The document discusses various cardiac function tests and markers. It describes tests like creatine kinase, cardiac troponin, and brain natriuretic peptide that are used to detect cardiac diseases. It provides details on each marker including what tissues they are found in and how levels change in different cardiac conditions.
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Cardiac Function Test
The document discusses various cardiac function tests and markers. It describes tests like creatine kinase, cardiac troponin, and brain natriuretic peptide that are used to detect cardiac diseases. It provides details on each marker including what tissues they are found in and how levels change in different cardiac conditions.
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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CARDIAC FUNCTION TEST
INDICATION FOR CARDIAC TESTING
Any chest pain
Palpitation Breathlessness Unstable angina Suspicious ECG changes Previous history of M.I. Following surgical coronary revascularization Patient with hypotension and dyspnea RISK FACTORS Modifiable – cigarette smoking, High total cholesterol, High LDL cholesterol, low HDL cholesterol, LVH. Diabetes mellitus, hypertension, physical inactivity, obesity, high triglycerides, stress.
Non modifiable factors -
age, male, family history. MARKERS FOR CARDIAC DISEASES Creatine kinase
Cardiac troponin
Brain natriuretic peptide ( indicator for ventricular
function)
C-Reactive protein
LDH & AST
CREATINE KINASE Catalyzes formation of phosphocreatine from creatine and ATP.
Types –cytosolic and mitochondrial.
Cytosolic enz. Dimer of two units. M and B.
Has 3 isoenzymes CK-3 (MM)- +nt in heart, skeleton muscle(96% of total) CK-2 (MB) – specific for heart ms.( 20% of total). CK-1(BB)- mainly in brain tissue, prostate, skeleton ms. CK-MM IS MAJOR ISOENZYME IN SERUM OF HEALTHY PERSONS
Separation of isoforms are done by electrophoresis, ion-
exchange chromatography, RIA, immunoinhibition. Interpretation-CK activity depends on age, race and sex. High activity seen in neonates,infants, adolesent Low activity seen in early pregnancy, women
CONTD. By electrophoresis separates band of CK-3 and CK-2. 3 CK3 and 2 CK2 forms exist. Tissue form of CK3 is known as CK-33. Tissue form of CK2 is known as CK-22. Conc of CK is more in pt. of heart diseases. Mitochondrial CK (CK-Mt) has two isoenzymes. CONTD. In skeleton muscles 1% is CK-2.
Persistent elevation of S. CK-2 occurs in muscle
dystrophies.
Total CK is used to measure polymyositis muscular
dystrophies and MB iso- enzyme is estimated in myocardial infarction.
Not present in RBCs
REMARKS Sensitive indicator of early stages of M.I. ( rise within 3-6 hrs, peak at 18-24 hrs).
More useful in subendocardial infarction.
Not increased in heart failure and coronary
diseases and hemolysis. NON PATHOLOGICAL CAUSES OF RAISED CK
After heavy exercise( max level after 24 hrs. of
exercise)
From i.m. injection of certain drugs rise may be
transient or remain upto 8 days.
After surgery( max .between 1-2 days after
surgery) OTHER CAUSES OF RAISED CK LEVELS Hypothyroidism Motor neuron diseases Hypothermia Hypoxia Convulsions Prolong immobilization Stroke Malignant hyperpyrexia (due to halothane, suxamethonium) LDH Catalyzes the reversible conversion of pyruvic acid and lactic acid. Normal serum level is – 60-250 IU/L. In AMI serum levels rises within first 12-24 hours, peak at 48 hours ,return to normal in 8- 14 days. LDH is nonspecific for myocardial tissue RBCs are rich in LDH CONTD. LDH -2 (H3M1)-- concentration in blood is more than LDH-1(H4). Pattern is reversed in M.I. this is known as flipped pattern. raised in – acute leukemia Pulmonary infarction Renal necrosis. Inflammatory hepatic disorders ISOENZYMES OF LDH TYPE POLYPEPTIDE ELECTROPHOR TISSUE RICH IN CHAINS ETIC MOBILITY FORM
LDH-1 (H4) FAST MOVING FOUND IN
HHHH MYOCARDIUM
LDH-2 (H3M) Kidney
HHHM
LDH-3 (H2M2) Spleen,
HHMM lung, ,pancreas, thyroid LDH-4 (HM3) Found in liver HMMM
LDH-5 (M4) SLOWEST FOUND IN LIVER
MMMM MOVING CHARACTERISTIC OF LDH ISOENZYMES Isoenzyme Subunits Electroph activity at tissue of % in s oretic 60ᵒ for 30 origin human mobility min serum at pH 8.6 LDH-1 H4 FASTEST N.D. Heart ms. 30%
LDH-2 H3M1 FASTER N.D. RBC 35%
LDH-3 H2M2 FAST P.D. Brain 20%
LDH-4 H1M3 SLOW D Liver 10%
LDH-5 M4 SLOWEST D. Skeleton 5%
ms. CONTD. NORMAL SERUM LDH-2 (H3M) most prominent isoenzymes
After MI, LDH-1 and LDH-2 predominates.
