Background: Sarpogrelate, a serotonin receptor blocker, increases collaterals via a platelet anti-aggregation effect and/or vasodilatation. However, a recent report showed a preconditioning effect of sarpogrelate that enhances the translocation of PKC-epsilon of cardiomyocytes, followed by opening of the mitochondrial K(ATP) channel via inhibition of serotonin release from platelets during ischemia, protecting against cellular injury in rabbit hearts without collaterals. The present study used a percutaneous coronary intervention (PCI) model to define the protective effect of sarpogrelate against ischemic injury and its mechanism in human coronary artery disease.
Methods and results: The study enrolled 20 patients with single vessel disease of 75% or 90% stenosis in the proximal left anterior descending (LAD) artery on coronary angiography (CAG). Patients were randomly divided into a control group (n=10) and a sarpogrelate group (n=10). The Delta STmax (maximum ST elevation) and Sigma ST (sum of ST elevation) on the 12-lead ECG recorded in the late stages (ie, 90 s and 120 s) after inflation were significantly smaller in the sarpogrelate group than in the controls. There was no significant difference in collaterals on the right and left CAG or between the 2 groups.
Conclusions: Sarpogrelate improves ischemic injury during PCI and may be related to a preconditioning-like mechanism rather than to stimulating collateral development.