Dyslipidaemia

@article{Durrington2003Dyslipidaemia,
  title={Dyslipidaemia},
  author={Paul N. Durrington},
  journal={The Lancet},
  year={2003},
  volume={362},
  pages={717-731},
  url={https://api.semanticscholar.org/CorpusID:208792416}
}
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94 Citations
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94 Citations

Percutaneous Coronary Intervention in Familial Hypercholesterolemia Is Understudied

Familial hypercholesterolemia is reviewed, unanswered questions in the interventional management of FH patients are identified, and barriers and opportunities for answering these questions are explored.

Update on the clinical utility of fenofibrate in mixed dyslipidemias: mechanisms of action and rational prescribing

Fenofibrate exerts a favorable effect on the atherogenic lipid profile of mixed dyslipidemia and can effectively reduce cardiovascular disease in patients with mixed dysipidemia.

Ezetimibe plus fenofibrate: a new combination therapy for the management of mixed hyperlipidaemia?

The combination of ezetimibe plus fenofibrate is a new alternative to improve the overall atherogenic lipid profile of patients with mixed hyperlipidaemia, and this combination therapy seems particularly useful for patients with a poor response or intolerance to statin monotherapy.

Lipid Disorders and Cardiovascular Risk: A Comprehensive Analysis of Current Perspectives

This review thoroughly investigates the complex terrain of lipid abnormalities, providing a detailed comprehension of the mechanisms that contribute to atherogenic processes and critically assesses the effects of lifestyle changes and nutritional interventions on lipid homeostasis.

Apolipoprotein A5 and hypertriglyceridemia.

The most common reason for an increase in circulating triglycerides is increased hepatic secretion of VLDL, and more than one mechanism may be involved in the increased risk of CHD associated with increased serum triglycerides.

PCSK9 inhibition and inflammation: A narrative review.

Demystifying the management of hypertriglyceridaemia

Patients with hypertriglyceridaemia usually present with obesity, insulin resistance, hepatic steatosis, ectopic fat deposition, and diabetes mellitus, and patients with a diagnosis of genetic lipoprotein lipase deficiency might benefit from LPL gene replacement therapy.

Apolipoproteins in the discrimination of atherosclerotic burden and cardiac function in patients with stable coronary artery disease

To compare the performance of apolipoproteins and oxidized LDL against routine clinical lipid profiles in the discrimination of atherosclerotic burden and cardiac function in stable coronary artery disease patients, a large number of patients were diagnosed with CAD.

Familial Hypercholesterolemia: A Literature Review of the Pathophysiology and Current and Novel Treatments

The major cause of FH is a mutation in the LDLR gene while other causes include mutation in various genes like apolipoprotein B, proprotein convertase subtilisin/kexin type 9, LDLR adaptor protein 1 (LDLRAP 1).

Statin policy and target populations: evidence-based or evidence-biased?

The target populations for statin therapy in the various national and international recommendations are likely to vary considerably, particularly in primary prevention, and terms such as familial hyperlipidaemia, metabolic syndrome, etc. are defined.
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