB determinations
 Like the troponins, MLC is released from reversibly
ischemic tissue.
 Although rapid testing of MLC is available, MLC
determination does not offer any advantage over cardiac
troponin assays.
 MLC remains of limited clinical significance as a routine
cardiac marker

lipoprotein phospholipase A2 (Lp-PLA2)
 Lp-PLA2 generates oxidized molecules within the blood
vessel wall that increase the potential of atherosclerosis
and irritability of the atherosclerotic plaque
 Elevations in the levels of Lp-PLA2 have been shown to
indicate greater risk of plaque formation and rupture
independent of the levels of either lipids or CRP
 Patients with elevated levels of Lp-PLA2 seem to be at a
greater risk of cardiac events

Patient Focused Cardiac Tests
Because the situation of patient of serious, special
care should be considered
The initial patient evaluation be performed within
20 minutes of arrival to the emergency department
(ED)
The optimum turnaround time from patient arrival
to the availability of test results for cardiac
markers should be about 30-60 minute

The role of lab in monitoring heart disease
The laboratory's role in monitoring heart function primarily involves:
 Measuring the effects of the heart on other organs, such as the lungs, liver
and kidney
 Arterial blood gases measure the patient's acid-base and oxygen status
 determine the respiratory acidosis and elevated carbon dioxide
levels that are often seen in patients with heart disease.
 electrolyte and osmolality :The patient with cardiac disease may develop
edema and fluid retention and ionic redistribution.
 Serum electrolyte determinations, including sodium, potassium, chloride,
and calcium, are important to monitor diuretic and drug therapy in
patients with heart disease
 Elevations of AST, ALT and ALP are often seen in patients with chronic
right ventricular failure and GGT value elevated in congestive heart
failure, suggesting liver congestion and damage.

The role of lab in monitoring heart disease
 Lipid evaluation will assess risk for coronary artery disease.
 Maintenance of near normal HDL-cholesterol, LDLcholesterol, and
triglyceride levels is highly recommended for cardiac patients.
 Determination of a lipoprotein similar to LDL may also be indicated as it
is an independent risk factor associated with development of premature
coronary artery and vascular disease.
 The patient who has secondary heart failure due to thyroid dysfunction can
be identified by a highly sensitive thyroid-stimulating hormone assay.
 The laboratory is also invaluable for monitoring therapeutic drugs following
the diagnosis of heart disease.
 The routine blood count
 Important for detecting anemia and infection
 Blood cultures
 To identify infections associated with pericarditis, endocarditis and
valvular problems

Available Blood-Based Tests for Heart
Disease
Substance Detected by
Blood Test
Patient Symptoms Indications of Elevations
Cardiac troponins (I and T)
Ischemia modified albumin
Natriuretic peptides (BNP)
Lipids (cholesterol, HDL,
LDL)
C-reactive protein
Lipoprotein phospholipase
A2
Chest pain or potential heart
attack
Chest pain or potential heart
attack
Shortness of breath; possible
heart failure
Current or future risk of
atherosclerosis
atherosclerosis
atherosclerosis
Injury to the heart
Possible diminished blood flow
to the heart
Probable congestive heart
failure
increased risk of
atherosclerosis
Increased risk of cardiac
events
Increased risk of cardiac
events

• An 83-year-old man with known severe coronary artery disease,
diffuse small vessel disease, and significant stenosis distal to a vein
graft from previous CABG (coronary artery bypass graft) surgery,
was admitted when his physician referred him to the hospital after
routine office visit. His symptoms included edema, jugular vein
distention and heart sound abnormalities. Significant laboratory data
obtained upon admission were as follows:
Urea nitrogen 53 6-24 mg/dl
Creatinine 2.2 0.5-1.4 mg/dl
Total protein 5.8 6.0-8.3 g/L
Albumin 3.2 3.5-5.3 g/L
Glucose 312 60-110 mg/dl
Calcium 4.1 4.3-5.3 mEq/L
Phosphorus 2.4 2.5-4.5 mg/dl
Total CK 134 54-186 U/L
CK-MB 4 0-5 ng/L
% CK-MB 3% <6%
Myoglobin 62 <70g/L
Troponin T 0.2 0-0.1 g/L

 Questions:
1. Do the symptoms of this patient suggest
AMI?
2.Based on lab data, would this diagnosis be
AMI? why or why not?
3.Based on the lab data, are there other
organ system abnormalities present?
4.What are the indicators of these organ
system abnormalities?
5.Is there a specific lab data that might
indicate congestive heart failure in this
patient?

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