Dyslipidaemia of Obesity, Metabolic Syndrome and Type 2 Diabetes Mellitus: the Case for Residual Risk Reduction After Statin Treatment
Vasilios G Athyros 1
, *, Konstantinos Tziomalos 2, Asterios Karagiannis 1, Dimitri P Mikhailidis 2
1 Second Propedeutic Department of Internal Medicine, Aristotle University, Hippocration Hospital, Thessaloniki, Greece
2 Department of Clinical Biochemistry (Vascular Prevention Clinic) and Department of Surgery, Royal Free Hospital Campus, University College Medical School, University College London (UCL), London, UK
Dyslipidaemia is frequently present in obesity, metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM). The predominant features of dyslipidaemia in these disorders include increased flux of free fatty acids (FFA), raised triglyceride (TG) and low high density lipoprotein cholesterol (HDL-C) levels, a predominance of small, dense (atherogenic) low density lipoprotein cholesterol (LDL) particles and raised apolipoprotein (apo) B values Posprandial hyperlipidaemia may also be present. Insulin resistance (IR) appears to play an important role in the pathogenesis of dyslipidaemia in obesity, MetS and T2DM. The cornerstone of treatment of this IR-related dyslipidaemia is lifestyle changes and in diabetic patients, tight glycaemic control. In addition to these measures, recent clinical trials showed benefit with statin treatment. Nevertheless, a substantial percentage of patients treated with statins still experience vascular events. This residual vascular risk needs to be addressed. This review summarizes the effects of hypolipidaemic drug combinations (including statins with cholesterol ester protein inhibitors, niacin, fibrates or fish oil, as well as fibrate-ezetimibe combination) on the residual vascular risk in patients with obesity, MetS or T2DM.
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* Address correspondence to this author at the Atherosclerosis and Metabolic Syndrome Units, Second Propedeutic Department of Internal Medicine, Aristotle University, Hippocration Hospital, Thessaloniki, 55 132, Greece; Tel: +30 2310 454 237; Fax: +30 2310 445 220; E-mail: email@example.com