Affiliations: Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI, USA | Mount Sinai Heart, Mount Sinai School of Medicine, New York, NY, USA
Note: [] Corresponding author: Robert S. Rosenson, MD, Mount Sinai Heart, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029 6574, USA. Fax: +212 849 2674; E-mail:: robert.rosenson@mssm.edu
Abstract: Reperfusion injury and no-reflow phenomenon are known entities that contribute to persistent impairment in myocardial perfusion and regional myocardial dysfunction following restoration of epicardial coronary blood flow after a myocardial infarction. Following prolonged ischemia, oxidative stress and inflammation-mediated alterations in erythrocyte mechanics and microvascular architecture play a major role in ischemia/reperfusion injury and no-reflow phenomenon. An increase in red cell rigidity is an important rheological aspect of RBCs, which facilitates platelet aggregation with the subendothelium. Dipyridamole inhibits the reuptake of adenosine which causes platelet inhibition and vasodilatation. Dipyridamole improves microvascular function by increasing RBC deformability and reducing blood viscosity. In addition, it has anti-oxidant and anti-inflammatory properties that provide protection to the microvasculature. This review discusses the potential role for dipyridamole therapy in the treatment of microvascular dysfunction.
