Background Cardiogenic shock complicates 5-10% of myocardial infarction (MI) cases. Data about the benefit of glycoprotein IIb/IIIa inhibitors (GPI) in these patients is sparse and conflicting. ...Methods We performed a systematic review, meta-analysis, and meta-regression of studies assessing the impact of GPI use in the setting of MI complicated cardiogenic shock on mortality, angiographic success, and bleeding events. We systematically searched for studies comparing GPI use as adjunctive treatment versus standard care in this setting. Random-effects meta-analysis and meta-regression were performed. Results Seven studies with a total of 1216 patients (GPI group, 720 patients; standard care group, 496 patients) were included. GPI were associated with a 45% relative reduction in the odds of death at 30 days (pooled OR 0.55; 95% CI 0.35-0.85; I.sup.2 = 57%; P = 0.007) and a 49% reduction in the odds of death at 1 year (pooled OR 0.51; 95% CI 0.32-0.82; I.sup.2 = 58%; P = 0.005). Reduction in short-term mortality seemed to be more important before 2000, as this benefit disappears if only the more recent studies are analyzed. GPI were associated with a 2-fold increase in the probability of achieving TIMI 3 flow (pooled OR, 2.05; 95% CI 1.37-3.05; I.sup.2 = 37%, P = 0.0004). Major bleeding events were not increased with GPI therapy (pooled OR, 1.0; 95% CI 0.55-1.83; I.sup.2 = 1%, P = 0.99). Meta-regression identified that patients not receiving an intra-aortic balloon pump seemed to benefit the most from GPI use (Z = - 1.57, P = 0.005). Conclusion GPI therapy as an adjunct to standard treatment in cardiogenic shock was associated with better outcomes, including both short- and long-term survival, without increasing the risk of bleeding. Keywords: Glycoprotein IIb/IIIa inhibitors, Abciximab, Eptifibatid, Cardiogenic shock
Les inhibiteurs de la glycoprotéine IIb/IIIa (anti-GPIIbIIIa) préviennent l’agrégation plaquettaire en empêchant leur liaison au fibrinogène. La thrombopénie est un effet secondaire connu, ...habituellement transitoire.
Un patient de 71 ans présentait une thrombopénie brutale et profonde après administration de tirofiban (anti-GPIIbIIIa). Les transfusions plaquettaires étaient peu efficaces et la persistance d’une thrombopénie sévère à j10 faisait indiquer une corticothérapie. Celle-ci permettait une correction progressive de la thrombopénie en faveur d’un mécanisme immunologique.
Les différents anti-GPIIbIIIa sont associés à un risque de thrombopénie d’installation brutale. Le mécanisme est mal compris. La gestion de ces thrombopénies, le plus souvent très transitoires, repose sur l’administration de concentrés plaquettaires. Rarement, un mécanisme immunologique peut être associé à une thrombopénie persistante qui peut répondre à une corticothérapie.
Glycoprotein IIb/IIIa inhibitors (anti-GPIIbIIIa) prevent platelet binding to fibrinogen. Transient sometimes-severe thrombocytopenia is a well-known side effect.
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.
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.
We studied the pharmacokinetic and pharmacodynamic properties or integrelin, a novel platelet glycoprotein IIb/IIIa receptor inhibitor, in patients undergoing elective percutaneous coronary ...intervention. Patients were randomized to placebo (n = 19) or to 1 of 4 integrelin dosing regimens (total n = 54) that were studied sequentially. All patients received aspirin and heparin. Patients were followed until discharge for the occurrence of adverse clinical events: death, myocardial infarction, coronary artery bypass surgery, repeat intervention, or recurrent ischemia. Bleeding was the primary safety end point. Frequent blood sampling was performed for adenosine diphosphate-induced platelet aggregations. Simplate bleeding times were performed. Adverse clinical events occurred less often in the integrelin-treated patients, although the overall numbers were too small to make a definitive statement as to clinical efficacy. There was no significant increase in serious bleeding among integrelin-treated patients. The 2 highest inregrelin boluses (180 and 135 gmg/kg) immediately (15 minutes after the bolus) provided >80% inhibition of adenosine diphosphate-induced platelet aggregation in >75% of treated patients. A constant inregrelin infusion of 0.75 μg/kg/min maintained this marked antiplatelet effect, whereas an infusion of 0.50 μg/kg/min allowed gradual recovery of platelet function. Elective coronary intervention was performed safely and with no significant increase in serious bleeding events using inregrelin with aspirin and heparin as an antithrombotic regimen. Integrelin provided rapid, intense, and persistent ex vivo platelet inhibition during coronary intervention. This new antiplatelet agent may be beneficial in reducing platelet-mediated ischemic complications of percutaneous coronary intervention.
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