This invention is a non-invasive treatment for myocardial infarctions.
Myocardial ischemia is a pathological state associated with coronary artery disease that results from reduced blood perfusion in the heart, leading to impaired oxygen supply to the heart. Current interventions for improving blood flow to damaged heart tissue are mostly invasive and high risk, including stent placement, coronary bypass surgery, angioplasty, and endarterectomy. This invention is a novel, non-invasive therapy for reducing tissue damaged caused by ischemia.
The inventors have discovered that heart disease may be treated with Apolipoprotein D (ApoD), a 169 residue, 29 kDa glycoprotein member of the lipocalin family that binds to several ligands, including progesterone and arachidonic acid, and is associated with HDL in plasma. It is expressed highly in nervous tissue and overexpressed in aging, neurological and psychiatric disorders. The inventors injected nontransgenic wild-type and homozygous null ApoD KO mice with 'empty' (control) or ApoD-encoding adenovirus (Ad). This experiment resulted in decreased relative infarct size (infarct areal area at risk) in ApoD overexpressors and increased size in ApoD KO mice indicating that tissue damage resulting from ischemia and ischemia/reperfusion stress can be treated by administering a prophylactic or therapeutic amount of ApoD. Furthermore, ApoD enhancements may treat other diseases, including but not limited to stroke, PAD, and surgery involving temporary disruption of blood flow (ischemia, e.g., kidney and liver surgeries). Lastly, testing for levels of ApoD would help determine the risk and severity of such diseases or surgeries in patients.
treatment for a number of diseases including myocardial ischemia