Reducing micro- and macrovascular residual vascular risk (RvR) is an unmet need of cardiovascular risk management. All known modifiable risk factors should be targeted from the outset in a given individual. Standards of care advise multifactorial intervention to achieve recommended levels of low-density lipoprotein cholesterol (LDL-C), blood pressure and glycaemic control in diabetes. Reducing RvR linked to LDL-C could be achieved with statins, bempedoic acid, ezetimibe or anti-PCSK9 monoclonal antibodies/ASO/siRNAs, the latter also reducing lipoprotein(a). Even in patients with controlled LDL-C, RvR linked to remnant cholesterol (RC) needs to be considered, with novel agents aimed at key components of atherogenic dyslipidaemia (AD) and triglycerides (TG)-rich lipoproteins metabolism, such as anti-apoC3 and anti-ANGPTL3. Targeting AD and/or RC in type 2 diabetes mellitus (T2DM), in addition to intensive LDL-C reduction, may provide additional macrovascular benefit when coupled with a decrease in non-high-density lipoprotein cholesterol (HDL-C), as shown in subgroups analyses of landmark fibrate trials. In contrast, there has been little progress in reducing residual microvascular risk beyond tight glycaemic control, except for the benefits of fenofibrate, whose mechanisms have yet to be determined. Another unmet need in reducing RvR of diabetic microvascular disease is the current lack of a validated risk calculator for predicting incident microangiopathy in diabetic patients.

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How to Evaluate and Reduce Micro- and/or Macrovascular Residual Risk?

  • Michel P. Hermans,
  • Fabian O. Lurquin,
  • Sylvie A. Ahn,
  • Michel F. Rousseau

摘要

Reducing micro- and macrovascular residual vascular risk (RvR) is an unmet need of cardiovascular risk management. All known modifiable risk factors should be targeted from the outset in a given individual. Standards of care advise multifactorial intervention to achieve recommended levels of low-density lipoprotein cholesterol (LDL-C), blood pressure and glycaemic control in diabetes. Reducing RvR linked to LDL-C could be achieved with statins, bempedoic acid, ezetimibe or anti-PCSK9 monoclonal antibodies/ASO/siRNAs, the latter also reducing lipoprotein(a). Even in patients with controlled LDL-C, RvR linked to remnant cholesterol (RC) needs to be considered, with novel agents aimed at key components of atherogenic dyslipidaemia (AD) and triglycerides (TG)-rich lipoproteins metabolism, such as anti-apoC3 and anti-ANGPTL3. Targeting AD and/or RC in type 2 diabetes mellitus (T2DM), in addition to intensive LDL-C reduction, may provide additional macrovascular benefit when coupled with a decrease in non-high-density lipoprotein cholesterol (HDL-C), as shown in subgroups analyses of landmark fibrate trials. In contrast, there has been little progress in reducing residual microvascular risk beyond tight glycaemic control, except for the benefits of fenofibrate, whose mechanisms have yet to be determined. Another unmet need in reducing RvR of diabetic microvascular disease is the current lack of a validated risk calculator for predicting incident microangiopathy in diabetic patients.