Key result
Early risk factor control produces sustained CV benefits after treatment cessation, likely via epigenetic changes.
Why the study?
Does early and intensive control of cardiovascular risk factors produce a sustained beneficial legacy effect on cardiovascular outcomes?
Does early and intensive control of cardiovascular risk factors produce a sustained beneficial legacy effect on cardiovascular outcomes?
This review highlights that early and intensive control of cardiovascular risk factors provides sustained long-term benefits (legacy effect), reinforcing the 'sooner the better' clinical approach.
May support earlier intensive risk-factor control; extends legacy-effect concept beyond diabetes but remains hypothesis-generating pending RCTs.
In medicine, a legacy effect is defined as the sustained beneficial effect of a given treatment on disease outcomes, even after cessation of the intervention. Initially described in optimized control of diabetes, it was also observed in clinical trials exploring intensification strategies for other cardiovascular risk factors, such as hypertension or hypercholesterolemia. Mechanisms of legacy were particularly deciphered in diabetes, leading to the concept of metabolic memory. In a more discreet manner, other memory phenomena were also described in preclinical studies that demonstrated long-lasting deleterious effects of lipids or angiotensin II on vascular wall components. Interestingly, epigenetic changes and reactive oxygen species (ROS) appear to be common features of “memory” of the vascular wall.
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Pothen et al. (2021) conducted a review in Cardiovascular diseases and risk factors (diabetes, hypercholesterolemia, hypertension). Early and optimized control of cardiovascular risk factors vs. Conventional therapy or delayed intervention was evaluated on Sustained cardiovascular benefits (legacy effect). Early and optimized control of cardiovascular risk factors produces a sustained beneficial legacy effect on cardiovascular outcomes even after treatment cessation, likely mediated by epigenetic changes.
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