Key lessons on LDL-c and CV risk
The following key messages have been formulated based on an expert meeting among European cardiologists and internists, as well as other PACE-CME educational activities.
Click on the statements to read brief explanations of what the statements are based on, including slides and references.
- Elevated LDL-c 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 lessons 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 triglyceride-rich lipoproteins and Lp(a)).
2. Blood pressure-lowering therapy: target SBP 120-130 mmHg (note U-curve).
3. Novel diabetes agents with CV benefit (CAD and/or risk of HF events with GLP-1ra and/or SGLT2i
4. Antithrombotic therapy: prolonged double antiplatelet therapy? 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.
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