Risk markers and primary prevention of cardiovascular disease
Absolute risk
- Absolute risk, not individual risk factors, drives treatment
- Treating one abnormal number in isolation both over- and under-treats
- Australian model: 5-year CVD risk from the Australian CVD risk calculator
| 5-yr risk | Category |
|---|---|
| <5% | Low |
| 5 to <10% | Intermediate |
| >=10% | High |
Burden and priority groups
- CVD remains a leading cause of death and DALYs in Australia
- Aboriginal and Torres Strait Islander Australians - CVD earlier and more severe
- Risk assessment from age 30, vs 45 in the general population
- General population assessment 45-79 yrs
- Age dominates every risk equation - it is the largest single term
Modifiable risk factors
Modifiable
- Smoking, hypertension, inc LDL-C, diabetes, obesity, inactivity, diet, alcohol
Non-modifiable risk factors
Non-modifiable
- Age, male sex, family history of premature CVD, ethnicity
Risk enhancers - not in the equation
- CKD, familial hypercholesterolaemia, elevated Lp(a)
- Chronic inflammatory disease - RA, SLE, psoriasis, HIV
- Severe mental illness, socioeconomic disadvantage
- Pre-eclampsia, gestational diabetes
Mechanism
- inc circulating LDL particles
- -> subendothelial retention and oxidation
- -> monocyte recruitment, foam cell formation
- -> fibrous cap over a lipid core
- -> inflammation thins the cap -> rupture -> thrombosis
- LDL is causal, and the exposure is cumulative (mmol/L x years)
Assessment
- BP, lipids, HbA1c or glucose, eGFR + ACR, smoking status, family history
High risk without calculating
High risk without calculating
- Known CVD
- eGFR <45, or CKD with significant albuminuria
- Familial hypercholesterolaemia
- SBP >=180 or DBP >=110 mmHg
- Total cholesterol >7.5 mmol/L
Coronary artery calcium score
- Use to reclassify intermediate risk when the treatment decision is genuinely uncertain
- Asymptomatic adults ~45-75 with intermediate risk
- CAC = 0 -> very low 10-yr event rate
- Measures plaque burden, not stenosis - it does not diagnose obstructive CAD
- Not for low-risk screening, and not for monitoring on statins - calcium increases as plaque stabilises
Low risk (<5%)
- Lifestyle; reassess every 5 years
Intermediate (5 to <10%)
- Intensive lifestyle; reassess in 2 years
- Consider CAC score, or start a statin if risk enhancers present
High (>=10%)
- Lifestyle + BP-lowering + lipid-lowering, started together
- Statin first line; add ezetimibe if target not reached
Lifestyle - every category
- Smoking cessation - the single largest gain
- Mediterranean-style diet, 150 min/wk activity, weight, alcohol, salt reduction
Secondary prevention - established CVD
- Aspirin + high-intensity statin + BP control in everyone
- LDL-C target <1.8 mmol/L
- ESC/EAS set <1.4 mmol/L plus >=50% reduction for very-high-risk patients - lower than current Australian practice
- Escalate: ezetimibe, then PCSK9 inhibitor (PBS criteria apply)
- Post-MI: beta blocker and ACEi/ARB, especially if EF impaired
- Cardiac rehabilitation
- *No benefit: CCBs for secondary prevention post-MI. Class I antiarrhythmics are harmful*
Aspirin in primary prevention
- Not routine - bleeding offsets benefit (ASPREE, ARRIVE, ASCEND)
Associated conditions
- Diabetes, CKD, obesity, metabolic syndrome, OSA
- Familial hypercholesterolaemia, elevated Lp(a)
- Chronic inflammatory disease - RA, SLE, psoriasis, HIV
- Severe mental illness, socioeconomic disadvantage
- Pre-eclampsia and gestational diabetes - female-specific risk enhancers
Why prevention works
- Atherosclerosis begins in adolescence and is silent for decades
- First presentation is MI or sudden death in a large minority
- Benefit is proportional to absolute risk and to LDL reduction
- Each 1 mmol/L LDL reduction -> ~20-25% relative reduction in major vascular events
Monitor
- Lipids and BP at 6-12 weeks after any change, then annually
- Adherence - the commonest reason a target is not met
- HbA1c, renal function, smoking status
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