Once again standing room only!
And managed to catch his eye to say 😀 for the camera 📸
Phil explaining how lipids have become unnecessarily complicated
We have gone from one medicine and one back up to multiple options for lipid management
Today going to take things back to fundamentals
How complicated lipids can be in one diagram 🖼️
Take away point: multiple mechanisms to lower lipids, work on different parts of the pathway
Lipoproteins broken down by size
- LDL will move cholesterol around the body
- Chylomicrons - smaller, risk of causing pancreatitis
What’s in a blood? What’s in a lipid profile?
So what tests do we need?
Initial sample does NOT need to be fasting. Make the most of every visit. Test if able.
Primary Prevention:
- don’t use QRISK for T1DM
- for males, T2DM over 51 QRISK will be over 10%
- for females, T2DM over 58 QRISK will be over 10%
Titrate up doses until getting a reduction of 40% of baseline
Causes of raised cholesterol
Important to take full history
Managing dyslipidaemia in DM
Secondary prevention:
Work backwards, start high and reduce as able
Ezetimibe:
- far lower CV benefits than a statin - particularly CV end points/events
PCSK9:
- rapidly recycle and clear lipid receptors
- imagine a snooker 🎱 table, more pockets
- increase uptake and recycling process
- tight criteria
- potent medicines - can see big drops
Negatives:
- cost and access
Bempedoic acid:
- work similarly to statins
- good for true statin intolerance patients
Inclisiran:
- works similarly to PCSK9 inhibitors
- limited outcome data
Statins:
- if you reduce LDL by 1mmol/L with statins you reduce CV risk by 20%
Is intolerance a no-cebo effect? As myopathy figures in RCTs are a lot less than reported in practice
Statin intolerance:
- simplified pathway
- washout period (longer washout if high CK)
- then re challenge
- if symptoms persist before rechallenge unlikely the cause was the statin
Consider potent statins once or twice a week E.g rosuvastatin
Lipid medicines compared by potency:
Summary slides:
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Let's start with the headline, drum roll please 🥁... Dapagliflozin in HFmrEF and HFpEF DELIVER Trial results
1. Background💔
HFpEF pts represent approx 50% of all people with HF
Currently limited Tx options in this group
Uncertainty remains re:
- People in highest part of EF range, ?attenuation of Tx effect
- People initiated on Tx during/soon after hospitalisation
- EF improved to >40%
2. Trial design, Endpoints and Flow
Note: either ambulatory or hospitalised patients
6236 patients. 3131 received dapagliflozin. Across 20 countries 🗺️
Follow up - 2.3 years
Equal drop out and incomplete follow up in Tx and in placebo arms