Dietary Fiber Modulates the Release of Gut Bacterial Products Preventing Cognitive Decline in an Alzheimer's Mouse Model.

Fiber intake is associated with a lower risk for Alzheimer´s disease (AD) in older adults. Intake of plant-based diets rich in soluble fiber promotes the production of short-chain fatty acids (SCFAs: butyrate, acetate, propionate) by gut bacteria. Butyrate administration has antiinflammatory actions, but propionate promotes neuroinflammation. In AD patients, gut microbiota dysbiosis is a common feature even in the prodromal stages of the disease. It is unclear whether the neuroprotective effects of fiber intake rely on gut microbiota modifications and specific actions of SCFAs in brain cells. Here, we show that restoration of the gut microbiota dysbiosis through the intake of soluble fiber resulted in lower propionate and higher butyrate production, reduced astrocyte activation and improved cognitive function in 6-month-old male APP/PS1 mice. The neuroprotective effects were lost in antibiotic-treated mice. Moreover, propionate promoted higher glycolysis and mitochondrial respiration in astrocytes, while butyrate induced a more quiescent metabolism. Therefore, fiber intake neuroprotective action depends on the modulation of butyrate/propionate production by gut bacteria. Our data further support and provide a mechanism to explain the beneficial effects of dietary interventions rich in soluble fiber to prevent dementia and AD. Fiber intake restored the concentration of propionate and butyrate by modulating the composition of gut microbiota in male transgenic (Tg) mice with Alzheimer´s disease. Gut dysbiosis was associated with intestinal damage and high propionate levels in control diet fed-Tg mice. Fiber-rich diet restored intestinal integrity and promoted the abundance of butyrate-producing bacteria. Butyrate concentration was associated with better cognitive performance in fiber-fed Tg mice. A fiber-rich diet may prevent the development of a dysbiotic microbiome and the related cognitive dysfunction in people at risk of developing Alzheimer´s disease.

Protective Effect of Tilia americana var. mexicana Against Kainic Acid-induced Damage in Brain, Liver, and Kidney: Behavioral and Biochemical Changes.

Tiliaamericana var. mexicana (Tilia) possesses anticonvulsant, antioxidant, neuroprotective, and hepatoprotective activities. The spectrum of anticonvulsant activity in status epilepticus models has not been sufficiently explored. We evaluated the effects of ethyl acetate (EAc), and methanol (ME) extracts on kainic acid (KA)-induced seizures by measuring rats'behavior (severity and latency) and lipoperoxidation in different brain areas (cerebellum, brain hemispheres, cortex, and medulla), kidneys, and liver. Male Wistar rats were administered KA (10 mg/kg, i.p.) after three days of pretreatment with Tilia extract (100 mg/kg). The EAc and ME Tilia extracts significantly decreased the severity of phase 1 and phase 2 seizures, respectively. The ME Tilia extract increased the latency to seizure (27 ± 2 min) compared to the control (13 ± 2 min). The ME and EAc Tilia extracts significantly prevented the increased lipid peroxidation caused by KA-induced seizures in the cerebellum, brain hemispheres, cortex, medulla, liver, and kidneys. The vehicle olive oil (OO) also showed anticonvulsant effects, decreasing the severity of seizures to phase 3 and lipoperoxidation levels in the cerebellum, brain hemispheres, cortex, medulla, liver, and kidneys. The anticonvulsant activity of Tilia is mediated by antioxidant effects in central and systemic areas that involve synergistic interactions among the chemical constituents of these extracts (glucosides of quercetin and kaempferol), while vehicle OO showed the same effects, probably due to its constituent oleuropein.

Exposure to Sub-Lethal Doses of Permethrin Is Associated with Neurotoxicity: Changes in Bioenergetics, Redox Markers, Neuroinflammation and Morphology.

Permethrin (PERM) is a member of the class I family of synthetic pyrethroids. Human use has shown that it affects different systems, with wide health dysfunctions. Our aim was to determine bioenergetics, neuroinflammation and morphology changes, as redox markers after subacute exposure to PERM in rats. We used MDA determination, protein carbonyl assay, mitochondrial O2 consumption, expression of pro-inflammatory cytokines and a deep histopathological analysis of the hippocampus. PERM (150 mg/kg and 300 mg/kg body weight/day, o.v.) increased lipoperoxidation and carbonylated proteins in a dose-dependent manner in the brain regions. The activities of antioxidant enzymes glutathione peroxidase, reductase, S-transferase, catalase, and superoxide dismutase showed an increase in all the different brain areas, with dose-dependent effects in the cerebellum. Cytokine profiles (IL-1ß, IL-6 and TNF-α) increased in a dose-dependent manner in different brain tissues. Exposure to 150 mg/kg of permethrin induced degenerated and/or dead neurons in the rat hippocampus and induced mitochondrial uncoupling and reduction of oxidative phosphorylation and significantly decreased the respiratory parameters state 3-associated respiration in complex I and II. PERM exposure at low doses induces reactive oxygen species production and imbalance in the enzymatic antioxidant system, increases gene expression of pro-inflammatory interleukins, and could lead to cell damage mediated by mitochondrial functional impairment.