Acute viral hepatitis LDH-5 and LDH-4 (HM3)
predominates. CARDIAC TROPONIN Complex of 3 protein subunits
Troponin C ( calcium binding component)
Troponin I (inhibitory component) Troponin T ( tropomyosin binding component)
Located mainly in myofibrils (94-97%)
Cytoplasmic fraction is only (3-6%) TROPONIN I AND T Troponin present in skeleton muscles and cardiac muscles but not in smooth muscles. Troponin I released in blood within 4 hrs. after onset of symptoms of M.I., peak at 14-24 hrs. and remains elevated for 3-5 days after infarction . Troponin T released in blood within 6 hrs. after onset of symptoms of M.I., peak at 72 hrs. and remains elevated for 7-14 days after infarction . CONTD. Two isoforms of cardiac TnT (TnT1, TnT2) present in adult human cardiac tissue.
Two more isoforms are present in fetal cardiac
tissue due to alternative splicing of mRNA.
TnT2 is 100% sensitive and 95% specific for
detection of M.I. CONTD.
cTnI is having 30 amino acid residues longer
than skeleton ms.
cTnT has unique 11 amino acid sequence
(specific for cardiac ms.)
Only cardiac specific is cTnI.
MEASUREMENT Cardiac troponin I (cTnI) - by monoclonal antibody based immunoassay Assay time range is 7-30 min. From different assay range varies. Troponin T - uses third generation reagent and antibodies which shows no cross reactivity with troponin of skeleton muscles MYOGLOBIN Composed of 153 amino acids and one iron atom in ferrous form., mol. wtg is 7,000.
Oxygen binding low molecular wtg. protein of cardiac
and skeleton ms.
Appears early in circulation after ms. injury.
Increased level is seen in trauma to cardiac, skeleton ms.
or AMI. MYOGLOBIN
Increased with in 1 hour after AMI, with peak
activity in 4-12 hours.
Activity decreases after 12 hours.
Rapidly cleared from kidney due to small size.
Increased level leads to kidney damage.
BNP synthesized and secreted from ventricles, in response with excessive stretching, present in brain also Pro –BNP consist of 108 amino acid Cleaved at cardiac myocytes into active C- terminal BNP(32 AA) and inactive pro BNP1-76. Raised in ventricular dysfunction Use to differentiate dyspnea caused by heart ds or lung C-REACTIVE PROTEIN
Bind with C-polysaccharide of cell wall of
streptococcus pneumoniae. Synthesized in parenchymal cells of liver. Raised in M.I. after 6-12 hrs. of symptoms. Indicator of- screening of organic diseases. Assessment of inflammatory diseases. Management of neonatal septicemias. ASPARTATE AMINO TRANSFERASE Or SGOT Needs pyridoxal phosphate as a coenzyme Good marker of cardiac ds. Normal level- 8-20 IU/L. Level > 350 IU/L is fatal Level> 150 IU/L is associated with high mortality. Level< 150 IU/L is associated low mortality. RISK DEPEND ON SIZE OF INFARCTION AST- ISOENZYME
m- AST (mitochondrial)- in serum
contributes less than 12% of total AST activity, but main in liver, heart, kidney, spleen and muscles.
s –AST (cytosolic).
Isoenzymes are separated by electrophoresis,
chromatography, immunochemical methods. CONTD. In AMI serum levels rises within first 12 hours, peak at 24 hours , return to normal in 3-5 days.
Also elevated in muscle diseases, hepatic disease.
NO RISE OF SGPT IN MYOCARDIAL
INFARCTION. GAMMA –GLUTAMYL TRANSPEPTIDASE
Also known as gamma glutamyl transferase.
Catalyzes transfer of ϒ- glutamyl group from one peptide to another peptide. Normal serum value-male 10-47 IU/L Female – 7-30 IU/L. High activity seen in kidney, liver, lung, pancreas and prostate. Heart contain very less amount. CONTD. Indicator of MI in later stages. Derived from vascular endothelium from angioblastic proliferation. Increased levels - also seen in Obstructive jaundice, cholangitis, cholecystitis. In alcoholics Pancreatic diseases Medicines ( anticonvulsant) INDICATION OF CHECKING LIPID PROFILE Suspected cardiovascular diseases, CAD, PVD.
All patients with diabetes mellitus, at least once
in 6 month.
Thyroid, and liver diseases.
All persons above 40 yrs.
SERUM CHOLESTEROL
Normal levels- 150-200mg/dl
Level at- 220mg/dl- moderate risk Level at- 240mg/dl- high risk. Women have low level of cholesterol LDL cholesterol- level should be under 130mg/dl. Level between 130-159 are borderline. Level above 160mg/dl high risk. HDL
HDL cholesterol – level above 60mg/dl
protect against heart disease. below 40mg/dl increases risk of heart diseases For every 1mg/dl drop in HDL risk of heart diseases increased by 3%. APO PROTEIN Apo-A-1 measures HDL cholestrol Apo-B measures LDL cholestrol Apo B: A-1 should be 0.4 Serum triglycerides- normal level is 50- 150 mg/dl. CHD RISK AND LIPID PARAMETERS
Low risk Borderline High risk
risk
Total cholestrol <200 200-240 >240
(mg/dl)
LDL cholestrol <130 130-160 >160
(mg/dl)
HDL cholestrol >60 35-60 <35
(mg/dl)
Triglycerides <150 200-400 >400
(mg/dl) CHOLINESTERASE Hydrolyze esters of choline to give choline and acid. Types – True and pseudo Normal value- 2.17 to 5.17 IU/mL. Serum enzyme activity is a sensitive index for cellular necrosis in myocardium. OTHER TESTS Lab tests - liver and renal function, lipids, glucose ECG Echo Cardiac catheterization CT/MRI chest Barium studies/upper GI endoscopy/abdominal US Thank you