Cardiovascular outcomes and their relationships to lipoprotein components in patients with and without chronic kidney disease: results from the IDEAL trial.
OBJECTIVE
In Incremental Decrease in Endpoints through Aggressive Lipid-lowering (IDEAL), we compared cardiovascular outcomes in patients with and without chronic kidney disease (CKD) (estimated glomerular filtration rate <60 mL min(-1) 1.73 m(-2)) and analysed relationships between lipoprotein components (LC) and major coronary events (MCE) and other cardiovascular (CV) events.


METHODS
Exploratory analysis of CV endpoints in a randomized trial comparing high dose of atorvastatin to usual dose of simvastatin on MCE.


METHODS
Patients with CKD were compared with the non-CKD patients. Cox regression models were used to study the relationships between on-treatment levels of LC and incident MCE.


RESULTS
Chronic kidney disease was strongly associated with cardiovascular end-points including total mortality. In patients with CKD, a significant benefit of high dose atorvastatin treatment was found for any CV events, stroke and peripheral artery disease, but not for MCE. However, all cardiovascular end-points except stroke and CV mortality were reduced in the non-CKD group. Differential changes in LC or relationships to LC could not explain the different treatment outcomes in MCE in the two groups.


CONCLUSIONS
Chronic kidney disease was a powerful risk factor for all cardiovascular end-points. The reason why the significant reductions achieved by high-dose statin treatment in most CV end-points in the non-CKD group were only in part matched by similar reductions in the CKD patients is not apparent. This difference did not result from differential changes in or relations to LC, but limited power may have increased the possibility of chance findings.
Holme
I
I
Oslo University Hospital, Ulleval, Centre of Preventive Medicine, Oslo, Norway. ingar.holme@nih.no
Fayyad
R
R
Faergeman
O
O
Kastelein
J J P
JJ
Olsson
A G
AG
Tikkanen
M J
MJ
Larsen
M L
ML
Lindahl
C
C
Holdaas
H
H
Pedersen
T R
TR
D000208:Acute Disease; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000097:blood* / Q000150:complications / Q000188:drug therapy / Q000401:mortality; D005260:Female; D005919:Glomerular Filtration Rate; D006323:Heart Arrest / Q000453:epidemiology / Q000517:prevention & control; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000453:epidemiology / Q000517:prevention & control; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use; D012044:Regression Analysis; D019821:Simvastatin / Q000627:therapeutic use
D000924:Anticholesteremic Agents; D015415:Biomarkers; D006538:Heptanoic Acids; D008074:Lipoproteins; D011758:Pyrroles; D000069059:Atorvastatin; D019821:Simvastatin