Acute coronary syndrome and transient global amnesia with sumatriptan.

Triptans are potent serotoninergic vasoconstrictors. They are generally avoided in elderly patients age greater than 65 or in patients with a history of CAD. Although there are reported cases of Acute Coronary Syndrome (ACS) or Transient Global Amnesia (TGA) in patients after ingesting therapeutic doses of triptan or dihydroergotamine, this is the first case report, up to our knowledge, of a patient, who had no previous cardiac history, that was diagnosed with both ACS and TGA. A 59-year-old woman with a long-standing history of migraine, gastroesophageal reflux disease, and hypothyroidism, presented to the Emergency Department (ED) complaining of amnesia, chest pain, and left arm numbness after ingesting a single dose of oral sumatriptan approximately 1-2 h prior to arrival. She had no recollection of the events that occurred after taking sumatriptan. No acute laboratory abnormalities were found except for an elevated troponin, which continued to trend upwards. Her EKG had no ST-T wave abnormalities. She was diagnosed with Acute Coronary Syndrome (ACS), non-ST elevation MI. She had a negative noncontrast CT head. Neurology was consulted for her amnesia and diagnosed her with Transient Global Amnesia (TGA). They recommended discontinuing sumatriptan and beginning topiramate as a prophylactic therapy. There is an increasing number of reports delineating sumatriptan's adverse effects. Emergency medicine physicians should promptly recognize the toxic effects and adverse reactions from triptans. Sumatriptan-induced vasoconstriction may lead to cardiac and cerebral ischemic events.

Statin decreases endothelial microparticle release from human coronary artery endothelial cells: implication for the Rho-kinase pathway.

OBJECTIVE: Elevated plasma levels of endothelial microparticles (EMPs) are associated with the presence of clinical atherosclerosis. Considering the anti-inflammatory properties of HMG-CoA reductase inhibitors on the endothelium, we studied the effect of fluvastatin on the release of EMPs in cultured human coronary artery endothelial cells (HCAEC). METHODS AND RESULTS: EMPs were generated in TNF-alpha-activated HCAECs. The absolute number of EMPs was enumerated using a novel two-color flow cytometric immunostaining technique with TruCount beads as an internal reference. EMPs are defined as EC membrane vesicles (1-2 microm in size) with a characteristic immunophenotype. The addition of fluvastatin to TNF-alpha-activated HCAECs significantly suppressed EMP release. Fluvastatin suppressed TNF-alpha-induced Rho activation. The Rho-kinase inhibitor, Y-27632, reproduced the effect of statin. CONCLUSION: EMP release from TNF-alpha-activated HCAECs is suppressed by fluvastatin. In addition, the Rho/Rho-kinase may play an important role in modulating EMP release.

Erythropoietin protects cardiac myocytes from hypoxia-induced apoptosis through an Akt-dependent pathway.

Apoptosis is a contributing cause of myocyte loss in ischemic heart disease. Recent work has shown that erythropoietin (EPO) offers protection against apoptosis in a wide variety of tissues. We demonstrate that the erythropoietin receptor (EPOR) is expressed in the neonatal rat ventricular myocyte (NRVM). Exposure of NRVMs to hypoxia, with recombinant human EPO, significantly decreased apoptosis as measured by TUNEL, flow cytometry, and caspase 3/7 like activity when compared to hypoxia treatment alone. EPO administered at the initiation of coronary artery occlusion in the rat significantly decreased apoptosis in the myocardial ischemic region. In the NRVM, EPO increased the activity of Akt. The anti-apoptotic effect of EPO was abrogated by co-treatment with LY294002, a specific blocker of phosphatidylinositol 3-kinase (PI3-K). Our study demonstrates that EPO inhibits apoptosis in the NRVM exposed to hypoxia, through an Akt-dependent pathway. EPO also inhibits apoptosis in the in vivo rat model of myocardial ischemia.