Abstract

The term cardiometabolic disease encompasses a range of lifestyle-related conditions, including Metabolic syndrome (MetS) and type 2 diabetes (T2D), that are characterized by different combinations of cardiovascular (CV) risk factors, including dyslipidemia, abdominal obesity, hypertension, hyperglycemia/insulin resistance, and vascular inflammation. These risk factors individually and interdependently increase the risk of CV and cerebrovascular events, and represent one of the biggest health challenges worldwide today. CV diseases account for almost 50% of all deaths in Europe and around 30% of all deaths worldwide. Furthermore, the risk of CV death is increased twofold to fourfold in people with T2D. Whilst the clinical management of CV disease has improved in Western Europe, the pandemic of obesity and T2D reduces the impact of these gains. This, together with the growing, aging population, means the number of CV deaths is predicted to increase from 17.1 million worldwide in 2004 to 23.6 million in 2030. The recommended treatment for MetS is lifestyle change followed by treatment for the individual risk factors. Numerous studies have shown that lowering low-density lipoprotein-cholesterol (LDL-C) levels using statins can significantly reduce CV risk in people with and without T2D or MetS. However, the risk of major vascular events in those attaining the maximum levels of LDL-C-reduction is only reduced by around one-third, which leaves substantial residual risk. Recent studies suggest that low high-density lipoprotein-cholesterol (HDL-C) (<1 .0 mmol/l; 40 mg/dl) and high triglyceride levels (≥1.7 mmol/l; 150 mg/dl) are independent risk factors for CV disease and that the relationship between HDL-C and CV risk persists even when on-treatment LDL-C levels are low (<1.7 mmol/l; 70 mg/dl). European guidelines highlight the importance of reducing residual risk by targeting these risk factors in addition to LDL-C. This is particularly important in patients with T2D and MetS because obesity and high levels of glycated hemoglobin are directly related to low levels of HDL-C and high triglyceride. Although most statins have a similar low-density lipoprotein-lowering efficacy, differences in chemical structure and pharmacokinetic profile can lead to variations in pleiotropic effects (for example, high-density lipoprotein-elevating efficacy), adverse event profiles, and drug-drug interactions. The choice of statin should therefore depend on the needs of the individual patient. The following reviews will discuss the potential benefits of pitavastatin versus other statins in the treatment of patients with dyslipidemia and MetS or T2D, focusing on its effects on HDL-C quantity and quality, its potential impact on atherosclerosis and CV risk, and its metabolic characteristics that reduce the risk of drug interactions. Recent controversies surrounding the potentially diabetogenic effects of statins will also be discussed.

Highlights

  • According to the World Health Organization, 63% of the 57 million deaths in 2008 were due to noncommunicable diseases [1]

  • Most statins have similar effects on low-density lipoprotein-cholesterol (LDL-C) levels [27,28,29,30,31,32,33,34,35,36,37], differences in chemical structure and pharmacokinetic profile can lead to variations in pleiotropic effects, adverse event profiles and drug–drug interactions

  • The Action to Control Cardiovascular Risk in Diabetes (ACCORD) study found that the primary event rate was reduced from 17.3% to 12.4% in the subgroup of type 2 diabetes (T2D) patients with both low baseline levels of high-density lipoprotein (HDL)-C (≤34 mg/dl or 0.88 mol/l) and high baseline TG (≥204 mg/dl or ≥2.3 mmol/l) [52]

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Summary

Introduction

According to the World Health Organization, 63% of the 57 million deaths in 2008 were due to noncommunicable diseases [1]. This relationship remained true even after event rates were adjusted for other risk factors, including baseline levels of LDL-C (Figure 2) Consistent with this observation, a post hoc analysis of intravascular ultrasound data from 1,455 people in four prospective randomized clinical trials showed that statinassociated changes in HDL-C were inversely associated with the progression of coronary atherosclerosis even in patients with low levels of LDL-C [61]. Recent studies have shown that, in addition to elevating HDL levels, some lipid-lowering agents are associated with pleiotropic effects that improve HDL structure and function [47,49,66,67,68] This observation is supported by a recent study, in which pitavastatin was associated with significantly greater reductions in plaque volume per 1% increase in HDL-C than other statins (atorvastatin, pravastatin, rosuvastatin, simvastatin) [67]. The Supplement Editors declare that they have no competing interests

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