Issue Section:
 CardioPulse > Epidemiology, Prevention, and Health Care Policies

Globally, almost one-third of all deaths are caused by cardiovascular diseases (CVD), mainly related to atherosclerosis.1 At present, atherosclerotic CVD (ASCVD) is by far first treated once symptoms arise (infarction, stroke, etc.) or when the risk factors reach dangerously high levels. However, this late-stage treatment is unsustainable. Novel preventive approaches against ASCVD are urgently needed.

Atherosclerosis often develops from early in life and progresses silently for decades before manifesting clinically.2 This silent phase represents a grossly underused window of opportunity. Cumulative lifetime exposure to even moderate or ‘high-normal’ levels of risk factors like LDL-C or blood pressure significantly increases ASCVD risk.3,4 Thus, early control of LDL-C has a greater impact on reducing future ASCVD events compared to interventions initiated later in life.5 This urges a redefinition of ‘normal’ risk factor levels in primary prevention,6 particularly for young people.

Silent atherosclerosis burden (detected by imaging) has been shown to be independently associated with ischaemic events7 and with all-cause mortality.8 In the early stages, the progression of atherosclerosis can be halted or even regress or disappear if risk factors are controlled.4 This forms the basis for the concept of early detection—visualization—of atherosclerosis allowing early interventions as a novel means to reduce ASCVD.

At present, primary prevention of ASCVD is based on the calculation of the mid-term (10 years) risk of suffering a major CVD event. However, risk scores, e.g. SCORE-2,9 do not consider individuals below 40 years of age, and below the age of 50 years, almost only smoking men reach the recommended threshold for interventions,9 leaving the young population unprotected. This is relevant since young individuals are more vulnerable to risk factors in terms of silent atherosclerosis progression.4

The broad individual variability in the susceptibility to risk factors explains that risk calculators, such as SCORE-2, work better at the population than at individual level. Overall, there seems to be a strong rationale for directing ASCVD prophylactics against identified—visualized—atherosclerosis rather than against a sum of risk factors with variable impact between individuals for developing atherosclerosis.

Coronary calcium scoring is a well-validated surrogate of future CVD events, but calcification occurs in mid- or late stages of atherosclerosis making it less ideal for early detection. Vascular ultrasound (VUS) of peripheral arteries accurately detects early stages (i.e. small plaques) of atherosclerosis.10 Detection and quantification of atherosclerotic plaques, and not intima-media thickness (IMT) determination, in carotid and femoral arteries, is a very good surrogate marker for global plaque burden.10

(Wow, NOTHING SPECIFIC TO CURE atherosclerosis! Why did you title the article 'cure'? Bad research allowed by your mentors and senior researchers!)