Biomedical Engineering Reference
In-Depth Information
Treatment
Treatment for limiting restenosis is shown in Table
9.1
.
Role of NO in the Management of Coronary Restenosis
One of the major problems related to the percutaneous transluminal coronary
angioplasty technique is the renarrowing of the vessel, a phenomenon known as rest-
enosis. NO and nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to
play a role in this pathology. NO counteracts several mechanisms involved in the
restenotic process after coronary angioplasty. During restenosis, an impairment of
NO-dependent pathways may occur. NO mediates an antiproliferative effect on
smooth muscle cells, inhibition of leukocyte-vessel wall interactions, and platelet
aggregation and adhesion. Because these effects are mainly dose dependent,
NO-releasing drugs have to be applied at a high dose to have an effect on restenotic
mechanisms. The main problem with the use of conventional NO donors is that they
affect blood pressure and flow, and for these reasons, they cannot be used safely in
clinical practice. Various novel methods for NO delivery have been investigated
including use of modified NO donors, NO-releasing stents, and eNOS gene therapy.
Modified NO Donors
Treatment with the NO donor molsidomine at a high dose for 6 months after coro-
nary angioplasty has no effect on the angiographic restenosis rate. Due to the vaso-
dilating effect of NO, the anginal status improves slightly more in patients receiving
molsidomine.
Table 9.1
Treatment of restenosis
Pharmacological agents
ACE inhibitors
Anticoagulants and thrombolytics
Antioxidants: probucol
Antiplatelet agents
Calcium channel blockers
Cytotoxic drugs
Growth factor inhibitors
Inflammatory mediator inhibitors
Lipid lowering agents
Monoclonal antibody: abciximab
Nitric oxide (NO)-based therapies and combination of NO with carbon monoxide
Radiation
Antisense therapy
Gene therapy
Stents and other devices
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