Expression of VEGF- and tight junction-related proteins in the neocortical microvasculature of patients with drug-resistant temporal lobe epilepsy.

The blood-brain barrier (BBB) maintains the optimal microenvironment for brain function. Tight junctions (TJs) allow endothelial cells to adhere to each other, leading to the formation of a barrier that prevents the penetration of most molecules via transcellular routes. Evidence has indicated that seizure-induced vascular endothelial growth factor (VEGF) type 2 receptor (VEGFR-2) pathway activation weakens TJs, inducing vasodilatation and increasing vascular permeability and subsequent brain injury. The present study focused on investigating the expression levels of VEGF-related (VEGF-A and VEGFR-2) and TJ-related proteins (claudin-5, occludin and ZO-1) in the neocortical microvasculature of patients with drug-resistant temporal lobe epilepsy (TLE). The results obtained from hippocampal sclerosis TLE (HS-TLE) patients were compared with those obtained from patients with TLE secondary to lesions (lesion-TLE) and autopsy samples. The Western blotting and immunofluorescence results showed that VEGF-A and VEGFR-2 protein expression levels were increased in HS-TLE and lesion-TLE patients compared to autopsy group. On the other hand, claudin-5 expression was higher in HS-TLE patients and lesion-TLE patients than autopsies. The expression level of occludin and ZO-1 was decreased in HS-TLE patients. Our study described modifications to the integrity of the BBB that may contribute to the pathogenesis of TLE, in which the VEGF system may play an important role. We demonstrated that the same modifications were present in both HS-TLE and lesion-TLE patients, which suggests that seizures modify these systems and that they are not associated with the establishment of epilepsy.

Drug-Resistant Temporal Lobe Epilepsy Alters the Expression and Functional Coupling to Gαi/o Proteins of CB1 and CB2 Receptors in the Microvasculature of the Human Brain.

Cannabinoid receptors 1 and 2 (CB1 and CB2, respectively) play an important role in maintaining the integrity of the blood-brain barrier (BBB). On the other hand, BBB dysfunction is a common feature in drug-resistant epilepsy. The focus of the present study was to characterize protein expression levels and Gαi/o protein-induced activation by CB1 and CB2 receptors in the microvascular endothelial cells (MECs) isolated from the brain of patients with drug-resistant mesial temporal lobe epilepsy (DR-MTLE). MECs were isolated from the hippocampus and temporal neocortex of 12 patients with DR-MTLE and 12 non-epileptic autopsies. Immunofluorescence experiments were carried out to determine the localization of CB1 and CB2 receptors in the different cell elements of MECs. Protein expression levels of CB1 and CB2 receptors were determined by Western blot experiments. [35S]-GTPγS binding assay was used to evaluate the Gαi/o protein activation induced by specific agonists. Immunofluorescent double-labeling showed that CB1 and CB2 receptors colocalize with tight junction proteins (claudin-5, occludin, and zonula occludens-1), glial fibrillary acidic protein and platelet-derived growth factor receptor-ß. These results support that CB1 and CB2 receptors are expressed in the human isolated microvessels fragments consisting of MECs, astrocyte end feet, and pericytes. The hippocampal microvasculature of patients with DR-MTLE presented lower protein expression of CB1 and CB2 receptors (66 and 43%, respectively; p < 0.001). However, its Gαi/o protein activation was with high efficiency (CB1, 251%, p < 0.0008; CB2, 255%, p < 0.0001). Microvasculature of temporal neocortex presented protein overexpression of CB1 and CB2 receptors (35 and 41%, respectively; p < 0.01). Their coupled Gαi/o protein activation was with higher efficiency for CB1 receptors (103%, p < 0.006), but lower potency (p < 0.004) for CB2 receptors. The present study revealed opposite changes in the protein expression of CB1 and CB2 receptors when hippocampus (diminished expression of CB1 and CB2) and temporal neocortex (increased expression of CB1 and CB2) were compared. However, the exposure to specific CB1 and CB2 agonists results in high efficiency for activation of coupled Gαi/o proteins in the brain microvasculature of patients with DR-MTLE. CB1 and CB2 receptors with high efficiency could represent a therapeutic target to maintain the integrity of the BBB in patients with DR-MTLE.

