ACS Flashcards
- What is acute coronary syndrome?
ACS is a spectrum of conditions including myocardial infarction with or without ST-segment-
elevation (STEMI or NSTEMI), and unstable angina.
- What causes ACS?
What causes ACS?
- Result from the formation of a thrombus of an atheromatous plaque in a coronary artery
- Presentation and management has similarities but also important differences.
- How can a diagnosis of ACS be made?
Clinical presentations, biochemical cardiac markers and ECG changes
What is STEMI caused by?
ASTEMIis generally caused by acompleteandpersistentblockage of the artery resulting in
myocardial necrosis with ST-segment elevation on ECG.
What is NSTEMI and unstable angina caused by?
In NSTEMI and unstable angina a partial or intermittent blockage of the artery occurs, which
usually results in myocardial necrosis in NSTEMI but not in unstable angina
- What causes myocardial ischaemia?
Results from imbalance in myocardial oxygen demand and supply.
What leads to an increased myocardial oxygen demand and what leads to a decreased myocardial supply?
Increased myocardial oxygen demand:
* increase in heart rate and ventricular contractility;
* Increase afterload and preload
* hypertension, high cardiac output (myocardial hypertrophy)
Decreased myocardial oxygen supply:
* reduced coronary blood flow and blood oxygen carrying capacity
* thrombosis, vasospasm
What is an atheroma and what does it consists of?
An accumulation of degenerative material in the tunica intima of artery walls (inner wall)
The material consists of:
Macrophage
Lipids such as cholesterol and fatty acids
Calcium deposits
Fibrous connective tissue
Explain the molecular mechanism of plaque formation in the artery./ Explain the process of plaque formation.
LDLs enter dysfunctional endothelium which causes three responses:
1. Causes the releases of inflammatory cytokines and growth factors which activates adhesion molecules (VCAM1) to attract leucocytes and monocytes into the cell
2. LDLs get engulfed by oxidised macrophages
Foam cell accumulates and smooth muscle cells proliferate causing the formation of plaque.
Inflammatory cell infiltration, smooth
muscle cell death through apoptosis, and matrix degradation through proteolysis (by matrix metalloproteinases- MMPs) generate a vulnerable plaque with a thin fibrous cap and a lipid- rich necrotic core. Plaque rupture can cause thrombosis which might be sufficient to cause vessel occlusion (or blockage).
How does fatty streak formation occur?
Foam cells eventually die propagating inflammatory cytokines which cause smooth muscle cells to proliferate and migrate. As the endothelium is dysfunctional it cannot release nitric oxide to prevent the proliferation of smooth muscle cells.
Explain the sequences in progression of atherosclerosis.
initial lesion
fatty streak
intermediate lesion
atheroma
fibroatheroma
Complicated lesion
What is the major difference between stable angina and unstable angina?
Stable angina - symptoms present on exertion but not at rest due to partially occluded artery. At rest flow although reduced by stenosis may be sufficient to serve cardiac oxygen needs
- Whilst in unstable angina the symptoms still occurs at rest. Angina of increasing severity, duration or frequency and occurring at rest or with a lesser degree of exertion
Exertion activates what pathway of the nervous system?
Sympathetic NS
What effect does exertion have on the SNS?
Exertion activates sympathetic nervous system, increasing:
* Heart rate
* Force of contraction
* Blood pressure
What are the key features of angina?
Myocardial oxygen consumption is increased during exertion
Demand > Supply = myocardial ischemia
Symptoms persist until oxygen balance restored
Detection usually by: ECG (depressed ST segment), exercise stress test, Holter monitor
