CASE STUDY Scenario A 46-year-old businessman was admitted to the hospital complaining of severe retrosternal pain of 2 hour’s duration. He was admitted to the hospital previously for the treatment of a small myocardial infarction (MI). He was a chronic smoker
On general examination his blood pressure was 150/90 mmHg, pulse 60/minutes and he was sweating profusely. There was no evidence of cardiac failure. His initial ECG showed ST segment elevation and other changes in certain leads, indicative of an acute anterior transmural infaction. Blood was taken at 4 hours and subsequently at regular intervals for measurement of CPK MB isoenzymes. He was given injection morphine to relieve his pain and apprehension and was immediately shifted to the cardiac care unit. Severe retroesternal pain
-Pain that occur behind the chest behind sternum
-Retrosternal chest pain can occur for various reasons, including
cardiac or heart-related issues and noncardiac conditions, such as gastroesophageal reflux disease (GERD).
https://www.medicalnewstoday.com/articles/retrosternal-chest-pain Small myocardial infarction
-Known as Heart attack
-caused by decreased or complete cessation of blood flow to a portion of the myocardium ( muscle of the heart )
https://www.ncbi.nlm.nih.gov/books/NBK537076/#:~:text=Myocardial%20infarction%20(MI)%2C%20colloquially,hemodynamic%20deterioration%20and%2 0sudden%20death General Examination Blood Pressure Blood pressure for the patient was 150/90 mmHg Pulse Patient’s pulse is 60/minutes Sweating No evidence of profusely cardiac failure
also known as diaphoresis in some cases acute
warning sign of heart attack myocardiac infarction blocked coronary artery would not lead to cardiac failure what is ECG? an electrocardiogram (ECG/EKG) represents a recording of the heart’s electrical activity (include rate and
ECG rhythm) anterior transmural infarction specific type of myocardial infarction (MI) that affect anterior wall of the heart muscle (transmural) “anterior” indicates that the infarction is affecting the front portion of the heart “transmural” indicates that the infarction extends through the entire thickness of the heart muscle wall anterior wall of the heart is supplied by the left anterior descending coronary artery blockage can cause ischemia and subsequent infarction of anterior wall of the heart REGULAR INTERVALS OF CPK MB ISOENZYME WHAT IS CREATINE KINASE? an enzyme (a molecule that helps speed up certain chemical reactions) found primarily in heart and skeletal muscle. Small amount found in brain, lungs, thyroid and adrenal gland
Normal range of CPK
Women: less than 4.4 ng/mL Men: less than 7.7 ng/mL
https://my.clevelandclinic.org/health/diagnostics/24519-ck-mb-test Question 1 What would be the status of creatine phosphokinase CPK enzymes and when the elevations are found? Explain Expected to elevate due to suspected acute myocardial infarction
Reason for this suspicion:
the patient come out with symptoms of severe retrosternal pain, sweating, and the presence of ST segment elevation on the initial electrocardiogram (ECG) ,suggests that he is experiencing a new myocardial infarction rather than a failure to recover from the previous one.
When heart muscle cells die due to heart attack (AMI), CPK-MB leaks into the bloodstream.
How can CPK level elevation be detected?
When someone having heart attack about 3-6 hours after the onset of chest pain. The level of CK-MB peaks in 12-24 hours and then returns to normal within about 48-72 hours. If there is a second heart attack or ongoing damage, then levels may rise again and/or stay elevated longer. Question 2 Briefly explain other enzymes/biomarkers of importance to detect the presence of acute MI such as creatine kinase CK/CPK isoenzymes, atypical isoenzymes (macro CK and mitochondrial CK), aspartate amino transferase (AST), lactate dehydrogenase (LDH) cardiac troponins including its normal value, in acute MI prognostic significance and involvement in other diseases? Creatine kinase CK/CPK isoenzymes CK is an enzyme that catalyzes the reversible transformation of creatine and ATP to creatine phosphate and ADP Found in most tissues, the best known marker for the identification of AMI CK is involved in mitochondria and cytosol in muscle cells. CK-MM, found in your skeletal muscle and heart CK-MB, found in the heart and rises when heart muscle is damaged CK-BB, found mostly in your brain. It's also found in smooth muscles such as the intestine or uterus When any of these tissues or muscle cells are damaged, they leak creatine kinase into bloodstream The level of the CK enzymes rises CK-MB generally rises after a heart attack, inflammation of the heart muscle, heart injury, heart surgery, muscular dystrophy, and other problems related to the heart. not related to any specific diseases Atypical isoenzymes (macro CK)
Macro-CK is a complex of creatine kinase (CK) enzyme bound to large
molecules, such as immunoglobulins or albumin. refers to high molecular weight forms of CK. , which are cleared more slowly from plasma than normal CK, resulting in a raised plasma level Normally, the concentration of macro-CK in the blood is very low, but in certain conditions, such as acute myocardial infarction (MI), the levels may rise. several reported disease associations, including hypothyroidism, neoplasia, autoimmune disease, myositis, and cardiovascular disease. Mitochondrial CK
Mitochondrial CK plays an important role in energy metabolism, which facilitates
the regeneration of ATP , the primary energy currency of cell During AMI, the myocardial cells undergo ischemic injury due to the interruption of blood flow to the heart. This ischemic insult leads to cellular damage and death, including damage to mitochondrial structures. Increase in CK-Mt levels following myocardial injury not related with any specific disease states but it has been detected in certain cases of malignant tumours Prognosistic significance Aspartate amino transferase (AST) Levels >350 IU/L are due to massive infarction (Fatal)
Known as serum Normal value: 0 In acute MI: >150 IU/L are associated with glutamate -Serum activity rise high mortality to 41 IU/L at oxoloacetatw sharply within first 37° 12 hours levels <50 IU/L are transminase -Peak at 24 hours associated with low mortality.
The rise in activity is also observed in muscle and
hepatic diseases. Can be differentiated by looking through SGPT enzyme activities Normal level: 55-140 IU/L at 30°C. The levels in the upper range are generally seen in children. In acute MI: LDH levels rise within 12 to 24 hours after AMI onset, peaking at around 48 hours. The increase in serum activity
The magnitude of LDH elevation is what is ST segment
of LDH is also seen in hemolytic anemias, hepatocellular proportional to the extent of myocardial damage, muscular dystrophies, infarction carcinoma, leukemias, and any condition which causes necrosis
lactate of the body cells.
dehydrogenase (LDH) Cardiac troponin Troponin complex: Troponin C (calcium binding), Troponin T: Two isoforms (TnT1 and TnT2) Troponin I (actomyosin ATPase inhibitory element), present in adult cardiac tissue; increases and Troponin T (tropomyosin binding element). within 6 hours of myocardial infarction; peaks at 72 hours; remains elevated for up to 7 to Normal Value: Troponin I < 0.04ng/mL; Troponin T 10 days. < 0.01 ng/mL Troponin I and Troponin T are specific Troponin I: Specific to cardiac muscle; released into markers of myocardial damage and are not circulation within 4 hours of myocardial infarction elevated in other muscle injuries. onset; peaks at 14 to 24 hours; remains elevated for 3 to 5 days. Troponin I sensitivity: 75%; Troponin T sensitivity: 100%. ** more than 1.5 ng/ml is indicative of significant myocardial damage
. References https://www.heart.org/en/health-topics/heart- attack/warning-signs-of-a-heart-attack https://www.nhlbi.nih.gov/ https://www.ncbi.nlm.nih.gov/books/NBK557536/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5491037/ Thank You For Today! QnA Session
