Key messages on LDL-c and CV riskLDL-c Key messages
The following key messages have been formulated based on an expert meeting (held December 14, 2018) among European cardiologists and internists, around the topic of ‘LDL-c and PCSK9 inhibition in high CV risk patients. Balancing science, guidelines and daily cardiology practice’.
Click on the statements to read brief explanations of what the statements are based on, including references.
- LDL is causal of atherosclerosis
- LDL-c level increases with age, so does the risk of atherogenesis
- The atherosclerosis disease process changes with time and LDL-c level, and treatment effect depends on the disease phase
- Regression of atherosclerotic plaque is possible with adequate lipid-lowering therapy
- Side-effects are not the effect of LDL-c lowering and achieved LDL-c level
- When lowering plasma cholesterol, this does not affect cholesterol present in membranes
- Lowering LDL-c profoundly to very low levels is safe
- Use combination therapy for additive LDL-c lowering effect to reduce CV risk
- Even below LDL-c target further LDL-c reduction gives additional CV benefit
- Greatest risk reduction can be achieved in the highest risk groups
- Statin therapy is remarkably safe
- When statin therapy is discontinued, the risk of CV events and mortality increases
- After an event; initiate the right treatment in hospital
- LDL-c lowering treatment impacts disease progression before clinical manifestation
- Screening for familial hypercholesterolemia after ACS pays off
Concept changes in lipid-lowering therapy to lower CV risk
Based on the key messages listed above, the following principles can be formulated that should form the basis of lipid-lowering therapy to lower CV risk.
1. Use combination therapy
2. Start early
3. Treat more aggressively
Emerging concept of multifactorial CV risk management
In addition to lipid-lowering, a broader concept of CV risk management in coronary disease is emerging, which should include:
1. Lipoprotein-modifying therapy: lower LDL-c earlier and more aggressively (and TRLP and Lp(a)).
2. Blood pressure-lowering therapy: target SBP 120-130 mmHg (note U-curve).
3. Antidiabetic therapy: lower CV risk (CAD and/or risk of HF events) with SGLT2i and/or GLP-1ra
4. Antithrombotic therapy: prolonged DAPT? Low-dose anticoagulation?
5. Anti-inflammatory therapy: target IL-1β
6. Future: target microbiome …?
Better algorithms on which patient to treat when with what, and better risk estimation are needed. Moreover, there is a need for better risk prediction of adverse events.