Cardiac Function Tests Heart disease Symptoms of heart disease Congenital heart disease Congestive...

Cardiac Function TestsHeart diseaseSymptoms of heart diseaseCongenital heart diseaseCongestive heart failureAcute coronary syndromeHypertensive heart diseaseInfective heart diseaseDiagnosis of heart diseaseLaboratory diagnosis of AMIEnzymes, cardiac proteins.Markers of inflammation and coagulationMarkers of congestive heart failureOther markersThe 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

Heart anatomy

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 dyspneaThe 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.

Symptoms of heart diseaseSyncope:

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 diseaseCongenital 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



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



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: .

Coronary arteries

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 Rheumatic fever is not caused by a direct infection or toxin but

because of the antibodies against the streptococcal antigens because of the antibodies against the streptococcal antigens

cross-react with similar antigens found in the heart and initiate a cross-react with similar antigens found in the heart and initiate a

cell-mediated immune response involving macro phages and cell-mediated immune response involving macro phages and

lymphocytes. 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 AMIHistory acute, severe and prolonged chest painECG 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 AMIEnzymes

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 Although the specificity of CK-MB for heart tissue is greater for heart tissue is greater

than 85%, it is also found in skeletal muscle and false-than 85%, it is also found in skeletal muscle and false-

positive results may be caused at clinical conditions such as positive results may be caused at clinical conditions such as

muscle disease and acute or chronic muscle injuries 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.

Troponins

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 CHFPatients 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 IMA is produced continually during ischemia and rises within 2-3

hours of an is chemic event hours of an is chemic 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 electrolyte and osmolality :The patient with cardiac disease may

develop edema and fluid retention and ionic redistribution. develop edema and fluid retention and ionic redistribution.

Serum electrolyte determinations, including sodium, potassium, Serum electrolyte determinations, including sodium, potassium,

chloride, and calcium, are important to monitor diuretic and drug chloride, and calcium, are important to monitor diuretic and drug

therapy in patients with heart disease therapy in patients with heart disease

Elevations of AST, ALT and ALP are often seen in patients with Elevations of AST, ALT and ALP are often seen in patients with

chronic right ventricular failure and GGT value elevated in chronic right ventricular failure and GGT value elevated in

congestive heart failure, suggesting liver congestion and damage. 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. Lipid evaluation will assess risk for coronary artery disease.

Maintenance of near normal HDL-cholesterol, LDL cholesterol, and Maintenance of near normal HDL-cholesterol, LDL cholesterol, and

triglyceride levels is highly recommended for cardiac patients.triglyceride levels is highly recommended for cardiac patients.

Determination of a lipoprotein similar to LDL may also be Determination of a lipoprotein similar to LDL may also be

indicated as it is an independent risk factor associated with indicated as it is an independent risk factor associated with

development of premature coronary artery and vascular disease. development of premature coronary artery and vascular disease.

The patient who has secondary heart failure due to thyroid dysfunction The patient who has secondary heart failure due to thyroid dysfunction

can be identified by can be identified by a highly sensitive thyroid-stimulating a highly sensitive thyroid-stimulating

hormone assayhormone assay. .

The laboratory is also invaluable for monitoring therapeutic drugs The laboratory is also invaluable for monitoring therapeutic drugs

following the diagnosis of heart disease. following the diagnosis of heart disease.

The routine blood countThe routine blood count

Important for detecting anemia and infectionImportant for detecting anemia and infection

Blood culturesBlood cultures

To identify infections associated with pericarditis, endocarditis and To identify infections associated with pericarditis, endocarditis and

valvular problemsvalvular 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 Current or future risk of atherosclerosis Current or future risk of 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

Glucose312 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 <70g/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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Cardiac Function Tests Heart disease Symptoms of heart disease Congenital heart disease Congestive...

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