Coronary Artery Disease: Acute coronary syndrome Flashcards
This is a term that covers a wide range of concepts:
- Blood stopped to the heart:
1) unstable angina with partial blockage of a vessel
2) acute myocardial infraction with full blockage of vessel - Rupture of an arthomatus plaque leading to possible thrombosis or embolism
How will a thrombus cap rupture?
IF there is a sturcutral defect in the fibrous cap, it exposes the thrombogenic core to the blood.
Where the cap is thinnest, there is infiltration of foam cells and loss of smooth muscle in the cap
The plaque will then rupture
WHen is thromus rupture likely to happen?
It is often spontaneous, but increase stress may increase the chance of a rupture e.g. winter between 6.30 and 9.00 monday morning
What happens to a ruptured cap?
This is called a STENOSIS which is a healed ruptured cap that will narrow the lumen.
What are the symptoms of Acture Coronary Symptoms?
Chest pain, tightness, pressure, pain, discomfort, shortness of breath, dizy, light headed, nausea, sweating
What differentiates these symptoms from Stable Angina?
It is NOT relieved by Nitrates.
What are the two types of Myocardial Infraction in Acute coronary syndrome?
ST-elevated myocardial infarction
Non-ST elevated myocardial infarction
What is a STEMI?
ST-elevated myocardial infarction: Persistent ST elevation on the ECG, and rise in Troponin levels.
What is NSTEMI?
Non-ST elevated myocardial infarction: ST is not elevated, but there are abnormalities in the ECG, either ST depression, or a T inversion. Also has a rise in Troponin levels
WHat if there are ST/T abnormalities, but the Troponin levels are normal?
This is UNSTABLE ANGINA
What if the ECG is normal or undetermined, but the Troponin levels are high?
NSTEMI
What is Troponin?
It is attached to tropomysin and is an actin filaments. Action potentials cause Calcium to attach to troponin, exposing the myosin binding site, cross bridge and contraction takes place.
What are Biomarkers and how are they used?
These are Troponins, Creatinine Kinase Isoforms, or Beta type natriuretic peptide. They are used in addition to ECG for diagnosis. They will appear in the plasma over a period of hours after first onset of symptoms if there is damage to muscle.
Advantage and Disadvantage of Creatinine Kinase Isoforms?
Less-selective but build up quicker
What is the molecular pathology of a Myocardial Infarction?
It is when a major vessel is completely occluded by a thrombus causing an area of the myocardium to be completely deprived from oxygen.
This causes hypoxia of the tissues.
Cessation of mitochondria producing ATP causing anaerobic glycolysis to try to compensate for this but only 7% of requirement is produced
Acid and Lactate build up and there is production of reactive oxygen species
There is impaired contration and contracture which is deformaties of the tissue (stunned myocyte)
This develops to cell death by oncosis, apoptosis and autophagy.
Necrosis at tissue level
What is the major determinant in the extent of irreversible injury from Myocardial Infarction?
TIME
Where does the Infarction progress from?
The endothelium to the epicardium
Is there collateral circulation?
Little or no collateral vcirculation
What is infarction?
Obstruciton of the blood flow by a thrombus or embolus causing local death to tissue
What are the goals for treating for Acute coronary Syndromes (heart attacks)
This can be fatal. The goals are:
1) reduce and relieve acute symptoms and distress
2) prevent or limit extent of myocardial necrosis
3) REduce risk of early death due to arrhythmia or acute heart failure
4) Reduce risk of reoccurance (secondary prevention)
5) Limit development of chronic iscahemic cardiomyopathy and heart failure
What is the Primary Treatment?
This is ttrreatment while waiting for diagnosis.
GTN to reduce the cardiac preload and oxygen demand
Loading dose of aspirin 300mg to reduce further thrombus formation
Morphine to relieve the pain
ANti-emetic to relieve nausea
What is the treatment after diagnosis of STEMI?
STEMI: Reperfusion therapy (emergancy)
DO this either with drugs that prevent fibrin build up or
Emergancy operation (PCI) within 12 hours of onset of symptoms and 2 hours of fibrinolytic therapy
What is the treatment after diagnosis of NSTEMI?
Clopidogrel loading dose of 300mg and asprin (unless contraindicated)
High risk patients may get the PCI operation or CABG ssurgery
What are the 2 class of drugs used for these primary treatment?
Anticoagulant
Antiarrhythmic
What is the long-term management post STEMI (prophylaxis)
Anti-platelet therapy: low dose aspirin for life and clopidogrel for 6-12 months
Anit-coagulation can be added or used as an alternative (warfarin or Rivaroxaban)
Statins regardless of HDL levels
ACE inhibitors or ARB if not already used
B-blocker
Aldosterone antagonist (spironoloctane) if Left ventricular dysfunction
