Lipid modification - CVD prevention
Aim
Modification of the blood lipid profile can reduce CVD risk.
Cardiovascular conditions caused by atherosclerosis
Coronary heart disease (including angina and myocardial infarction).
Stroke.
Transient ischaemic attack (TIA).
Peripheral arterial disease.
Lipid profile
High-density lipoprotein cholesterol (HDL-C) x
Non-HDL-cholesterol (non-HDL-C) y
Total cholesterol x + y
Triglycerides
A fasting sample is not needed.
Total cholesterol, non-HDL-C and triglycerides are important prognostic indicators of CVD events.
Non-HDL-C has replaced low-density lipoprotein cholesterol (LDL-C) as the primary target for reducing cardiovascular risk with lipid-modifying treatment.
HDL-C is inversely related to CV risk.
Elevated triglyceride levels (greater than 2.3 mmol/L), especially when HDL-C levels are low, is a risk factor for CVD and is independent of total cholesterol.
Extreme levels of triglycerides (greater than 20 mmol/L) are associated with pancreatitis and a high risk of morbidity and mortality.
A total cholesterol of more than 7.5 mmol/L and a family history of premature coronary heart disease — consider the possibility of familial hypercholesterolaemia.
A total cholesterol of more than 9.0 mmol/L, or non-HDL cholesterol concentration of more than 7.5 mmol/L— arrange for specialist assessment.
Primary prevention of CVD, high intensity statin e.g. atorvastatin 20 mg daily
Without the need for formal risk assessment
Age>40y with Type 1 diabetes with diabetes >10y OR nephropathy or other CVD risk factors.
Chronic kidney disease
Familial hypercholesterolaemia
Offer statin
All people with Type 1 diabetes
Aged ≥ 85y (particularly if at risk such as smoker or hypertensive etc)
Consider offering statin
Formal risk assessment (by QRISK 3)
Age ≤ 84y AND 10-year risk of developing CVD is ≥10% and lifestyle modification is ineffective or inappropriate.
Offer statin
Secondary prevention of CVD, atorvastatin 80 mg daily
Pre-existing CVD
history of MI, angina, stroke, TIA or peripheral arterial disease.
Baseline investigations before starting lipid modification therapy
A non-fasting lipid profile.
Liver function tests (transaminases).
Renal function, including estimated glomerular filtration rate.
HbA1c.
Creatine kinase (if the person has persistent generalized unexplained muscle pain).
Thyroid stimulating hormone
Aim of treatment
Measure Lipids, LFTs, U&Es [and CK only if symptomatic] in all people after 3 months of statin treatment. LFTs should be checked 3m and 12m after starting treatment.
Stop statin treatment if CK is five or more times the upper limit of normal.
Aim: to achieve greater than 40% reduction in baseline non-HDL-C levels.
If not achieved, consider
Compliance, Diet and lifestyle measures.
Increasing the dose of atorvastatin up to 80 mg
Consider ezetimibe AND atorvastatin if primary hypercholesterolaemia (seek specialist advice).
Secondary care treatment options
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor (alirocumab or evolocumab), alone or in combination with a statin and/or other lipid-lowering drugs for people with primary non-familial hypercholesterolaemia or mixed dyslipidaemia at:
High risk of CVD — only if LDL-C level is persistently above 4.0 mmol/L.
Very high risk of CVD— only if LDL-C level is persistently above 3.5 mmol/L
Management for primary and secondary prevention of CVD
Addressing other modifiable CVD risk factors, such as smoking and obesity and diabetes.
Identifying and managing secondary causes of dyslipidaemia (such as excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome).
Arranging follow-up to monitor for adverse effects and to review drug treatment.