TY  - JOUR
A1  - Fruchart, Jean-Charles
A1  - Davignon, Jean
A1  - Hermans, Michael P.
A1  - Al-Rubeaan, Khalid
A1  - Amarenco, Pierre
A1  - Assmann, Gerd
A1  - Barter, Philip
A1  - Betteridge, John
A1  - Bruckert, Eric
A1  - Cuevas, Ada
A1  - Farnier, Michel
A1  - Ferrannini, Ele
A1  - Fioretto, Paola
A1  - Genest, Jacques
A1  - Ginsberg, Henry N.
A1  - Gotto Jr., Antonio M.
A1  - Hu, Dayi
A1  - Kadowaki, Takashi
A1  - Kodama, Tatsuhiko
A1  - Krempf, Michel
A1  - Matsuzawa, Yuji
A1  - Núñez-Cortés, Jesús Millán
A1  - Monfil, Calos Calvo
A1  - Ogawa, Hisao
A1  - Plutzky, Jorge
A1  - Rader, Daniel J.
A1  - Sadikot, Shaukat
A1  - Santos, Raul D.
A1  - Shlyakhto, Evgeny
A1  - Sritara, Piyamitr
A1  - Sy, Rody
A1  - Tall, Alan
A1  - Tan, Chee Eng
A1  - Tokgözoğlu, Lale
A1  - Toth, Peter P.
A1  - Valensi, Paul
A1  - Wanner, Christoph
A1  - Zambon, Albertro
A1  - Zhu, Junren
A1  - Zimmet, Paul
T1  - Residual macrovascular risk in 2013: what have we learned?
JF  - Cardiovascual Diabetology
N2  - Cardiovascular disease poses a major challenge for the 21st century, exacerbated by the pandemics of obesity, metabolic syndrome and type 2 diabetes. While best standards of care, including high-dose statins, can ameliorate the risk of vascular complications, patients remain at high risk of cardiovascular events. The Residual Risk Reduction Initiative (R(3)i) has previously highlighted atherogenic dyslipidaemia, defined as the imbalance between proatherogenic triglyceride-rich apolipoprotein B-containing-lipoproteins and antiatherogenic apolipoprotein A-I-lipoproteins (as in high-density lipoprotein, HDL), as an important modifiable contributor to lipid-related residual cardiovascular risk, especially in insulin-resistant conditions. As part of its mission to improve awareness and clinical management of atherogenic dyslipidaemia, the R(3)i has identified three key priorities for action: i) to improve recognition of atherogenic dyslipidaemia in patients at high cardiometabolic risk with or without diabetes; ii) to improve implementation and adherence to guideline-based therapies; and iii) to improve therapeutic strategies for managing atherogenic dyslipidaemia. The R(3)i believes that monitoring of non-HDL cholesterol provides a simple, practical tool for treatment decisions regarding the management of lipid-related residual cardiovascular risk. Addition of a fibrate, niacin (North and South America), omega-3 fatty acids or ezetimibe are all options for combination with a statin to further reduce non-HDL cholesterol, although lacking in hard evidence for cardiovascular outcome benefits. Several emerging treatments may offer promise. These include the next generation peroxisome proliferator-activated receptor alpha agonists, cholesteryl ester transfer protein inhibitors and monoclonal antibody therapy targeting proprotein convertase subtilisin/kexin type 9. However, long-term outcomes and safety data are clearly needed. In conclusion, the R(3)i believes that ongoing trials with these novel treatments may help to define the optimal management of atherogenic dyslipidaemia to reduce the clinical and socioeconomic burden of residual cardiovascular risk.
KW  - phospholipid fatty acids
KW  - term fenofibrate therapy
KW  - cardiovascular munster procam
KW  - residual cardiovascular risk
KW  - atherogenic dyslipidaemia
KW  - type 2 diabetes
KW  - therapeutic options
KW  - high denisty lipoprotein
KW  - randomized controlled-trial
KW  - coronary artery disease
KW  - type-2 diabetes mellitus
KW  - triglyceride-rich lipoproteins
KW  - alpha/delta agonist GFT505
KW  - placebo-controlled trial
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-117546
SN  - 1475-2840
VL  - 13
IS  - 26
ER  -