3- acute coronary syndromes Flashcards
what are risk factors for acute coronary syndromes?
- gender
- family history
- age
- obesity
- high cholesterol
- drug abuse
- alcohol
- hypertension
- smoking
- stress
for chronic stable angina, what is
a) type of stenosis?
b) type of ischaemia?
a) fixed stenosis = - consistent, unchanging narrowing of a coronary artery (stenosis = abnormal narrowing of artery)
b) demand led ischaemia = occurs when heart has increased demand for oxygen
*stable angina is a predictable & safe condition
what is presenting history of angina?
cardiac chest pain
- heavy feeling, weight on chest, pressure, tightness
- radiates along arm, jaw, epigastrium, back
what is acute coronary syndrome?
= any acute presentation of coronary artery disease (only provisional diagnosis that covers a spectrum of conditions)
*it’s an umbrella term that includes angina, STEMI etc
what are types of myocardial infarction (MI)?
STEMI = ST elevation MI
NSTEMI = non ST elevation MI
what is pathogenesis of acute coronary syndrome?
normal →fatty streak →atherosclerotic plaque →fibrous plaque →plaque rupture/thrombosis
what causes coronary thrombosis?
Coronary thrombosis may occur as a result of either spontaneous plaque rupture or percutaneous coronary interventions, such as placement of an intracoronary stent.
The resulting 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.
describe the formation of atheroma?
- damage to endothelium, usually caused by risk factors like hypertension, smoking & diabetes
- inflammation in response to endothelial injury where inflammation cells migrate & accumulate and they engulf LDL cholesterol that’s accumulated in endothelium forming foam cells
- foam cells accumulate making fatty streaks
- the fatty streaks progress into atheromas which are made of lipids, cholesterol and debris covered by fibrous cap
what are the factors affecting plaque rupture?
for plaque:
- lipid content of plaque
- thickness of fibrous cap
- plaque shape
for artery:
- sudden changes in intraluminal pressure or tone
- bending & twisting of an artery during heart contraction
- mechanical injury
what is PCI?
inserting stent with balloon and catheter to keep vessel wide to allow blood flow
what is the coagulation pathway?
it happens if fibrous cap ruptures and happens at same time as platelet cascade
TF (tissue factor) that’s released from damaged tissues forms a complex with factor VII →activation of factor VIIa which initiates coagulation cascade. Activated VIIa + factor X →factor Xa which in combination with others activates prothrombin (factor II) →thrombin (factor IIa). Thrombin catalyses the conversion of fibrinogen (soluble) to fibrin (insoluble). The fibrin molecules join together forming long fibrous chains →develop into a dense fibrous mesh engulfing not only the aggregation of platelets, but also other blood cells
what is the bodies response to PCI?
- the stent can disrupt the plaque so may cause a release of plaque debris into the bloodstream and can lead to a temporary state of vascular injury
- In response to the vascular injury, the body’s natural response is to initiate blood clotting mechanisms to repair the damaged area. Platelets, a type of blood cell involved in clotting, may adhere to the injured arterial wall and aggregate, forming a blood clot
*this is why also given anti-platelet to prevent another clot forming
what happens in platelet cascade?
it happens when plaque ruptures:
platelets adhere to exposed collagen by ADP receptors and once adhered they become active and release activators such as ADP (which acts as signalling molecule to attract & activate other platelets in vicinity). Thromboxane A2 is also generated by arachidonic acid through cyclooxygenase (COX) enzyme which promotes further activation & aggregation
how does atheroma lead to symptoms like angina or claudication (muscle pain)?
when the atheroma grows and narrows the vessel, less blood can get through so less oxygen ->pain
*more likely to come on when exercising as increased oxygen demand
how does atherosclerotic plaque lead go MI or stroke etc?
The atherosclerotic plaque, particularly when it is mature and calcified, is a relatively inflexible structure and is prone to fissuring and rupture.
This may trigger the development of a thrombus which can cause acute vascular stenosis, leading to local ischaemia and possibly to infarction. Depending on the vessel involved, this can become manifest as a myocardial infarction, stroke, critical leg ischaemia, or even cardiovascular death
what is vessel like in
a) STEMI?
b) NSTEMI?
a) vessel occlusion →cell death
b) subtotal occlusion (not completely blocked off vessel)
what is arrhythmia of STEMI?
ventricular fibrillation = rapid & chaotic contractions of ventricles
what is difference in appearance of normal heart LV and infarcted heart LV?
infarcted heart is darker in colour and the ventricle is dilated
what are the most important diagnosis factors for acute coronary syndrome?
- history
- ECG
*troponin levels are useful but only alongside history
what would be presenting history of STEMI MI?
- SEVERE crushing central chest pain
- radiating to jaw & arms, especially the left
- similar to angina but more severe, prolonged and not soothed by GTN
- associated with sweating, nausea and often vomiting
what presenting history differences between angina and MI?
duration - longer for MI (10 mins for angina & 30 mins or longer for MI)
severity - much more severe for MI
GTN spray - relives for angina but doesn’t for MI
associated symptoms - usually none for angina and sweating, nausea, vomiting for MI
