[Long-lasting thrombocytopenia induced by glycoprotein IIb/IIIa inhibitor]. / Thrombopénie sévère et prolongée induite par un inhibiteur de la glycoprotéine IIb/IIIa.

INTRODUCTION: Glycoprotein IIb/IIIa inhibitors (anti-GPIIbIIIa) prevent platelet binding to fibrinogen. Transient sometimes-severe thrombocytopenia is a well-known side effect. OBSERVATION: A 71-year-old patient presented severe thrombocytopenia after the administration of tirofiban (anti-GPIIbIIIa). Corticosteroid treatment was initiated at day 10 because of persistence of severe thrombocytopenia with poor platelet transfusion efficacy. Corticosteroid treatment led to platelet recovery evoking an immune mediated mechanism for thrombocytopenia. CONCLUSION: Anti-GPIIbIIIa are associated with a risk of dramatic thrombocytopenia. The underlying mechanism is poorly understood. The management of these usually transient thrombocytopenias is based on platelet transfusion. As report here, in some cases persistent thrombocytopenia can respond to corticosteroids.

[AS heterozygote hemoglobinopathy and coronary risk]. / Hémoglobinopathie hétérozygote AS et risque coronaire.

There have been several reports of vaso-occlusive events and sudden death in subjects with sickle cell trait. However, the precise mechanism underlying these episodes remains unclear. The clinical observations have been supported by in vitro studies in which haemoglobin AS (Hb AS) red cells showed abnormalities of their filterability, probably related to gelling or polymerisation of the Hb AS. These in vitro studies and reports in the literature of sickle-cell hearts led the authors to investigate the possible association between AS subject and coronary risk. The results of coronary angiography in 9 patients with Hb AS, paired with respect to the usual cardiovascular risk factors, were compared with those of 18 AA subjects. The number of patients who underwent coronary bypass surgery for three-vessel disease was much greater in the AS subjects. However, the difference was not statistically significant. This tendency of AS subjects to develop thrombosis and coronary artery disease requires further study with larger numbers of patients.

Genetic polymorphisms of the renin-angiotensin system and angiographic extent and severity of coronary artery disease: the CORGENE study.

Genetic polymorphisms of the renin-angiotensin system (RAS) have been associated with coronary artery disease (CAD) but no relation between these polymorphisms and coronary atherosclerosis has yet been systematically evaluated. The CORGENE study is a cross-sectional study involving 463 Caucasians who underwent standardized coronary angiography for established or suspected CAD [156 patients with a previous myocardial infarction (MI), 307 without MI]. Four angiographic scores assessing the extent and severity of the coronary lesions were obtained from a double visual analysis of each angiogram, arbitration being achieved by a quantitative measurement. Three different genotypes were analyzed: the angiotensin I-converting enzyme insertion/deletion (ACE I/D) polymorphism, the Met to Thr change at position 235 of the angiotensinogen gene (AGT M235T) and the A to C transition at position 1166 of the angiotensin II type-1 receptor gene (AT1R A1166C). No significant association was observed between these polymorphisms and the clinical characteristics of MI and non-MI subjects. While most classical risk factors were positively correlated with the angiographic scores, no significant relationship could be established with the three genotypes (r ranging from -0.08 to 0.05). Only one significant correlation was observed: between the presence of the AGT 235T allele and the extent of the coronary lesions (r = -0.19, P = 0.04) in patients with low-risk status. These overall results are not in favor of a role of these RAS genetic polymorphisms in the development of coronary atherosclerosis.