Hans Schneider, Week 12 MED1022; Pathology
Cardiac tissue necrosis is not visible in the first few hours but then becomes coagulation necrosis. Heart cells get ischaemic injury, go through apoptosis and necrosis, cell membrane becomes damaged, intracellular molecules traverse the membrane and appear in the interstitial fluid and eventually in blood (troponin, creatine kinase). Old markers are creatine kinase and lactate dehydrogenase. Troponin T binds troponin to tropomyosin strand, troponin C binds calcium and initiates contraction. Troponin I inhibits contraction in the resting state.
Detection of rise of biomarkers above the 99th percentile shows evidence of ischaemia, ECG shows changes of new ischaemia or development of pathological Q waves, imaging may show loss of viable myocardium. CK is only seen in STEMI and NSTEMI, troponin also in ACS. Elevated troponin may also be seen in demand ischaemia (sepsis/SIRS, hypotension/hypovolaemia, supraventricular tachycardia/atrial fibrillaiton, left ventricular hypertrophy), MI (intracranial haemorrhage or stroke, coronary vasospasm, ingestion of sympathomimetic agents), direct myocardial damage (cardiac contusion, direct current cardioversion, cardiac infiltrative disorders, chemotherapy), myocardial strain (CHF, PE, pulmonary hypertension), chronic renal insufficiency. Troponin high sensitivity can see all heart problems. BNP/NTproBNP is elevated in heart failure and might help with diagnosis and management of patients with heart failure. Increased levels of markers are associated with worse outcomes and may indicate lipid lowering therapy.
Type 1 is due to an atherosclerotic rupture leading to clotting and stenosis of a coronary vessel, also known as a primary coronary event. Type 2 myocardial infarction is where increased oxygen demand, or decreased supply, causes ischemia: this can be due to causes such as coronary artery spasm, embolism, anaemia, arrhythmia or hypo/hypertension. Type 3 is when you die from a coronary incident and it is too late to do anything.