Ischaemic Heart Disease Flashcards
Lipid Guidelines
No longer a specific target for LDL High risk = high CVD risk = history of IHD = >21yrs with high LDL >4.9 = people with diabetes High intensity = 40mg rosuvastatin
Side effects of statins
Muscle pains Rhabdomyolysis LFT derangement Death Cognitive impairment New onset diabetes
Anatomical Vs functional study as initial investigation of coronary artery stenosis
Nil significant difference in primary endpoint of death, MI, unstable angina and major complications between Cardiac CT and stress echo/nuclear perfusion/exercise ECG
HOWEVER Cardiac CT reduces the number of normal angiograms done
PROMISE STUDY
What is coronary calcification?
Not in normal vessels
Increases with age
Associated with coronary atheroma
Does not correspond with the degree of luminal stenosis
What is the coronary calcium score
Agatston score
Non con CT
Detects individuals at risk of cardiovascular events that are not detectable by traditional risk factors
Recommended for those at intermediate risk of CVD - 10-20% 10 yr risk
Fractional flow reserve
Ischaemia is defined as FFR <0.8
FAME study = reduces MI and death at 1 yr compared to angiogram guided PCI in multivessel disease
Antiplatelet drugs - Ticagrelor Vs Clopidogrel
PLATO study
Ticagrelor has significantly less adverse outcomes and no significant increase in bleeding after 12 months
Antiplatelet drugs - Prasugrel Vs Clopidogrel
TRITON study
Prasugrel significantly reduced primary endpoint of death, MI and stroke compared to clopidogrel
Given AFTER coronary anatomy was known
Mechanism of action of new antiplatelet agents
T+P act on platelet P2Y12 ADP receptor
Differences between prasugrel and ticagrelor?
Prasugrel is a prodrug
Prasugrel binds irreversibly, ticagrelor has reversible binding
Mechanism of ticagrelor-mediated dypnoea and ventricular pauses
Adenosine mediated
Contraindications for prasugrel?
Prior stroke or TIA, weight < 60kgs, age >75yrs
Why clopidogrel is bad?
Prodrug
Must be activated by cytochrome P450
A significant proportion of population are slow metabolism
Radial Vs femoral access in ACS
Meta-analysis = radial access –> less bleeding complications –> less death, MI and stroke
Role of thrombus aspiration during primary PCI for STEMI?
TOTAL trial
Routine thrombectomy was associated with increased risk of stroke within 30days
Fix all disease at STEMI or only culprit lesion?
Current practice = fix only culprit lesion
COURAGE trial = fix only culprit lesion
PRAMI trial = fix all lesions
CAGs Vs PCI in 3VD and left main disease
Low risk score = PCI but increased risk of revascularisation
High risk +/- diabetes = CAGs but increased risk of stroke
SYNTAX, FREEDOM and EXCEL studies
Medical therapy Vs. PCI for stable angina
PCI did not reduce risk of AMI or death when added to optimal medical therapy
COURAGE trial
Stop or continue aspirin pre CAGs
Nil increased risk of death or thrombosis
Nil increased risk of major bleeding
= continue aspirin
ATACAS trial
Mechanism of action of proprotein converatase subtilisin/kexin type 9 inhibitors?
Inhibition of LDl receptor degradation
What is the GRACE score?
Risk of in hospital mortality after ACS
Age Heart rate Systolic BP Creatinine ST elevation
> 140 = coronary angiogram within 24hrs
What are the different types of MI?
Type 1 = acute plaque rupture with thrombus
Type 2 = vasospasm or endothelial dysfunction
Type 3 = fixed plaque –> decreased supply
Type 4 = Decreased supply only