Target lipid concentrations

Mach, 2020

Target lipid concentrations for patients taking lipid-modifying therapy are shown in Target lipid concentrations according to ASCVD risk estimate for patients taking lipid-modifying therapy. The recommended target lipid concentrations were previously based on indication (either primary or secondary prevention of atherosclerotic cardiovascular disease [ASCVD]); however, these have been modified and are now based on ASCVD risk estimation. Review target lipid concentrations in any patient who has been taking long-term lipid-modifying therapy, because the targets may have changed since the last assessment or initiation.

Note: Reconsider target lipid concentrations in patients who have been taking long-term lipid-modifying therapy—targets may have changed since the last assessment or initiation.

The low-density lipoprotein cholesterol (LDL-C) concentration is the primary target of lipid-modifying therapy. Although intervention studies have not been designed to determine lipid targets, clinical trials have shown a continuous relationship between the extent of lowering of LDL-C and a reduction in the number of cardiovascular events. This benefit has been demonstrated in randomised controlled trials of statins alone and in combination with either ezetimibe or a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor.

When triglycerides are significantly elevated, the non–high-density lipoprotein cholesterol (non–HDL-C) concentration may better reflect ASCVD risk (compared with LDL-C alone), because it includes atherogenic triglyceride-rich lipoproteins in addition to LDL-C. Although the non–HDL-C target has not been evaluated as extensively as the LDL-C target, it is a useful secondary target in patients with elevated triglycerides.

To assess the response to lipid-modifying therapy, recheck lipid concentrations around 6 weeks after starting or adjusting therapy¹.

Although efforts should be made to meet the recommended target lipid concentrations, in patients where this is difficult to achieve, movement towards these concentrations, even if they are not reached, is likely to be beneficial.

In some patients, lipid-lowering therapy achieves lipid concentrations lower than the target concentrations. The continuous relationship between the extent of LDL-C lowering and the reduction in cardiovascular events extends well below the target LDL-C concentrations (down to LDL-C concentrations of less than 0.2 mmol/L)Giugliano, 2017. These ultra-low LDL-C concentrations are not associated with any increase in adverse events. There is no clinical indication to reduce or stop lipid-lowering therapy in a patient who has reached a low LDL-C concentration.

Table 1. Target lipid concentrations according to ASCVD risk estimate for patients taking lipid-modifying therapy
[NB1]

Mach, 2020
Established ASCVD or very high ASCVD risk [NB2]
established ASCVD (CAD, stroke or TIA, PAD) unequivocal documented imaging findings of multivessel CAD greater than 50% stenosis, or disease in more than one vascular bed chronic kidney disease (eGFR less than 30 mL/min/1.73 m²) familial hypercholesterolaemia with atherosclerosis or another major risk factor diabetes with end-organ damage diabetes with at least 3 major risk factors [NB3] type 1 diabetes of early onset and duration of more than 20 years
LDL-C target	at least 50% reduction in LDL-C from baseline and less than 1.4 mmol/L, whichever is lowest
non–HDL-C target	less than 2.2 mmol/L
triglycerides target	less than 1.7 mmol/L
High ASCVD risk
LDL-C target	At least 50% reduction in LDL-C from baseline and less than 1.8 mmol/L, whichever is lowest
non–HDL-C target	less than 2.6 mmol/L
triglycerides target	less than 1.7 mmol/L
Intermediate ASCVD risk
LDL-C target	less than 2.6 mmol/L
non–HDL-C target	less than 3.4 mmol/L
triglycerides target	less than 2.0 mmol/L
Low ASCVD risk
LDL-C target	less than 3.0 mmol/L
non–HDL-C target	less than 3.8 mmol/L
triglycerides target	less than 2.0 mmol/L
Note: ASCVD = atherosclerotic cardiovascular disease; CAD = coronary artery disease; eGFR = estimated glomerular filtration rate; LDL-C = low-density lipoprotein cholesterol; non–HDL-C = non–high-density lipoprotein cholesterol; PAD = peripheral artery disease; TC = total cholesterol; TIA = transient ischaemic attack NB1: For advice on estimating ASCVD risk, see Atherosclerotic cardiovascular disease risk estimation . NB2: The 2019 European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines for the management of dyslipidaemias provide lipid targets according to ASCVD risk estimated using a European ASCVD risk calculator. This calculator includes an additional risk category of 'very high risk' for patients with specific risk factors. More aggressive lipid targets are recommended for this group. Although the 'very high risk' category is not included in the Aus CVD risk calculator, it is still appropriate to consider more aggressive lipid targets for patients with these risk factors. NB3: Major risk factors for atherosclerotic cardiovascular disease are diabetes, smoking, elevated blood pressure, dyslipidaemia and central obesityVisseren, 2021.

¹ Do not use coronary artery calcium scoring to assess the response to lipid-modifying therapy. While lipid-modifying therapy reduces the extent of atherosclerotic plaque, it may conversely increase the extent of plaque calcification.Return