Myocardial infarction due to late stent thrombosis following epileptic convulsive seizures.

We report the first case in the literature of acute myocardial infarction due to very late (5 years) drug-eluting stent (DES) thrombosis presenting with inferior ST-elevation myocardial infarction immediately after epileptic convulsive seizures in a patient with known coronary artery disease. A bare-metal stent had been implanted in the left anterior descending coronary artery in 2002, and a drug-eluting stent implanted in the right coronary artery in 2003. We discuss the possible pathogenetic mechanisms implied in convulsive epileptic crisis resulting in development of very late DES thrombosis.

Recurrent very late drug-eluting stent thrombosis.

In-stent thrombosis is a severe and potentially fatal event. The incidence of this pathological process does not differ significantly after implantation of either bare metal or drug-eluting stents (DESs) in the first month after intervention, but stent thrombosis (ST) continues to occur over a long period of time after implantation of DESs, a phenomenon known as late and very late ST. Multiple predictors of late ST have been identified, and among others, patient's adherence to medical therapy as well as an optimal interventional technique of stent implantation emerge as crucial variables. Scarce data is available about the occurrence of recurrent very late ST. We report three cases of recurrent very late thrombosis of first generation DESs in middle-aged patients with different degrees of coronary artery disease, presenting with acute myocardial infarction.

Inflammation and platelet activation in peripheral arterial occlusive disease.

OBJECTIVES: Epidemiological evidence indicates that inflammation accompanies the progression of atherosclerosis. The aim of the present cross-sectional study was to define relationships between platelet activation and inflammation in patients with mild to severe (stages II to IV) peripheral arterial occlusive disease (PAOD) and matched controls. The effect of chronic administration of low-dose acetylsalicylic acid was investigated. METHODS: Subjects were studied on a single occasion. C-reactive protein (CRP) and two indexes of in vivo platelet activation were measured - the urinary excretion of 11-dehydrothromboxane (TX) B(2) by immunoassay and circulating platelet-monocyte aggregates (PMAs) by flow cytometry. RESULTS: Plasma PMAs and urinary 11-dehydro-TXB(2) were significantly increased in PAOD patients compared with controls (P<0.01 for all). A positive correlation between 11-dehydro-TXB(2) and CRP was found in the study population (r(s)=0.63, P<0.001). Using logistic regression analysis, CRP was the only independent correlate of 11-dehydro-TXB(2) (ß(CRP)=11.9, P<0.01), whereas only the presence of PAOD was an independent predictor of high PMA levels (ß(PAOD)=13.7, P=0.001). Chronic administration of acetylsalicylic acid reduced 11-dehydro-TXB(2), but not PMA and CRP. CONCLUSIONS: There is evidence that platelet activation in patients with PAOD is related to the vascular disease and is dependent on the severity of inflammation.