Acute Myocardial Infarction Flashcards
Chronic Stable Angina features
Fixed stenosis which causes demand led ischaemia and prodcues predictable and safe symptoms
Advise for patients who have flare ups of Chronic Stable Angina
Stop what they are doing
Sit to reduce the demand on the heart
Spray the GTN spray
Chest pain associated with chronic stable angina
Heavy feeling
Weight on the chest
Pressure and tightness
Acute Coronary Syndrome
Any acute presentation of coronary artery disease and is only a provisional diagnosis that covers a spectrum of conditions
Acute coronary syndromes include…
STEMI
NSTEMI
Unstable Angina
Pathogenesis of NSTEMI and STEMI
Artherosclerotic plaque rupture
Acute Coronary Syndrome features
Dynamic stenosis
Supply led ischaemia causing symptoms at rest which are unpredictable and dangerous
Factors affecting plaque rupture
Lipid content Thickness of fibrous cap Sudden changes in intraluminal pressure Bending and twisting of an artery during heart contraction Plaque shape Mechanical injury
Platelet Cascade initiation (use of stenting)
Causes coronary thrombosis resulting in vascular damage exposes subendothelial collagen and von willebrand factor to the circulating blood. Platelets rapidly adhere to the sites of tissue damage via glycoproteins and integrins.
Platelet Cascade Adhesion
Unactivated platelets are rapidly recruited and ahere to the site of vascular damage forming a monolayer.
Platelet Cascade Activation
Glycoprotein mediated binding to the exposed tissue elements stimulates platelet signalling which results in a shape change from the usual disk-like form to spheres with extended pseudopodia thereby enhancing the ability of the platelets to interact with each other and with the subendothelial surface.
Platelet Cascade (release of activators)
Platelets now begin to release numerous prothrombotic activators with platelet activation becoming highly amplified. Preformed ADP is released from platelet dense granules. Thromboxane A2 is generated from platelet membrane lipids. Both ADP and thromboxane A2 cause further activation and recruitment. This platelet activation leads to aggregation and eventual thrombus formation
Platelet Cascade (Surface Receptors)
Secreted ADP binds to the ADP receptor, a G-coupled receptor on the platelet surface which stimulates thrombus growth and stability by recruiting additional platelets to the site of injury, potentiating platelet granule release of ADP, fibrinogen and factor V and exposure of inflammatory markers on the platelet surface including P-selectin
Platelet Cascade (amplification of platelet activation)
Platelet activation rapidly results in platelet aggregation, a detrimental process, which may progress to thrombosis and acute vessel occlusion with ischemic injury including myocardial infarction and stroke
Platelet Cascade (activation triggers inflammatory cascade)
Platelet activation results in the expression of platelet surface inflammatory markers, P-selectin and CD40 ligand (CD40L). Platelet-leukocyte conjugates form via P-selectin interacting with its ligand PSGL-1 on the leukocyte surface. CD40L interacts with monocytes, endothelial cells and smooth muscle cells. Thus activation of platelets triggers an inflammatory process emphasising the need to manage platelet activation.
