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Biochemical Markers for Diagnosis of Myocardial Infarction

Biochemical Markers for Diagnosis of Myocardial Infarction. What is Myocardial Infarction?. Myocardial ischemia results from the reduction of coronary blood flow to an extent that leads to insufficiency of oxygen supply to myocardial tissue

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Biochemical Markers for Diagnosis of Myocardial Infarction

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  1. Biochemical Markers for Diagnosis of Myocardial Infarction

  2. What isMyocardial Infarction? • 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 ---this is defined as: Myocardial Infarction is the death & necrosis of myocardial cells as a result of coronary prolonged & irreversible ischemia

  3. 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 ECG changes clinical manifestations (chest pain) release of intracellular contents to blood BIOCHEMICAL MARKERS

  4. Diagnosis of Myocardial Infarction WHO criteria for the diagnosis of myocardial infarction ( at least 2/3): 1- Clinical Manifestations 2- ECG 3- Biochemical Markers

  5. Criteria of ideal markers for myocardial infarction 1- Specific: to myocardial muscle cells (no false positive) 2- Sensitive: - rapid release on onset of attack (diagnose early cases) - so, can detect minor damage - no miss of positive cases (no false negative) 3- Prognostic: relation between plasma level & extent of damage 4- Persists longer: so, can diagnose delayed admission 6- Reliable: procedure depends on evidenced principle 5- Simple, inexpensive: - can be performed anywhere by low costs - no need for highly qualified personnel 7- Quick: low turnaround time

  6. Types of Biochemical Markers for Diagnosis of Myocardial Infarction 1- Cardiac enzymes (isoenzymes): Total CK CK-MB activity CK-MB mass LDH AST 2- Cardiac proteins: Myoglobin Troponins

  7. Time-course of enzyme changes • Plasma enzymes follow a pattern of activities after a MI • Theinitial lag phase lasts for about 3 hours • Enzymes rise rapidly to peak levels in 18-36 hours • The levels return to normal based on enzyme half-life • Rapid rise and fall indicates diagnostic value.

  8. Cardiac Enzymes • Total CK (sum of CK-MM, CK-MB & CK-BB) non specific to cardiac tissue (available also in skeletal muscles) • CK-MB (CK-2) activity More specific than total CK BUT: less specific than cardiac troponin I (as CK-MB is also available in skeletal muscles) Appears in blood: within 4 - 6 hours of onset of attack (used for early cases) Reaches maximum peak within: 12 - 24 hours Returns to normal: after 2 - 3 days of onset (nolong stay in blood. So, notfor delayed admissions) Advantages: - useful for earlydiagnosis of MI - useful for diagnosis reinfarction Disadvantages: notused for delayed admission (more than 2 days) not 100% specific (elevated in skeletal muscle damage)

  9. Cardiac Enzymes cont. • CK-MB mass -Appears one hour earlierthan CK-MB activity (more sensitive) - So, useful for diagnosis of early cases & reinfarction - BUT: notfor diagnosis of delayed admission cases & less specific than cardiac troponin I • Relative index = CK-MB mass / Total CK X 100 more than 5 % is indicative for MI

  10. Cardiac Enzymes cont. • Lactate dehydrogenase (LDH) LDH is a tetramer, each chain may be one of two types (H & M) where: LDH1 is (H4) while LD5 is (M4) 5 isomers are available, but, each predominates in a certain organ. LD1 & LD2 predominates in heart Detected in blood: 18-16 hours after onset of MI attacks (not for early cases) Reaches a maximum peak level: in 48 h Remains elevated for: 5-6 days after MI (may remain elevated up to 14 days) Disadvantages: A non-specific marker of as it is also elevated in diseases of liver, lung, kidney, RBCs etc

  11. Cardiac Enzymes cont. • Aspartate aminotransferase (AST) • A non-specific marker of MI as it appears also in liver & other organs diseases • (N.B. AST is somewhat more heart-specific than ALT) • Detected in blood: 6-12 hours after onset of MI attacks (not for early cases) • Reaches a maximum peak level: in 30 hours • Returns to normal : after 2 - 6 days after MI

  12. Cardiac Proteins • Myoglobin - Non specificfor cardiac tissue (as it is elevated also in skeletal muscle & renal tissue) - Appears in blood earlierthan other markers (within 1-4 hours) So, with high sensitivity - BUT: Returns to normal in 24 hours So, NOT for delayed admission cases (after one day of onset of attack)

