U12C3 MI Flashcards
What is angina?
- Pain in the chest of cardiac origin due to inadequate blood and O₂ supply to myocardium from occlusion of coronary arteries
- Atheroma = very common, mostly asymptomatic
- Atheromatous deposits → plaques → atherosclerosis
- Stable → unstable angina → thrombosis/MI
- Vasospasm of coronary arteries - rare (Prinzmetal’s)
What is atherosclerosis?
- Disease of arterial vessels
- Progressive and cumulative
What are lipids and the different types?
Fatty acids:
- SFA = saturated fatty acid (0 double bonds)
- MUFA = mono-unsaturated fatty acid (1 double bond)
- PUFA = poly-unsaturated fatty acid (>1 double bond)
Cholesterol
Triglycerides
Lipoproteins (= lipids + proteins):
- Chylomicrons
- VLDL = very low density lipoprotein
- IDL = intermediate-density lipoprotein
- LDL = low-density lipoprotein (1 copy of ApoB-100)
- HDL = high-density lipoprotein
What is the LDL receptor and how can it be mutated?
- Single-pass type I membrane protein (839 amino acids)
- Widely distributed
- Binds LDL, the major cholesterol-carrying lipoprotein, and transports it into cells by endocytosis
- Familial hypercholesterolaemias →↑ serum LDL
Type I = mutation in LDL-R
- Autosomal dominant (many known mutations) →
- ↓ expression levels; ↓ affinity for LDL; ↓ uptake of LDL;
Type II = mutation in ApoB
- Autosomal dominant
- Defective ApoB-100
- Prevents binding to LDL-R
How is lipid/cholesterol transported?
From gut via lymph to body/liver = exogenous pathway
- “fat absorption”
- Chylomicrons
- TGs → FAs + glycerol – absorbed into cells
- Cholesterol esters → liver → endogenous pathway or bile acids
From liver to body = endogenous pathway
- “cholesterol transport” to body
- Liver → VLDL → IDL → LDL (LP density ↓ as they deliver lipids to cells)
- Deliver TGs (FAs & glycerol) and cholesterol to cells (via LDL-R)
From body to liver
- “reverse cholesterol transport”
- Non-liver cells → HDL using ApoA and ABCA1 containing cholesteryl esters
- HDL binds to Scavenger Receptor B1 (SCARB1) on liver
From liver to gut and back again…
- “enterohepatic circulation”
- Bile acid synthesis requires a large amount of cholesterol
- Synthesised de novo, re-cycled via EHC or from blood (LDL)
How is cholesterol recycled?
How is choleseterol synthesised?
What is the physiology of angina?
Stable vs unstable angina pathophysiology
Stable angina occurs when there’s a temporary imbalance between the heart’s demand for oxygen and its supply due to narrowed coronary arteries, often caused by atherosclerosis. Unstable angina involves more unpredictable and severe symptoms, typically due to a partially blocked artery or a blood clot forming on a ruptured plaque, leading to decreased blood flow to the heart. This can progress to a heart attack.
What is the pathophysiology of an MI?
What is the pathogenesis of atherosclerosis?
What is the progression of a plaque?
What are the risk factors for coronary artery disease?
Obesity – total blood volume and cardiac output are increased with cardiac workload normally higher leading to hypertension as well as associated with dyslipidaemia, insulin resistance and inflammation which can lead to atherosclerosis
Smoking – oxidant compounds of cigarette smoke cause endothelium dysfunction which leads to the atherosclerotic process as well as the plaques of smokers having a high vulnerability of rupture due to a higher lipid content
Hypertension - in picture
Physical activity – decreases vascular inflammation, improves endothelial function and coronary circulation preventing myocardial ischaemia
Hypocholesterolaemia – leads to the formation of more plaques within the coronary arteries leading to atherosclerosis and increase MI risk
Diabetes mellitus – higher risk of insulin resistance, hyperinsulinemia and vascular calcification which not only promote the occurrence of atherosclerosis but also accelerate the progression of stable plaques to unstable plaques or plaque rupture leading to thrombosis
Men - historically, men had higher rates of unhealthy habits such as smoking and stress as well as naturally occurring hormones in women playing a protective role as heart disease risk increases after menopause
Advancing age – potentially to do with oxidative stress caused by excess production of ROS leading to inflammation (IL-6, TNF-α) which then leads to cardiac remodeling of ECM caused by impaired ECM turnover causing fibrosis that can lead to AF… also are more likely to develop hypertension, diabetes and atherosclerosis which also contributes
Socioeconomic status – limited access to healthcare services, higher stress level (crime and unemployment), poorer dietary habits, higher smoking and alcohol levels, higher rates of depression as well as higher education and income are associated with higher acceptance and compliance with CVD
Geographic location – fewer visits to doctors, less lipid screening, poorer blood pressure control and less use of stains in older adults with diabetes
What is QRISK3?
- Adults aged 40-74 who attend NHS health checks have their cardiovascular disease risk score calculated using the QRISK calculator
- QRISK is an algorithm that calculate an individual’s 10 year risk of having a heart attack or stroke… it is in review and updated every year… for example, NICE recommended adding severe mental illness
- It is not to be used opportunistically in unselected people – rather use systemic strategy
- It can be used for people aged 25 to 84 years old
- Don’t use in people who already have CVD
What are the different types of angina?
-
Atypical angina:
is described by NICE as chest pain with two out of three of the features classical angina.-
Non-angina chest pain:
is described by NICE as chest pain with one out of three of the features above. -
Variant (Prinzmetal’s) angina:
caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest. Characteristically, there is ST segment elevation on the ECG during the pain. -
Unstable angina:
increases rapidly in severity, occurs at rest, or is of recent onset (less than 24 hours) (acute coronary syndrome) -
Refractory angina:
refers to patients with severe coronary disease in whom revascularization is not possible and angina is not controlled by medical therapy. -
Microvascular angina:
symptoms of angina, a positive exercise test and normal coronary arteries on angiogram. It is thought to result from functional abnormalities of the coronary microcirculation. While it has a good prognosis, it is often highly symptomatic and can be difficult to treat.
-
Non-angina chest pain:
What are the symptoms of angina? Stable vs unstable
- ‘Heavy’, ‘tight’ or ‘gripping’ central or retrosternal pain which may radiate to the jaw and/or arms.
- Pain which occurs with exercise or emotional stress.
- Pain which eases rapidly with rest or with GTN (glyceryl trinitrate)
What are the symptoms of a MI?
What is the Canadian Cardiovascular Society functional classification of Stable angina?
What does each coronary artery supply?
NSTEMI vs STEMI
What are the features of a 1st, 2nd and 3rd degree heart block on an ECG?
What are the manifestations of MI?
How does a coronary angiogram work?
What would the cardiac bio markers show?
What is the flow diagram of treatment for stable angina?
What is a primary coronary angioplasty?
What are the types of infarcts?
What are the complications of an MI?
What is cardiac rehab?
