919-8 High-speed Coronary Rotational Atherectomy. Are Angiographic Factors Predictive of Failure, Major Complications or Restenosis? A Multivariate Analysis

In order to determine if angiographic factors are predictive of Failure (F), Major Complications (Me) or Restenosis (R) after Rotational Atherectomy with Rotablator, 16 angiographic variables were analyzed in 243 coronary arteries of 228 patients using a multivariate logistic regression technique (quasi Newton method and maximal probability technique).F was defined as the impossibility to complete the procedure; MC as the occurrence of O-wave myocardial infarctiön, in-hospital death or the need for emergency bypass graft surgery; R as recurrent ischemia due to an angiographic reduction of the lumen of the culprit vessel within 6 months following the procedure.Angiographic variables analized were: 1: Vessel treated. 2: Type of obstruction (A-B-C Task Force AHA-ACC). 3: Lesion lenhgth. 4: Lesion eccentricity. 5: Lesion angulation. 6: Lesion calcification. 7: Ostial lesion. 8: Lesion at a bifurcation. 9: Restenosed lesion. 10: Preprocedural stenosis. 11’ Postatherectomy stenosis. 12: Final stenosis. 13: Difficult access. 14: Number of vessels diseased>70% (1 vessel/multiple vessels). 15: Ejection fraction (40%/>40%).16: Arterial diameter (<3 mm/>3 mm).Primary success rate was 95.5% (232/243 arteries) and MC rate was 1.7% (infarction 2 cases and coronary surgery 2 cases, no deaths were recorded). F occurred in 6 cases.None of the covariates analized was statistically significant for F or MC. R was observed in 28.3% of cases and was 1.86 times more likely in longer lesions (p<0.03) and 2.54 times more likely in non calcified lesions (p<0.04). When lesion length and the presence of calcium were associated in a logistic regression manner, the following was obtained:LengthCalciumRestenosis % probability<10mm+6.3%10-20 mm+11.1%>20mm+18.9%<10 mm-14.6%10-20 mm-24.2%>20mm-37.2Conclusions1) The angiographic variables considered were not prediclive of F or Me. 2) Restenosis ocurred more frequenlly in long and non calcified lesions

Differential Regional Immune Response in Chagas Disease

Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool of memory cells develops, providing long-term immunity to subsequent reinfection. The extent of infection and rate of pathogen clearance are thought to determine both the magnitude of cell expansion and the homeostatic contraction to a stable number of memory cells. This straight correlation between the kinetics of T cell response and the dynamics of lymphoid tissue cell numbers is a constant feature in acute infections yielded by pathogens that are cleared during the course of response. However, the regional dynamics of the immune response mounted against pathogens that are able to establish a persistent infection remain poorly understood. Herein we discuss the differential lymphocyte dynamics in distinct central and peripheral lymphoid organs following acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. While the thymus and mesenteric lymph nodes undergo a severe atrophy with massive lymphocyte depletion, the spleen and subcutaneous lymph nodes expand due to T and B cell activation/proliferation. These events are regulated by cytokines, as well as parasite-derived moieties. In this regard, identifying the molecular mechanisms underlying regional lymphocyte dynamics secondary to T. cruzi infection may hopefully contribute to the design of novel immune intervention strategies to control pathology in this infection