Impact of heart failure on ischaemic preconditioning in humans

Stenotic lesions ultimately can cause ischemic events. Reperfusion therapy
(either pharmacologic, endovascular or surgical) is mandatory for salvage of
ischemic tissue. However, during reperfusion several deleterious events take
place causing further damage, commonly referred to as ischaemia
reperfusion(IR)-injury. A detrimental feature of IR-injury is endothelial
damage. A recent study found that advanced age is associated with a larger
decrease in endothelial function compared to young subjects, possibly through
the presence of an a priori lower endothelial function. Also heart failure is
associated with the presence of significant endothelial dysfunction. However,
no previous study examined whether heart failure is associated with a larger
decrease in endothelial function.
Ischaemic preconditioning (IPC) refers to the reduction of IR-injury induced by
brief (repeated) preceding periods of ischemia. Also the arterial endothelium
can be protected by IPC. Several studies performed in animals and humans have
demonstrated that the protective effects of IPC are attenuated with aging.
However, no previous study in humans examined whether the protective effects of
IPC on the endothelial function are preserved in heart failure.

To examine the impact of heart failure on the change in endothelial function in
response to ischaemia reperfusion injury. A secondary objective is to explore
the ability of ischaemic preconditioning to protect against the decrease in
endothelial function in heart failure.

cross-sectional observation

n/a

Non-invasive cuff occlusion is used to examine endothelial function (5-minute
ischaemia), apply ischaemic preconditioning (3 cycles of 5-minute ischaemia)
and produce the stimulus that induces ischaemia-reperfusion injury (20-minute
ischaemia). This repeated cuff inflation is non-invasive and not associated
with a health risk f or the subject. The volunteers will not benefit directly
from participating in this study.