In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Treating dyslipidemia. How aggressive should we be?

Cardiovascular Pharmacology and Pharmacotherapy

Case presentation slidesSlides from the presentations


Ulf Landmesser (Zürich, Switzerland) presented a 54-year old patient at very high risk of cardiovascular (CV) disease, who suffered from two acute coronary syndromes (ACS) in a very short time period (slide 1). This case opened the stage for a discussion about intensive statin therapy, really targeting low LDL cholesterol levels. Although the patient was already on simvastatin 20mg, his lipid levels were well above the cut-off for secondary prevention and therefore atorvastatin 80mg was started (slide 2). Indeed, the results from the PROVE-IT trial and other studies, as well as the CTT meta-analysis have clearly demonstrated that aggressively lowering LDL cholesterol with high dosage statins effectively cuts down hard endpoints following an ACS.

In addition, the number of patients suffering from life-threatening or at least worrying side-effects on high statin doses is low and acceptable in terms of benefit-risk ratio. Another interesting question that was raised following this presentation was whether in this patient, who also had low HDL and high triglyceride levels, additional therapy should be considered. Although it has been demonstrated that even with low LDL levels, reduced HDL concentration considerably increases risk, the jury is still out on this issue and data on combined lipid lowering strategies including other drugs (i.e.; extended-release niacin, ezetimibe, fibrates, daltetrapib) are awaited.

Switching from secondary to primary prevention, John Deanfield (London, UK) presented the history of a 45-year old man with multiple risk-factors but without overt disease yet (slide 3). Based on the characteristics of this relatively young subject, the issues of age on the one hand and short-term versus lifetime risk of CV disease were extensively covered. Prof. Deanfield first simulated the risk assessment that increased significantly by simply adding 10 years to the current age of the patient presented. Secondly, he rightfully pointed out that most scoring systems provide us with relatively short-term risk assessment (i.e.; 10 years), which is not very useful in younger patients, whereas lifetime CV risk really deserves to be addressed in future studies. In this way, rethinking the concept of CV risk will probably set the way to earlier treatment of risk factors and could also help in persuading patients to change their lifestyle. Finally, the fact of whether biomarkers and recently introduced imaging techniques could be of help in fine-tuning CV risk and decision making was addressed.

Finally, Prof. Ian Graham (Dublin, Ireland) summarized the recently updated European guidelines on CV prevention. He extensively went through the different issues that were raised during the case presentations and wrapped it up with a very useful mnemonic (4).




Treating dyslipidemia. How aggressive should we be?

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.