Eddy Edson
Well-Known Member
- Relationship to Diabetes
- Type 2
Update to 2017 Roadmap with detailed reviews of new evidence. The WHF is the leading global NGO for CV stuff, bringing together experts and institutions from everywhere.
Background: Atherosclerotic cardiovascular diseases (ASCVD) including myocardial infarction, stroke and peripheral arterial disease continue to be major causes of premature death, disability and healthcare expenditure globally. Preventing the accumulation of cholesterol-containing atherogenic lipoproteins in the vessel wall is central to any healthcare strategy to prevent ASCVD. Advances in current concepts about reducing cumulative exposure to apolipoprotein B (apo B) cholesterol-containing lipoproteins and the emergence of novel therapies provide new opportunities to better prevent ASCVD. The present update of the World Heart Federation Cholesterol Roadmap provides a conceptual framework for the development of national policies and health systems approaches, so that potential roadblocks to cholesterol management and thus ASCVD prevention can be overcome.
Methods: Through a review of published guidelines and research papers since 2017, and consultation with a committee composed of experts in clinical management of dyslipidaemias and health systems research in low-and-middle income countries (LMICs), this Roadmap identifies (1) key principles to effective ASCVD prevention (2) gaps in implementation of these interventions (knowledge-practice gaps); (3) health system roadblocks to treatment of elevated cholesterol in LMICs; and (4) potential strategies for overcoming these.
Results: Reducing the future burden of ASCVD will require diverse approaches throughout the life-course. These include: a greater focus on primordial prevention; availability of affordable cholesterol testing; availability of universal cholesterol screening for inherited dyslipidaemias; risk stratification moving beyond 10-year risk to look at lifetime risk with adequate risk estimators; wider availability of affordable cholesterol-lowering therapies which should include statins as essential medications globally; use of adequate doses of potent statin regimens; and combination therapies with ezetimibe or other therapies in order to attain and maintain robust reductions in LDL-C in those at highest risk. Continuing efforts are needed on health literacy for both the public and healthcare providers, utilising multi-disciplinary teams in healthcare and applications that quantify both ASCVD risk and benefits of treatment as well as increased adherence to therapies.
Conclusions: The adverse effects of LDL-cholesterol and apo B containing lipoprotein exposure are cumulative and result in ASCVD. These are preventable by implementation of different strategies, aimed at efficiently tackling atherosclerosis at different stages throughout the human life-course. Preventive strategies should therefore be updated to implement health policy, lifestyle changes and when needed pharmacotherapies earlier with investment in, and a shift in focus towards, early preventive strategies that preserve cardiovascular health rather than treat the consequences of ASCVD.
The "8 Pillars":
1. Atherosclerosis results from the retention of apolipoprotein B (apo B) containing lipoproteins mostly in the form of low- density lipoproteins (LDL) in the vessel wall. LDL cholesterol (LDL-C) is not only causal but a cumulative risk factor, over the lifespan, for ASCVD.
2. Individuals have differential retention of apo B containing lipoproteins and hence differential vulnerability to the effects of LDL-C exposure. Therefore, LDL-C and apo B should not be considered in isolation without considering other factors.
3. Most cardiovascular events occur among individuals without extreme elevations in LDL-C, hence global risk should be considered.
4. Extreme elevations in LDL-C from birth with a monogenic basis (familial hypercholesterolaemia) are more common than previously recognised and are prevalent across all regions of the world, and their consequences are largely preventable through early screening and treatment.
5. ASCVD can be reduced through reductions in LDL-C through multiple different pathways, with benefit reliably quantifiable and proportional to both the absolute reduction in LDL-C and the duration of that reduction, hence treatments could be interchanged or combined as needed.
6. As the majority of the total atherogenic cholesterol content (non-HDL-C) consists of LDL-C and as the majority of apo B containing lipoproteins are LDL particles, LDL-C reductions will provide largely predictable parallel proportional reductions in nonHDL-C and apo B.
7. The increasing prevalence of cardio-metabolic diseases such as obesity and diabetes has resulted in an increase in other lipid disorders which increase ASCVD risk. These are characterised by elevated triglyceride rich apo B containing lipoproteins which are atherogenic. Therefore, pragmatically moving towards estimation of atherogenic particle number in the form of apo B measurements with a single measure, or if this is not feasible, total atherogenic cholesterol content (non-HDL-C) may improve risk assessment and measures of benefit irrespective of therapeutic modality.
8. The recognition that elevations in lipoprotein (a) are common (but poorly detected) and are an independent causal risk factor of ASCVD.
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