Residual vascular risk and the possibilities of therapy.

Czech version

Authors: V. Bláha
Published in: Kardiol Rev Int Med 2012, 14(3): 161-171
Category:

Overview

Residual cardiovascular risk can be defined as the residual risk of incident vascular events or progression of established vascular damage persisting in patients treated with current evidence-based recommended care including the risk that established from risk factors, such as dyslipidemia, characterized by low HDL-cholesterol, elevated triglycerides and apolipoprotein B, small dense LDL and sometimes also high lipoprotein(a), high blood pressure, and the risk related to emerging or newer risk factors. High residual risk is common in patients with metabolic syndrome, type 2 diabetes mellitus, insulinoresistance and abdominal obesity. Current evidence supports a causal association between elevated triglyceride-rich lipoproteins and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for triglyceride-rich lipoproteins and remnants, together with the epidemiological data suggestive of the association for circulating triglycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The concept clearly derives from intervention trials, mainly the statin trials, and there is a lot of debate about the residual risk conferred by other lipid components, in particular low levels of HDL cholesterol and high levels of triglycerides. A meta-analysis of 53 fibrates (16,802 subjects) and 30 niacin trials (4,749 subjects) revealed an average HDL-C increase of 10% with fibrates and 16% with niacin, a triglyceride decrease of 36% with fibrates and 20% with niacin, and a LDL-C decrease of 8% with fibrates and 14% with niacin. These lipid changes resulted in similar overall reductions in major coronary events evidenced by a 25% decrease with fibrates and 27% with niacin. The experts believe that therapeutic targeting of elevated triglycerides (≥ 1.7 mmol/L), a marker of triglyceride-rich lipoproteins and their remnants, and/or low HDL-C (< 1.0 mmol/L) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.

Keywords:
residual cardiovascular risk – metabolic syndrom – diabetes mellitus type 2 – aterogenic dyslipidaemia – statin – fibrate – niacin

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