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Objectives: In the treatment of acute myocardial infarction (MI), the time delay to achieve reperfusion of the infarction-related artery has been linked to survival rates. Primary or direct angioplasty has been found to be an excellent means of achieving reperfusion in acute ST-elevation MI compared to thrombolytic therapy in randomized trials. However, no mortality benefit of primary angioplasty over thrombolysis was observed in several registries, in which delays in performing primary angioplasty were longer. Our objectives were to evaluate the door-to-balloon time (DBT) in our institution and investigate its relationship with clinical and prognostic variables. Methods:We studied, retrospectively, 67 patients submitted to primary angioplasty, from January 1999 to November 2000. We divided our patient population into two groups. Group A (GA) included patients with DBT less than 120 min and group B (GB) patients with DBT greater or equal to 120 min. We evaluated several clinical variables, such as left ventricular ejection fraction (LVEF) on their first echocardiogram during hospitalization, admission Killip classification, in-hospital length of stay (LOS) and major cardiovascular events (MACE) during hospitalization and up to 6-month follow-up (in 23 patients). Results:The median DBT was 132 min and the mean was 165 min, with a standard deviation of 137 min for all the cases. We had 32 patients in the GA and 35 patients (52%) in the GB. We observed four in-hospital deaths, all in GB. The mean LVEF was 53.1 ± 9% in GA and 46.1 ± 13% in GB (P = 0.059). Admission Killip class greater than 1 was noted in three patients of each group. The in-hospital LOS was similar for both groups (GA = 8.35 ± 4 and GB = 8.33 ± 4 days; NS). In-hospital events occurred in eight patients of GA (25%) and seven patients of GB (20%; NS). Only five follow-up events occurred during the first 6 months, three events in GA patients and two in GB patients (NS). Conclusion:DBT greater than or equal to 2 h are common and in our population it occurred in more than half of the primary angioplasties. Greater than 2 h DBTs were associated with a trend to larger left ventricular dysfunction early after MI. Monitoring and measures to reduce DBT are crucial for the potential prognosis improvement offered by primary angioplasty and for the broadening of its use in the management of acute MI. P2Primary angioplasty versus streptokinase in elderly patients with acute myocardial infarction PF Leite, M Park, VS Kawabata, MS Barduco, S Timerman, LF Cardoso, JAF Ramires Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil Because only a few studies about acute myocardial infarction (AMI) include elderly patients, we compared outcomes of patients aged 70 years or older with AMI who underwent thrombolysis or primary angioplasty treatment. Methods:From April 1995 to June 1999, 64 patients within 12 h of symptom onset and no contraindications for thrombolytic therapy were randomized in two groups. Group I (32 patients, 20 men) sub...

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plays a critical role in the inflammatory response and, potentially, a polymorphism in IRAK1 may alter the immune response impacting clinical outcome. P2Gene expression and intracellular NF-κ κB activation after HMGB1 and LPS stimuli in neutrophils from septic patients E Silva, Introduction Neutrophils play a major role in sepsis-induced organ dysfunction, especially in the lung. HMGB1 has emerged as a late cytokine and is implicated in the perpetuation of inflammatory stimulus and organ dysfunction development as well. There are limited data about neutrophil response patterns to HMGB1 in septic patients, and whether those patterns could be different from those following LPS exposure. Objectives To evaluate the differences of gene expression and activation of NF-κB, Akt, and p38MAPK in blood neutrophils from septic patients exposed to HMGB1 and LPS; and to compare response patterns between blood neutrophils from patients and healthy volunteers. Methods Twenty-two sepsis-induced acute lung injury patients and 34 healthy volunteers were enrolled in this study. The primary clinical variables collected were the 28-day survival and the presence of shock at ICU admission. Peripheral blood was obtained and neutrophils were isolated by plasma-percoll gradients after dextran sedimentation of erythrocytes. Neutrophils were resuspended in RPMI and cultured with or without 1000 ng/ml rHMGB1 or with or without 100 ng/ml LPS for 15, 30, and 60 min. The electrophoretic mobility shift assay technique was used to measure the NF-κB translocation, while western blot analysis was used to determine Akt phosphorylation and an ELISA was used to determine p38MAPK phosphorylation. Microarray analysis was used to evaluate the neutrophil gene expression in unstimulated neutrophils and after either HMGB1 stimulus or LPS stimulus. P < 0.05 was considered significant. Results Although with some similarities, HMGB1 and LPS induced distinct patterns of gene expression in peripheral blood neutrophils from septic patients. A Venn diagram ( Fig. 1) displays genes upregulated greater than twofold that are both common and unique after both stimuli. Using functional ontology, the genes upregulated by both HMGB1 and LPS primarily consisted of cytokines, chemokines, coagulation-related proteins, phosphatases, and transcriptional regulators factors. Importantly, while HMGB1 induced an HMGB1-related gene downregulation, LPS did not induce any changes in HMGB1 gene expression in these patients. Regarding intracellular activation, both HMGB1 and LPS increased translocation of NF-κB and the phosphorylation of Akt and p38MAPK in neutrophils from septic patients. However, there were some differences in terms of the degree and kinetics of activation between neutrophils cultured with LPS and HMGB1 (Fig. 2). There are no important differences in terms of intracellular activation when we compared neutrophils from septic patients with those from volunteers. Finally, neither NF-κB translocation nor kinase phosphorylation was associated with sepsis severity. However...

Objectives To characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state model