Sunitinib and Atrial Trabeculae Contractility (SCAR)
Recently, sunitinib (a tyrosine kinase inhibitor that is used for treatment of metastatic renal carcinoma and gastrointestinal stroma tumors) has been associated with development of heart failure, possibly by off-target inhibition of AMP-protein kinase. The investigators hypothesize that sunitinib reduces the contractile ability of myocardium and the tolerance against ischemia-reperfusion and that activators of AMP-protein kinase such as atorvastatin and AICAR reverse this unwanted effect of sunitinib.
The primary objective of the study is to investigate the effect of sunitinib on ex-vivo atrial contractile force in absence and presence of ischemia-reperfusion.
A secondary objective is to explore if atorvastatin or AICAR prevent sunitinib-induced deterioration of contractile function of human atrial trabeculas. Study design: Lab
|Study Design:||Observational Model: Case-Only|
|Official Title:||The Influence of Sunitinib on Contractility of Human Atrial Trabeculae|
- Force [ Time Frame: 200 minutes ] [ Designated as safety issue: No ]The developed force in ex vivo atrial trabeculae during standardized stimulation.
- Speed [ Time Frame: 200 minutes ] [ Designated as safety issue: No ]The difference in averaged maximal speed of tension reduction during relaxation between two trabeculae
- Maximal Speed [ Time Frame: 210 minutes ] [ Designated as safety issue: No ]The difference in averaged maximal speed of tension development during contraction between two trabeculae.
Biospecimen Retention: None Retained
|Study Start Date:||November 2010|
|Study Completion Date:||April 2014|
|Primary Completion Date:||April 2014 (Final data collection date for primary outcome measure)|
Two trabeculas will be isolated and one will be exposed to sunitinib and the other to normal buffer solution. Both will be stimulated to contraction during 200 minutes.
With/without sunitinib IP
Two trabeculas will be isolated and one will be exposed to sunitinib and the other to normal buffer solution. Both will be stimulated to contraction and ischemia/reperfusion
Please refer to this study by its ClinicalTrials.gov identifier: NCT01246778
|Radboud University Nijmegen Medical Centre|
|Nijmegen, Netherlands, 6500HB|
|Principal Investigator:||G. A. Rongen||Radboud University|