Effects of Simvastatin Alone Versus Fenofibrate Alone Versus Simvastatin Plus Fenofibrate on Lipoprotein Subparticle Profiles in Patients With Diabetes Mellitus and Mixed Dyslipidemia

Athyros, Vasilios G.; Kakafika, AI; Karagiannis, Asterios; Mikhailidis, DP

doi:10.1016/j.amjcard.2008.02.087

Cited by 2 publications

(2 citation statements)

References 8 publications

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“…Glycaemic control appears to improve but does not normalize these abnormalities [146]. Statin or fibrate monotherapy can improve the lipid profile in patients with T2DM; however, they affect different aspects of lipoprotein metabolism [147-149]. Hence, it is difficult to normalize all lipid abnormalities in patients with T2DM using monotherapy with either a statin or a fibrate [114].…”

Section: Treatmentmentioning

confidence: 99%

Dyslipidaemia of Obesity, Metabolic Syndrome and Type 2 Diabetes Mellitus: the Case for Residual Risk Reduction After Statin Treatment

Athyros¹

2011

TOCMJ

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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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Section: Treatmentmentioning

confidence: 99%

Dyslipidaemia of Obesity, Metabolic Syndrome and Type 2 Diabetes Mellitus: the Case for Residual Risk Reduction After Statin Treatment

Athyros¹

2011

TOCMJ

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“…Additional reductions in lipid and lipoprotein concentrations were observed in statin/ fenofibrate combination therapy, in comparison to statin monotherapy. [149][150][151][152][153][154][155][156][157][158][159][160][161][162][163] Also, the combination therapy reduced inflammatory markers including fibrinogen, high-sensitivity C reactive protein, and plasminogen activator inhibitor-1 levels; 156,158 and improved postprandial endothelial dysfunction. 145 As seen in Table 1, eight randomized double-blind efficacy studies using simvastatin/fenofibrate combination therapy were compared to statins alone.…”

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confidence: 99%

Simvastatin/fenofibrate combination in the treatment of dyslipidemia: current evidence

Jiménez-Montero¹,

Haft²

2014

RRED

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Background: It has been demonstrated that statins can reduce major cardiovascular complications throughout a broad range of patients with dyslipidemia and multiple cardiovascular risk. Despite the impact of statin therapy on cardiovascular morbidity and mortality, a residual cardiovascular risk remains following lowering of low-density lipoprotein cholesterol. In many patients, optimization of the lipid profile cannot be achieved with statin therapy. Therefore, pharmacologic interventions with non-statin therapy can be used. Aims: The objective of this review was to analyze current clinical evidence of the effects of simvastatin/fenofibrate combination therapy. Methods: We searched and analyzed the evidence up to June 2014, regarding the effects of statin/fibrate combination therapy for reducing cardiovascular complications. Results: Forty-nine studies reporting the efficacy and safety of statin/fibrate combination therapy were analyzed. Of the forty-nine, 19 analyzed the simvastatin/fenofibrate combination therapy. This therapy was demonstrated to be safe and superior to the statin monotherapy in modifying atherogenic dyslipidemia, including lipoprotein subclasses. Nevertheless, in randomized clinical trials cardiovascular endpoints were not significantly different when fenofibrate was added to a standard low-density lipoprotein cholesterol reducing therapy. Of note, in the subgroup analysis, positive results were observed in patients with high triglycerides and low high-density lipoproteins. The inclusion of heterogeneous populations in these studies may explain the mixed results of cardiovascular outcomes seen in randomized clinical trials. Conclusion: Future clinical studies that rigorously address the effects of simvastatin/ fenofibrate in patients with triglycerides .2.25 mmol/L and high density lipoprotein cholesterol ,0.90 mmol/L, will provide a more accurate conclusion regarding the use of simvastatin/ fenofibrate combination therapy. For now, emphasis must be put on non-pharmacological interventions that effectively induce weight loss and strict glycemic control in diabetics. The initiation of simvastatin/fenofibrate combination therapy among patients with residual cardiovascular risk should be employed at the physician's discretion, as this strategy lacks hard cardiovascular end points.

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Effects of Simvastatin Alone Versus Fenofibrate Alone Versus Simvastatin Plus Fenofibrate on Lipoprotein Subparticle Profiles in Patients With Diabetes Mellitus and Mixed Dyslipidemia

Cited by 2 publications

References 8 publications

Dyslipidaemia of Obesity, Metabolic Syndrome and Type 2 Diabetes Mellitus: the Case for Residual Risk Reduction After Statin Treatment

Dyslipidaemia of Obesity, Metabolic Syndrome and Type 2 Diabetes Mellitus: the Case for Residual Risk Reduction After Statin Treatment

Simvastatin/fenofibrate combination in the treatment of dyslipidemia: current evidence

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