Clopidogrel effect on platelet reactivity in patients with stent thrombosis: results of the CREST Study.

OBJECTIVES: We investigated whether patients who suffered subacute stent thrombosis (SAT) have higher post-treatment reactivity than those who do not encounter stent thrombosis. BACKGROUND: High post-treatment platelet reactivity has been reported after coronary stenting after clopidogrel therapy and may be an important factor in the occurrence of SAT. METHODS: We identified patients with SAT treated at two tertiary care centers over a 1.5-year period. Light transmittance aggregation induced by adenosine diphosphate (ADP) and arachidonic acid, total and activated glycoprotein (GP) IIb/IIIa after stimulation with ADP, and vasodilator-stimulated phosphoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and compared with an age-matched group of patients without SAT (n = 100). High post-treatment platelet reactivity was defined as >75th percentile ADP-induced aggregation in the group without SAT. RESULTS: The SAT patients had higher mean platelet reactivity than those without SAT by all measurements (p < 0.05): 49 +/- 4% versus 33 +/- 2% for 5 micromol/l ADP-induced aggregation and 65 +/- 3% versus 51 +/- 2% for 20 micromol/l ADP-induced aggregation (p < 0.001), 69 +/- 5% versus 46 +/- 9% for P2Y12 reactivity ratio (p = 0.03), and 138 +/- 19 mean fluorescence intensity (MFI) versus 42 +/- 4 MFI for stimulated GP IIb/IIIa expression (p < 0.001). Of patients with SAT, 60% had high platelet reactivity. CONCLUSIONS: High post-treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT. Measures to uniformly determine platelet reactivity after coronary stenting and treatment strategies to improve P2Y12 receptor inhibition in patients with high post-treatment platelet reactivity should be further investigated.

The possible role of uric acid in renal hyper-echogenicity in neonatal hypoxic acute shock.

Sonographic examinations as well as blood and urine chemistry tests were carried out in 4 neonates (3 mature, 1 premature) with transient renal failure, who were suffering from the effects of neonatal asphyxia of varying etiology. The first ultrasound examinations of the kidneys were performed within 24 hours after the hypoxic event. Simultaneously, blood and urine tests for parameters of renal function and purine metabolites were also carried out. Transient insufficiency of renal function could be detected in all cases with hyper-uricemia and hyper-uricosuria with no hypercalciuria. Ultrasonographic examinations showed hyper-echogenicity of the renal pyramids in all of the cases and hyper-reflectivity of the renal cortex in cases 2 and 4. In 3 cases, hyper-echogenicity appeared within 24 hours and disappeared in a short time, while in case 3 it could be detected from day 4 until day 14. These findings demonstrate, that the neonatal kidney is very sensitive to hypoxia and that hypoxic renal failure is accompanied by hyper-echogenicity of the kidneys. Uric acid is a possible cause of the renal hyper-echogenicity.