Implementation of a chest pain management service improves patient care and reduces length of stay

Objective Chest pain is one of the most common complaints in patients presenting to an emergency department. Delays in management due to a lack of readily available objective tests to risk stratify patients with possible acute coronary syndromes can lead to an unnecessarily lengthy admission placing pressure on hospital beds or inappropriate discharge. The need for a co-ordinated system of clinical management based on enhanced communication between departments, timely and appropriate triage, clinical investigation, diagnosis, and treatment was identified. Methods An evidence-based Chest Pain Management Service and clinical pathway were developed and implemented, including the introduction of after-hours exercise stress testing. Results Between November 2005 and March 2013, 5662 patients were managed according to a Chest Pain Management pathway resulting in a reduction of 5181 admission nights by more timely identification of patients at low risk who could then be discharged. In addition, 1360 days were avoided in high-risk patients who received earlier diagnosis and treatment. Conclusions The creation of a Chest Pain Management pathway and the extended exercise stress testing service resulted in earlier discharge for low-risk patients; and timely treatment for patients with positive and equivocal exercise stress test results. This service demonstrated a significant saving in overnight admissions.

Change to costs and lengths of stay in the emergency department and the Brisbane protocol: An observational study

- Objective To compare health service cost and length of stay between a traditional and an accelerated diagnostic approach to assess acute coronary syndromes (ACS) among patients who presented to the emergency department (ED) of a large tertiary hospital in Australia. - Design, setting and participants This historically controlled study analysed data collected from two independent patient cohorts presenting to the ED with potential ACS. The first cohort of 938 patients was recruited in 2008–2010, and these patients were assessed using the traditional diagnostic approach detailed in the national guideline. The second cohort of 921 patients was recruited in 2011–2013 and was assessed with the accelerated diagnostic approach named the Brisbane protocol. The Brisbane protocol applied early serial troponin testing for patients at 0 and 2 h after presentation to ED, in comparison with 0 and 6 h testing in traditional assessment process. The Brisbane protocol also defined a low-risk group of patients in whom no objective testing was performed. A decision tree model was used to compare the expected cost and length of stay in hospital between two approaches. Probabilistic sensitivity analysis was used to account for model uncertainty. - Results Compared with the traditional diagnostic approach, the Brisbane protocol was associated with reduced expected cost of $1229 (95% CI −$1266 to $5122) and reduced expected length of stay of 26 h (95% CI −14 to 136 h). The Brisbane protocol allowed physicians to discharge a higher proportion of low-risk and intermediate-risk patients from ED within 4 h (72% vs 51%). Results from sensitivity analysis suggested the Brisbane protocol had a high chance of being cost-saving and time-saving. - Conclusions This study provides some evidence of cost savings from a decision to adopt the Brisbane protocol. Benefits would arise for the hospital and for patients and their families.

O peptídeo natriurético tipo B (BNP) como preditor de mortalidade a longo prazo em pacientes com síndrome coronariana aguda sem supradesnível do segmento ST

Fundamentos: Apesar dos conhecimentos adquiridos sobre marcadores preditores de mortalidade na síndrome coronariana aguda (SCA), a capacidade de avaliação a longo prazo permanece desconhecida. O peptídeo natriurético tipo B (BNP) tem sido extensamente utilizado, porém as evidências existentes se restringem ao seguimento de curto e médio prazos. Objetivos: Determinar se o BNP é um preditor independente de mortalidade por todas as causas a longo prazo em pacientes com síndrome coronariana aguda sem supradesnível do segmento ST (SCASSST). Métodos: No período de 1o de Janeiro de 2002 a 31 de Dezembro de 2003, foram selecionados 224 pacientes consecutivos atendidos na sala de emergência com SCASSST. A dosagem do BNP à admissão foi incorporada no protocolo diagnóstico, tendo o seu valor sido correlacionado com a mortalidade ao final do seguimento. Resultados: Os pacientes foram acompanhados por 9,34 anos (mediana), tinham 71,5 anos (intervalo IQ=60,5;79,0) e com predomínio do gênero masculino (62,9%). A hipertensão arterial esteve presente em 82,1% e o diabetes em 23,7%. A angina instável (AI) foi diagnosticada em 52,2% e o infarto agudo do miocárdio sem supradesnível do segmento ST (IAMSSST) em 47,8%. O BNP mediano foi de 81,9 pg/ml (intervalo IQ 22,2; 225). A mortalidade se correlacionou com os quartis crescentes do BNP: 14,3; 16,1; 48,2; e 73,2% (p<0,0001). A curva ROC determinou o BNP=100 pg/ml como o melhor ponto de corte, tendo apresentado área sobre a curva (AUC) de 0,79 (IC 95%=0,72-0,85) e sendo preditor de mortalidade ao final do seguimento: 17,3% vs. 65,0%, p<0,001, RR=3,76 (IC 95%=2,49-5,63). O BNP teve poder prognóstico tanto nos pacientes com (26,7 vs. 71,2%, p<0,001) como nos sem (12,9 vs. 56,8%, p<0,001) alteração da função ventricular, e também conforme o diagnóstico de AI (18,7 vs. 48,6%, p=0,001) e IAMSSST (14,9 vs. 75,0%, p<0,001). Na análise de regressão logística, a idade>72 anos (OR=3,79, IC 95%=1,62-8,86, p=0,002), o BNP≥100 pg/ml (OR=6,24, IC 95%=2,95-13,23, p<0,001) e a taxa de filtração glomerular estimada (TFGE)(OR=0,98, IC 95%=0,97-0,99, p=0.049) foram preditores independentes de mortalidade. Conclusões: O BNP dosado à admissão dos pacientes com SCASSST é um forte e independente preditor de mortalidade a longo prazo.

