http://circinterventions.ahajournals.org/content/10/9/e005805?etoc=
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- Editorials
- heart failure
- percutaneous coronary intervention
- renal artery obstruction
- ST elevation myocardial infarction
Ischemia
of organs, including that of the heart, kidney, and brain, account for
major morbidity and mortality in the United States. When an organ is
ischemic, the logical approach is to relieve the ischemia by
re-establishing blood flow as is accomplished by percutaneous
interventions, such as angioplasty and placing a stent in an occluded
coronary artery or occluded renal artery. However, even after
establishing patency of the large obstructed blood vessel, a degree of
organ damage may persist because of reperfusion injury.1
In the heart, this may manifest as reperfusion arrhythmias, stunned
myocardium (postischemic left ventricular dysfunction), and no reflow or
microvascular obstruction. Whether reperfusion actually kills
myocardial cells remains debatable. In the kidneys, reperfusion injury
may manifest as microvascular damage, loss of glomerular filtration, and
damage because of reactive oxygen species that includes loss of
cortical structure. It has been postulated that abrupt reperfusion
results in reactive oxygen species production by the mitochondria,
opening of the mitochondrial permeability transition pore, an influx of
calcium into the mitochondria, release of cytochrome C, and peroxidation
of cardiolipin in the inner mitochondrial membrane.2
Certainly, angioplasty/stenting for renal artery stenosis alone for the
treatment of hypertension has been disappointing in its effect on major
adverse clinical outcomes.3
Most patients need to remain on medical therapies, and there is limited
evidence of preservation of renal function. One potential explanation is
that reperfusion injury has contributed to the disappointing outcomes.
See Article by Saad et al
Numerous therapies have been tested in preclinical models to try to reduce ischemia/reperfusion injury.4
In the setting of clinical ST-elevation–myocardial infarction (STEMI),
various adjunctive agents have been tried along with reperfusion to
further reduce myocardial infarct size and limit ischemia/reperfusion
injury. Although many of these therapies showed promise in preclinical
studies, most did not work …
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