  13. Cardiac Proteins cont. • Cardiac Troponins Protein complex located on the thin filament of striated muscles consists of 3 subunits: cTn T, cTn I & cTn C with different structures & functions • Troponins are involved in the interaction between actin and myosin for contraction • Troponins are also present in cytosol of cardiac myocytes cTnI & cTnTareused are biomarkers for MI diagnosis Cardiac troponins (cTn)are different from skeletal muscle troponins So, more specific for MI diagnosis

  14. Cardiac Proteins cont. • Cardiac Troponin I (cTn I) 100 % cardiac specific With greater sensitivityfor diagnosing minordamage of MI Appears in blood: within 6 hours after onset of infarction Reaches maximum peak: around 24 hours Disappears from blood: after about 10 days (stays longer) So, useful for diagnosis of delayed admission Prognostic marker : Matching relation between level in blood & extent of cardiac damage

  15. Recommendations for use of biochemical markers for diagnosis of myocardial infarction 1- Recommended for all patientscomplaining of chest pain (with clinical examination & ECG) 2- Sample Type: plasma Timing: i. on admission ii. serial ( at least every one hour in a period 6-9 hours) should be referenced to admission & onset of pain 3- Testshould be with low turnaround time Less than one hour (accepted) Less than half an hour is preferred 4-Types of Markers used: Early markers: as Myoglobin: Appears in blood early (within less 4 hours) BUT not specific & not persists for long period (less than 2 days) Definitive markers: Troponin: Appears in blood later than myoglobin (within 6 hours) BUT 100% specific, prognostic & stays longer (one week) 5- Troponinis currently the marker of choice should be available in all cardiac & emergency centers (if not, CK-MB mass is the second choice)

  16. Time Course for Biomarkers of Myocardial Infarction

  17. Diagnosis of Heart Failure • Heart failure is a complex clinical condition in which the heart ‘s ability to pump is compromised. • The prognosis is poor if untreated, with a two-year survival rate of under 50% • The diagnosis can be difficult, especially the presenting symptoms can be due to many diseases. • The definitive diagnosis is best by echocardiography ( which can be limited or delayed

  18. Diagnosis of Heart Failureb-natriuretic peptide (BNP) • BNP is a neurohormone secreted by cardiac myocytes in response to volume expansion & pressure overload , • It plays a role in circulatory homeostasis (natriuresis, diuresis & vasodilatation). • In heart failure, it increases. So we can differentiate between breathlessness due to cardiac disease or pulmonary cause. • The accuracy of its measurement is greatest in patients with more severe disease and poorest in those already receiving treatment

  19. A 9-year-old boy is brought to the ER by his parents after 2 days of worsening nausea/vomiting and abdominal pain. The abdominal pain is located in the epigastric region and radiates to his back • He has had several episodes of similar pain in the past but none quite as severe. His parents deny fever/chills and change in bowel habits. In the ER, the patient is afebrile and in moderate dis- tress. • Both the liver and spleen appear to be enlarged and he has epigastric tenderness.

  20. Several small yellow-white papules were noted on his back and buttocks. Laboratory tests reveal elevated amylase and lipase levels. On further questioning, the father reports having high triglyceride levels and several members of the mother's family have had early heart disease. Laboratory tests performed after hospitalization revealed elevated triglyceride levels and reduced lipoprotein lipase activity.

  21. What is etiology of the boy's abdominal pain? • What is the likely underlying biochemical disorder? • What is the role of lipoprotein lipase?

  22. Hypertriglyceridemia can be the result of: • a genetic disorder in one of the pro- teins involved in lipoprotein metabolism, • or it can arise secondarily to a number of other disorders, including diabetes mellitus, obesity, and alcohol abuse, • and as a side effect of some medications such as -blockers, oral estrogens, and some diuretics.

  23. Laboratory results for a patient with uncontrolled Type I diabetes mellitus reveal hyperglycemia (634 mg/dL) and hypertriglyceridemia (498 mg/dL). The most likely cause of the hypertriglyceridemia in this patient is which of the following? Deficiency in apoprotein C-II • Increased hepatic triglyceride synthesis • Decreased lipoprotein lipase activity • Deficiency in LDL receptors • Absence of hormone-sensitive lipase

  24. A teenage boy presents with moderate to severe epigastric pain. • Physical examination reveals extensive eruptive xanthomas and hepatosplenomegaly. A blood sample reveals milky plasma. Which of the following is the most likely lipoprotein to be elevated in this • patient's plasma? • Chylomicrons • Chylomicron remnants • HDL IDL • LDL

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