Dose-Dependent Behavioral and Antioxidant Effects of Quercetin and Methanolic and Acetonic Extracts from Heterotheca inuloides on Several Rat Tissues following Kainic Acid-Induced Status Epilepticus.

Kainic acid (KA) has been used to study the neurotoxicity induced after status epilepticus (SE) due to activation of excitatory amino acids with neuronal damage. Medicinal plants can protect against damage caused by KA-induced SE; in particular, organic extracts of Heterotheca inuloides and its metabolite quercetin display antioxidant activity and act as hepatoprotective agents. However, it is unknown whether these properties can protect against the hyperexcitability underlying the damage caused by KA-induced SE. Our aim was to study the protective effects (with regard to behavior and antioxidant activity) of administration of natural products methanolic (ME) and acetonic (AE) extracts and quercetin (Q) from H. inuloides at doses of 30 mg/kg (ME30, AE30, and Q30 groups), 100 mg/kg (ME100, AE100, and Q100 groups), and 300 mg/kg (ME300, AE300, and Q300 groups) against damage in brain regions of male Wistar rats treated with KA. We found dose-dependent effects on behavioral and biochemical studies in the all-natural product groups vs. the control group, with decreases in seizure severity (Racine's scale) and increases in seizure latency (p < 0.05 in the ME100, AE100, Q100, and Q300 groups and p < 0.01 in the AE300 and ME300 groups); on lipid peroxidation and carbonylated proteins in all brain tissues (p < 0.0001); and on GPx, GR, CAT, and SOD activities with all the treatments vs. KA (p ≤ 0.001). In addition, there were strong negative correlations between carbonyl levels and latency in the group treated with KA and in the group treated with methanolic extract in the presence of KA (r = -0.9919, p = 0.0084). This evidence suggests that organic extracts and quercetin from H. inuloides exert anticonvulsant effects via direct scavenging of reactive oxygen species (ROS) and modulation of antioxidant enzyme activity.

Expression and localization of the polarity protein CRB2 in adult mouse brain: a comparison with the CRB1rd8 mutant mouse model.

Acquisition of cell polarization is essential for the performance of crucial functions, like a successful secretion and appropriate cell signaling in many tissues, and it depends on the correct functioning of polarity proteins, including the Crumbs complex. The CRB proteins, CRB1, CRB2 and CRB3, identified in mammals, are expressed in epithelial-derived tissues like brain, kidney and retina. CRB2 has a ubiquitous expression and has been detected in embryonic brain tissue; but currently there is no data regarding its localization in the adult brain. In our study, we characterized the presence of CRB2 in adult mice brain, where it is particularly enriched in cortex, hippocampus, hypothalamus and cerebellum. Double immunofluorescence analysis confirmed that CRB2 is a neuron-specific protein, present in both soma and projections where colocalizes with certain populations of exocytic and endocytic vesicles and with other members of the Crumbs complex. Finally, in the cortex of CRB1rd8 mutant mice that contain a mutation in the Crb1 gene generating a truncated CRB1 protein, there is an abnormal increase in the expression levels of the CRB2 protein which suggests a possible compensatory mechanism for the malfunction of CRB1 in this mutant background.

The nuclear receptor FXR, but not LXR, up-regulates bile acid transporter expression in non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. Patients with non-alcoholic steatohepatitis (NASH) have increased plasmatic and hepatic concentrations of bile acids (BA), suggesting that they can be associated with the progression of the disease. Hepatic nuclear receptors are known to modulate genes controlling BA metabolism; thus, in this work we aimed to compare the expression of liver nuclear receptors -farnesoid X (FXR), small heterodimer partner (SHP) and liver X alpha (LXRα) receptors- and BA transporters -sodium+/taurocholate cotransporting polypeptide (NTCP) and bile salt export pump (BSEP)- in liver biopsy samples of patients with simple steatosis (SS) and NASH. MATERIAL AND METHODS: Forty patients with biopsy-proven NALFD were enrolled between 2009 and 2012; liver biopsies were classified as SS (N = 20) or NASH (N = 20) according to the NAFLD activity score. Gene expression of nuclear FXR, LXRα, SHP, NTCP and BSEP was analyzed by real-time reverse transcription polymerase chain reaction and protein level was quantified by western blot. RESULTS: Gene expression of FXR, SHP, NTCP and BSEP was significantly up-regulated in the NASH group in comparison with SS patients (P < 0.05). In contrast, protein level for FXR, SHP and NTCP was decreased in the NASH patients vs. the SS group (P < 0.05). Gene and protein profile of LXRα did not show differences between groups. CONCLUSIONS: The results suggest that liver nuclear receptors (FXR and SHP) and BA transporters (NTCP and BSEP) are associated with the progression of NAFLD.