Investigation on acute biochemical effects of Ce(NO3)(3) on liver and kidney tissues by MAS H-1 NMR spectroscopic-based metabonontic approach

High resolution magic angle spinning (MAS)-H-1 nuclear magnetic resonance (NMR) spectroscopic-based metabonomic approach was applied to the investigation on the acute biochemical effects of Ce(No-3)(3). Male Wistar rats were administrated with various doses of Ce (NO3)(3)(2, 10, and 50 mg(.)kg(-1) body weight), and MAS H-1 NMR spectra of intact liver and kidney tissues were analyzed using principal component analysis to extract toxicity information. The biochemical effects of Ce (NO3)(3) were characterized by the increase of triglycerides and lactate and the decrease of glycogen in rat liver tissue, together with an elevation of the triglyceride level and a depletion of glycerophosphocholine and betaine in kidney tissues. The target lesions of Ce (NO3)(3) on liver and kidney were found by MAS NMR-based metabonomic method. This study demonstrates that the combination of MAS H-1 NMR and pattern recognition analysis can be an effective method for studies of biochemical effects of rare earths.

Pre-hospital body surface potential mapping improves early diagnosis of acute coronary artery occlusion in patients with ventricular fibrillation and cardiac arrest

Aims: To determine whether 80-lead body surface potential mapping (BSPM) improves detection of acute coronary artery occlusion in patients presenting with out-of-hospital cardiac arrest (OHCA) due to ventricular fibrillation (VF) and who survived to reach hospital. Methods and results: Of 645 consecutive patients with OHCA who were attended by the mobile coronary care unit, VF was the initial rhythm in 168 patients. Eighty patients survived initial resuscitation, 59 of these having had BSPM and 12-lead ECG post-return of spontaneous circulation (ROSC) and in 35 patients (age 69±13 yrs; 60% male) coronary angiography performed within 24. h post-ROSC. Of these, 26 (74%) patients had an acutely occluded coronary artery (TIMI flow grade [TFG] 0/1) at angiography. Twelve-lead ECG criteria showed ST-segment elevation (STE) myocardial infarction (STEMI) using Minnesota 9-2 criteria - sensitivity 19%, specificity 100%; ST-segment depression (STD) =0.05. mV in =2 contiguous leads - sensitivity 23%, specificity 89%; and, combination of STEMI or STD criteria - sensitivity 46%, specificity 100%. BSPM STE occurred in 23 (66%) patients. For the diagnosis of TFG 0/1 in a main coronary artery, BSPM STE had sensitivity 88% and specificity 100% (c-statistic 0.94), with STE occurring most commonly in either the posterior, right ventricular or high right anterior territories. Conclusion: Among OHCA patients presenting with VF and who survived resuscitation to reach hospital, post-resuscitation BSPM STE identifies acute coronary occlusion with sensitivity 88% and specificity 100% (c-statistic 0.94). © 2012 Elsevier Ireland Ltd.

Favorable effect on acute and chronic graft-versus-host disease with cyclophosphamide and in vivo anti-CD52 monoclonal antibodies for marrow transplantation from HLA-identical sibling donors for acquired aplastic anemia

Between August 1989 and November 2003, 33 patients at our center with acquired aplastic anemia underwent bone marrow transplantation (BMT) from HLA-identical sibling donors with cyclophosphamide and in vivo anti-CD52 monoclonal antibodies (MoAb) for conditioning. The median age at BMT was 17 years (range, 4-46 years). Before BMT, 58% were heavily transfused (>50 transfusions), and 42% had previously experienced treatment failure with antithymocyte globulin-based immunosuppressive therapy. Unmanipulated bone marrow was used as the source of stem cells in all patients except 1. Graft-versus-host disease (GVHD) prophylaxis was with cyclosporine alone in 19 (58%) patients; 14 received anti-CD52 MoAb in addition to cyclosporine. The conditioning regimen was well tolerated without significant acute toxicity. Graft failure was seen in 8 patients (primary, n = 4; secondary, n = 4). Of those whose grafts failed, 4 survived long-term (complete autologous recovery, n = 2; rescue with previously stored marrow, n = 1; second allograft, n = 1). The cumulative incidence of graft failure and grade II to IV acute and chronic GVHD was 24%, 14%, and 4%, respectively. None developed extensive chronic GVHD. With a median follow-up of 59 months, the 5-year survival was 81% (95% confidence interval, 68%-96%). No unexpected early or late infectious or noninfectious complications were observed. We conclude that the conditioning regimen containing cyclophosphamide and anti-CD52 MoAb is well tolerated and effective for acquired aplastic anemia with HLA-matched sibling donors. The favorable effect on the incidence and severity of GVHD is noteworthy in this study and warrants further investigation.

