Lipid Therapy and Age

Role of Age (≥70 years)

  • Advanced age substantially increases cardiovascular risk
  • SCORE2 (and SCORE2-OP) already classify individuals ≥70 years into higher risk categories
  • Age + plaques = cumulative risk increase

High Risk vs Very High Risk

Clinical constellation

ESC/EAS risk category

Carotid plaques without symptoms

High risk

Carotid plaques + additional risk factors (e.g., diabetes, CKD, smoking)

Very high risk

Carotid plaques + prior stroke/TIA

Very high risk (secondary prevention)

Therapeutic Consequences

LDL-C Targets According to ESC/EAS

Risk category

LDL-C target

High risk

<70 mg/dL and ≥50% reduction

Very high risk

<55 mg/dL and ≥50% reduction

Statin therapy is indicated even at advanced age, provided there are no contraindications.

Important Clarification Regarding Age

Age ≥75–80 years is not a contraindication to statin therapy.

The ESC/EAS emphasize:

  • Benefit persists even in advanced age
  • Decisions should be individualized (frailty, life expectancy, polypharmacy)
  • Start with a low dose and titrate upward if appropriate

Core Message

A patient >70 years with carotid plaques is at least high risk according to ESC/EAS; with additional risk factors (CAD, hypertension, smoking, etc.), the patient is very high risk.

This results in a clear indication for LDL-lowering therapy with a high-potency statin at plaque-stabilizing doses
(e.g., rosuvastatin ≥20 mg, atorvastatin ≥40 mg).

ESC/EAS guidelines do not recommend age-based discontinuation, but rather an individualized, target-oriented approach.

Monitoring & Re-evaluation

  • Tolerability is more important than dose
  • CK only if muscle symptoms occur
  • ALT/AST at baseline and after dose changes
  • Regular re-evaluation of:
    • Functional status
    • Therapeutic goals
    • Patient preferences

Risk classification is not primarily age-based, but driven by evidence of atherosclerotic vascular disease.

Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal. 2020;41(1):111–188. doi:10.1093/eurheartj/ehz455.

Carotid Plaques

  1. Significance of Carotid Plaques
  • Carotid plaques are considered clinical evidence of subclinical atherosclerosis
  • They are independent predictors of:
    • Myocardial infarction
    • Stroke
    • Cardiovascular death

Thus, they fulfill a high-risk criterion per se.

Plaque / “Carotid Atherosclerosis” (Ultrasound, Vessel Wall Finding)

In population-based ultrasound studies, prevalence in the 75–84-year age group is approximately 75–85%:

  • Men: 76.5%
  • Women: 81.2%

(Definition: carotid atherosclerosis/plaques on B-mode ultrasound)

Practical implication:
In individuals >75 years, carotid plaques are the rule rather than the exception when actively assessed.

Stenosis

Prevalence is much lower, as most plaques do not cause high-grade luminal narrowing:

  • ≥50% stenosis: typically several percent up to ~10% (population- and risk-profile dependent; increases with age)
  • ≥70% stenosis (severe asymptomatic): approximately 0.1–3.1% in the general population (age-dependent)

A plaque / “carotid atherosclerosis” detected on ultrasound (vessel wall finding) is an independent marker of systemic atherosclerosis and is considered a risk factor for coronary artery disease, myocardial infarction, and stroke.
Clinically, it justifies a higher cardiovascular risk classification, even if not explicitly included in many risk scores.

  1. Atherosclerosis Is a Systemic Disease
  • Carotid plaques serve as a surrogate for coronary plaques
  • Frequent coexistence of:
    • Carotid plaques
    • Coronary plaques
    • Peripheral arterial disease

A plaque indicates that the patient has manifest atherosclerosis, even if still asymptomatic.

  1. Evidence Base (Simplified Key Messages)
  • Carotid plaques are stronger predictors of cardiovascular events than:
    • isolated intima–media thickness (IMT)
  • Associated with:
    • higher incidence of coronary artery disease
    • increased risk of myocardial infarction
    • increased overall cardiovascular risk

 The finding is not only locally relevant but systemically prognostic.

Consequences for Risk Stratification

Formally (Risk Scores)

  • Traditional scores (e.g., SCORE2) include:
    • age, sex, blood pressure, lipids, smoking
  • Carotid plaques are usually not directly incorporated

Clinically (Decisive)

A documented carotid plaque is considered a “risk modifier” and typically results in:

  • A higher risk category than suggested by the score alone
  • A more aggressive prevention strategy

Many guidelines essentially state:

Evidence of subclinical atherosclerosis = higher true risk than numerically estimated

Practical Consequences (Typical Scenario)

A patient with:

  • low to intermediate calculated risk
  • plus carotid plaque on ultrasound

is often classified as having:

  • high cardiovascular risk

with implications for:

  • stricter LDL targets
  • clearer statin indication
  • tighter blood pressure and lifestyle goals
  • more intensive follow-up strategies

 

References:

  1. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111–188. doi:10.1093/eurheartj/ehz455.
  2. SCORE2 working group and ESC Cardiovascular Risk Collaboration. SCORE2 risk prediction algorithms: revised models to estimate 10-year risk of cardiovascular disease in Europe. Eur Heart J. 2021;42(25):2439–2454. doi:10.1093/eurheartj/ehab309.
  3. SCORE2-OP working group and ESC Cardiovascular Risk Collaboration. SCORE2-OP risk prediction algorithms: estimating incident cardiovascular event risk in older persons in four geographical risk regions. Eur Heart J. 2021;42(25):2455–2467. doi:10.1093/eurheartj/ehab312.
  4. Inaba Y, Chen JA, Bergmann SR. Carotid plaque, compared with carotid intima-media thickness, more accurately predicts coronary artery disease events: a meta-analysis. Atherosclerosis. 2012;220(1):128–133. doi:10.1016/j.atherosclerosis.2011.06.044.
  5. Joakimsen O, Bønaa KH, Stensland-Bugge E, Jacobsen BK. Age and sex differences in the distribution and ultrasound morphology of carotid atherosclerosis: the Tromsø Study. Arterioscler Thromb Vasc Biol. 1999;19(12):3007–3013. doi:10.1161/01.ATV.19.12.3007.
  6. de Weerd M, Greving JP, Hedblad B, et al. Prevalence of asymptomatic carotid artery stenosis in the general population: an individual participant data meta-analysis. Stroke. 2010;41(6):1294–1297. doi:10.1161/STROKEAHA.110.581058.
  7. Johnsen SH, Mathiesen EB. Carotid plaque compared with intima-media thickness as a predictor of coronary and cerebrovascular disease. Curr Cardiovasc Risk Rep. 2009;3:21–27. doi:10.1007/s11886-009-0004-1.