Metabolic syndrome and nonalcoholic fatty liver disease. The role of endothelial progenitor cells.

BACKGROUND: Endothelial dysfunction has been previously described in metabolic syndrome patients. The levels of circulating endothelial progenitor cells (EPCs) inversely correlates with the incidence of cardiovascular disease. The aim of this study was to investigate the association between NAFLD, metabolic syndrome and EPC levels. MATERIAL AND METHODS: A cross-sectional pilot study was performed at a university hospital in Mexico. Two groups of patients without previously known chronic diseases were studied and classified according to the presence of NAFLD. Anthropometric, dietary, and biochemical variables, and circulating EPC number were measured and compared between the groups. RESULTS: Forty subjects were included and classified into two groups: patients with NAFLD (n = 20) and a control group (n = 20). The overall prevalence of insulin resistance and metabolic syndrome was 25% and 17.5%, respectively. EPC levels were found to be higher in the NAFLD group (p < 0.05) as in the patients with insulin resistance (p < 0.01) and metabolic syndrome (p < 0.01). These levels showed correlation with the severity of steatosis. CONCLUSIONS: Patients with NAFLD have increased levels of EPC, such levels are associated with the severity of NAFLD. These findings may suggest that these cells may play a role in the early natural history of NAFLD. EPC might be increased in an attempt to repair the endothelial damage resulting from metabolic alterations accompanying NAFLD. Further studies are needed to establish the dynamics of these cells in NAFLD.

A metal mixture induces transformation upon antioxidant depletion in a hepatic cell line.

INTRODUCTION: Metals are ubiquitous soil, air, and water pollutants. A mixture of arsenic cadmium and lead, in particular, has commonly been found in the vicinity of smelter areas. The mixture of As-Cd-Pb has been shown to be carcinogenic, and transforming potential and oxidative stress have been proposed as principal mechanisms involved in this process. The aim of this work was to explore the role of the antioxidant barrier in the establishment of cell transformation upon chronic exposure to a metal mixture containing 2 µM NaAsO(2), 2 µM. CdCl(2), and 5 µM Pb(C(2)H(3)O(2))(2)∙3H(2)O in WRL-68 cells-a non-transformed human hepatic cell line. MATERIAL AND METHODS: In this study, we used a WRL-68 cell model of human embryonic hepatic origin treated with antioxidant inhibitors (L-Buthionine-sulfoxamine and aminotriazole) to test the role of the antioxidant barrier in the establishment of cell transformation upon chronic exposure to a metal mixture of As-Cd-Pb (2 µM NaAsO(2), 2 µM CdCl(2) and 5 µM Pb(C(2)H(3)O(2))(2)∙3H(2)O). We evaluated oxidative damage markers, including reactive oxygen species, lipid peroxidation, and genotoxicity, as well as antioxidant response markers, including glutathione concentration, catalase activity, and superoxide dismutase activity, which promote morphological transformation, which can be quantified by foci formation. RESULTS: As expected, we found an increase in the intracellular concentration of the metals after treatment with the metal mixture. In addition, treatment with the metal mixture in addition to inhibitors resulted in a large increase in the intracellular concentration of cadmium and lead. Our results describe the generation of reactive oxygen species, cytotoxicity, genotoxicity, and oxidative damage to macromolecules that occurred exclusively in cells that were morphologically transformed upon exposure to a metal mixture and antioxidant barrier inhibition. CONCLUSION: Our results show the importance of the antioxidant barrier role in the protection of cellular integrity and the transformation potential of this metal mixture via free radicals.

Bilirubin alone as a biomarker for short-term mortality in acute-on-chronic liver failure: an important prognostic indicator.