Special issue on the 6th Portuguese Conference on Automatic Control (Controlo 2004)

The Portuguese Association of Automatic Control (APCA) organizes, every two years, the Portuguese Conference on Automatic Control. Its 6th edition (Controlo 2004) was held from 7 to 9 June, 2004 at the University of Algarve, Faro, Portugal, by its Centre for Intelligent Systems (CSI). CONTROLO 2004 International Program Committee (IPC) has decided, from the very start, to ask for submission of full draft papers, to encourage special sessions with well-defined themes, and for student papers. All papers have been reviewed by three separate reviewers. From the 122 contributions submitted, the IPC selected 89 oral papers, 20 special session papers, and 5 student posters. CONTROLO 2004 Technical Programme consists of 33 oral sessions (5 being special sessions) and 1 poster session, covering a broad range of control topics, both from theory and applications. The programme also includes three plenary lectures, given by leading experts in the field, Professors Ricardo Sanz, João Miranda Lemos and Rolf Isermann.

Rôles physiopathologiques du complément dans le syndrome coronarien aigu et implications thérapeutiques

Les efforts investis pour diminuer les risques de développer un infarctus du myocarde sont nombreux. Aujourd’hui les médecins prennent connaissance des divers facteurs de risque connus prédisposant aux syndromes coronariens aigus (SCA) dans le but de prendre en charge les patients «à risque» [1]. Bien que le suivi rigoureux et le contrôle de certains facteurs de risque modifiables aient permis une meilleure gestion des cas de SCA, les cas d’infarctus persistent de manière encore trop fréquente dans le monde. Puisque d’importantes études ont démontré que les SCA pouvaient survenir sans même la présence des facteurs de risque conventionnels [2, 3], les chercheurs se sont penchés sur un autre mécanisme potentiellement responsable de l’avènement des SCA : l’inflammation. L’inflammation joue un rôle prépondérant dans l’initiation, la progression et les complications de l’athérosclérose [4, 5] mais aussi dans les situations post-infarctus [6, 7]. Au cours des dernières années, le contrôle du processus inflammatoire est devenu une cible de choix dans la prévention et le traitement des SCA. Cependant, malgré les efforts investis, aucun de ces traitements ne s’est avéré pleinement efficace dans l’atteinte du but ultime visé par une diminution de l’inflammation : la diminution de la mortalité. Le complément est un système complexe reconnu principalement pour son rôle primordial dans l’immunité [2]. Cependant, lorsqu’il est activé de manière inappropriée ou excessive, il peut être à l’origine de nombreux dommages cellulaires caractéristiques de plusieurs pathologies inflammatoires dont font partie les complications de l’athérosclérose et des événements post-infarctus. Le travail effectué dans le cadre de mon doctorat vise à établir les rôles physiopathologiques du complément dans les interactions de l’axe thrombose-inflammation caractéristiques des SCA dans le but ultime d’identifier des cibles thérapeutiques permettant le développement de nouvelles approches pour la prévention et le traitement de ces pathologies. Les principaux résultats obtenus durant mon cursus suggèrent d’abord que la voie alterne du complément peut représenter une cible thérapeutique de choix dans les maladies coronariennes aiguës puisque l’activation terminale du complément semble y être principalement causée par l’activation du cette voie. De faibles niveaux sériques de MBL (mannan-binding lectin) et une activation terminale négligeable du complément caractérisent plutôt la maladie coronarienne stable. En comparant l’activité relative de chacune des voies du complément chez des cohortes de patients traités ou non par un anticorps spécifique à la protéine C5 du complément (pexelizumab), un second volet démontre quant à lui qu’une inhibition de l’activation du C5 n’a pas d’effet bénéfique majeur sur l’inhibition de la formation du complexe sC5b-9 ou sur les événements cliniques subséquents. Par conséquent, nous avons exploré, à l’aide d’un modèle in vitro, les raisons de l’inefficacité du traitement. Les résultats révèlent que le blocage du C5 avec le pexelizumab inhibe la production de l’anaphylatoxine pro-inflammatoire C5a et du complexe terminal du complément sans toutefois avoir d’effet sur l’apoptose des cellules endothéliales produites induite par le sérum des patients atteints de STEMI. Finalement, une autre section stipule que l’atorvastatine diminue l’activation du complément induite par les plaquettes sanguines chez des patients hypercholestérolémiques, mettant en évidence l’importance du rôle de cette statine dans la réduction des effets délétères de l’activation du système du complément médié par les plaquettes. Ensemble, l’étude du rôle spécifique des différentes voies d’activation du complément dans des contextes pathologiques variés, l’analyse des effets d’une inhibition spécifique de la protéine C5 du complément dans la progression des SCA et la mise en évidence des interactions entre l’activation du complément et les plaquettes activées ont contribué au développement d’une meilleure connaissance des rôles physiopathologiques du complément dans la progression de la maladie coronarienne.