Myocardial Infarction
Also written as MI.
• Is due to Pericarditis whose causes include:- bacterial and viral pericarditis, myocardial infarction, rheumatic fever, connective tissue disorder, trauma, uraemia
Myocardial Infarction
- Troponin I — rises 2–4hrs, peaks 24hrs, lasts 10 days. It is the most specific biomarker.
- CK-MB — rises 4–6hrs, back to normal in 48–72hrs. This marker is useful for detecting reinfarction.
- Myoglobin — first to rise (1–2hrs), but it is not specific.
- –24 hrs: Arrhythmia ( VF ) — the 1 cause of early death.
- –5 days: Free wall rupture → tamponade ; VSD rupture ; papillary muscle rupture → acute MR .
Read this in Heart Pathology: Comprehensive Short Notes
What our notes say
- • Is due to Pericarditis whose causes include:- bacterial and viral pericarditis, myocardial infarction, rheumatic fever, connective tissue disorder, trauma, uraemia (Cardiovascular system examination revised 2012 — Past Paper Questions & Answers)
- Myocardial infarction is associated with faster utilisation of creatine phosphate (bchem EOY 2011 — Past Paper Questions & Answers)
- A 51-year-old man is hospitalized for acute myocardial infarction. (renal pathology — Past Paper Questions & Answers)
- A 60-year-old woman is admitted with sudden onset of chest pain and is diagnosed with an acute myocardial infarction. (renal pathology — Past Paper Questions & Answers)
- She had a myocardial infarction last year but recovered and is doing well following angioplasty. (CNS PATHOLOGY — Past Paper Questions & Answers)
- Low cardiac output: heart failure, myocardial infarction, arrhythmias, cardiac tamponade, pulmonary embolism. (Junior Clerkship in Internal Medicine (MBIM4100) main exam, Paper One: 31 Januar)
Study material on Myocardial Infarction
- CARDIOVASCULAR PATHOLOGY
- Cardiovascular system examination revised 2012
- Comprehensive Heart Pathology Notes 🫀
- Heart Pathology: Comprehensive Short Notes
- CARDIOVASCULAR PATHOLOGY
- CLINICAL BIOCHEMISTRY LAQs & SAQs
- Clinical Enzymes: Functions and Applications
- Clinical Enzymology and Biomarkers
- Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019
- CRUSH COURSE YEAR 3 SEM 1 WORK (Part 1)
- Cardiovascular Disease and Biochemical Markers MCQs
- Weekly Pathology Exam - June 19, 2026 (Section A: MCQs)
Practice questions on Myocardial Infarction
A 55-year-old man has a history of hypercholesterolemia with coronary artery disease and suffered a myocardial infarction 2 years ago. He now presents with crushing substernal chest pain. Which of the following laboratory tests is most useful in diagnosing the cause of his chest pain?
- Increased white blood cell count
- Elevated sedimentation rate
- Decreased serum complement
- Increased serum troponin
- Decreased platelet count F. Increased serum cholesterol
Answer: D. Troponins are released from the damaged striated muscle. Cell damage leads to leakage of intracellular contents, such as enzymes or other proteins. Some of these are more specific for certain tissues to aid in diagnosis. ---
A patient receives a COX-2 selective inhibitor for chronic arthritis but develops a myocardial infarction. What best explains this adverse effect?
- COX-2 inhibition increases leukotriene synthesis via shunting of arachidonic acid
- Selective inhibition of endothelial PGI2 production without affecting platelet TxA2 favors thrombosis
- COX-2 inhibitors enhance neutrophil adhesion to vascular endothelium
- Inhibition of COX-2 increases production of pro-inflammatory cytokines
- COX-2 blockade impairs hepatocyte regeneration leading to coagulopathy
Answer: B. This is a critical clinical point about selective COX-2 inhibitors. Endothelial cells produce prostacyclin (PGI2) via COX-2, which is a vasodilator and inhibits platelet aggregation. Platelets produce thromboxane A2 (TxA2) via COX-1, which promotes vasoconstriction and platelet aggregation. Selective COX-2 inhibitors block endothelial PGI2 production but leave platelet TxA2 production intact (since platelets use COX-
What is the most common histological change seen within 24 hours following a myocardial infarction?
- Pallor and oedema
- Increased collagen deposition
- Liquefactive necrosis
- Disintegration of dead myofibers
- Neutrophilic infiltration
Answer: D. Within 24 hours of a myocardial infarction, the primary histological change is coagulative necrosis, characterized by the loss of nuclei and striations, and disintegration of dead myofibers.
Which of the following is the most specific marker for myocardial infarction?
- CK-MB
- Troponin I
- Myoglobin
- LDH Correct
Answer: B. Troponin I is highly specific for cardiac muscle and remains elevated longer than other markers, making it gold standard for MI diagnosis. ---
Which cardiac biomarker has the SHORTEST time to return to normal levels after myocardial infarction?
- Troponin I
- CK-MB
- Troponin T
- NT-proBNP
Answer: B. ** CK-MB typically returns to normal within a few days after myocardial infarction, helping determine the timing of myocardial injury. Troponins remain elevated for several days longer. ---
What is the advantage of using troponins over CK-MB in diagnosing myocardial infarction?
- Troponins rise earlier
- Troponins are more specific to cardiac muscle
- CK-MB remains elevated longer
- Troponins are less expensive
Answer: B. ** Troponins are highly specific to cardiac muscle injury, making them the gold standard for diagnosing myocardial infarction, whereas CK-MB can be less specific. ---