BACKGROUND AND AIMS. Acute-on-chronic liver failure has been recognized as a sudden deterioration of cirrhosis, with a high short-term mortality. Prognostic scores are used to assess liver dysfunction. However, there is not enough information on a score to predict short term mortality in those patients. We aimed to investigate the prognostic value of bilirubin concentration in predicting the 1-week outcome of patients with acute-on-chronic liver failure. MATERIAL AND METHODS. We performed a retrospective analysis with a cohort of 65 patients (33 women/32 men), age average of 64 years, diagnosed with acute-on-chronic liver failure with at least 1 week follow-up. Demographics, clinical and biochemical variables were analyzed. Most patients died (59 %) within 1 week of follow-up. RESULTS. In univariate logistic regression analysis, admission to the intensive care unit, use of vasoactive drugs, need for parenteral nutrition, and levels of conjugated, unconjugated, and total bilirubin at the time of hospital admission were significantly associated with 1-week mortality; in a multivariate logistic regression, conjugated (p = 0.01), unconjugated (p =0.01), and total bilirubin (p = 0.009) were independently associated with 1-week mortality. In ROC curve analysis, conjugated (0.751, p < 0.05) and total bilirubin (0.746, p < 0.05) levels were significantly the best short-term mortality predictors. CONCLUSIONS. High levels of bilirubin are able to predict short-term mortality in these patients. Also, we suggest that bilirubin can be used as a biochemical marker to improve triage of patients with acute-on-chronic liver failure especially with emerging interventions such as extracorporeal liver assist devices and possibly improved early phase pharmacological therapies.

High coffee intake is associated with lower grade nonalcoholic fatty liver disease: the role of peripheral antioxidant activity.

BACKGROUND & AIMS: Some phytochemicals present in coffee have a potential antioxidant role which seems to protect the human body against cardiovascular diseases, liver disease and malignancies. Nonalcoholic fatty liver disease is a common disease with limited therapeutic options. This study investigated the antioxidant effect of coffee by measuring antioxidant enzymes and lipid peroxidation markers in patients with nonalcoholic fatty liver disease. MATERIAL AND METHODS: We performed a case-control study at the University Hospital, Mexico City. Anthropometric, metabolic, dietary and biochemical variables of all patients were determined and compared. The presence of nonalcoholic fatty liver disease was established by ultrasonography. All patients completed a dietary questionnaire in order to determine their of coffee consumption. Catalase, superoxide dismutase and thiobarbituric acid reactive substances were measured in all of the patients. RESULTS: Seventy-three subjects with and 57 without nonalcoholic fatty liver disease were included. Patients with nonalcoholic fatty liver disease had significantly higher body mass index, blood glucose, homeostasis model of assessment-insulin resistance and insulin values in comparison to patients without nonalcoholic fatty liver disease. On the one hand, there was a significant difference in coffee intake between the groups (p < 0.05, for all comparisons). There was no significant difference between groups in catalase (0.39 ± 0.74 vs. 0.28 ± 0.69 nM/min/mL), superoxide dismutase (5.4 ± 3.45 vs. 4.7 ± 2.1 U/mL) or thiobarbituric acid-reactive substances (4.05 ± 1.87 vs. 3.94 ± 1.59 µM/mL). CONCLUSIONS: A high intake of coffee has a protective effect against nonalcoholic fatty liver disease however there was no significant difference in the antioxidant variables analyzed.

Estudio del grado de satisfacción de los pacientes intervenidos encirugía mayor ambulatoria en un periodo de seis meses / No disponible

Introducción: La calidad asistencial está íntimamente relacionada con la satisfacción de los pacientes. En los pacientes intervenidos en cirugía mayor ambulatoria, la satisfacción cobra especial relevancia, puesto que los pacientes permanecen durante un breve espacio de tiempo en el hospital. Las expectativas sanitarias de los usuarios están centradas sobre todo en los servicios que reciben por parte de los profesionales. El personal de enfermería es, por lo tanto, una pieza clave en la prestación de los cuidados y en la percepción que los usuarios tienen de los mismos. Objetivos: Determinar el grado de satisfacción de los pacientes intervenidos en el servicio de CMA. Conocer cuáles son los aspectos del proceso asistencial que generan una mayor satisfacción o insatisfacción, para así poder realizar programas de mejora. Material y métodos: Se realizó un estudio observacional descriptivo de la satisfacción de los pacientes intervenidos en cirugía mayor ambulatoria. Mediante la realización de una entrevista telefónica, se estudió la opinión de los pacientes dos meses después de haber sido sometidos a una intervención quirúrgica, a través de un cuestionario validado de 14 ítems que considera tres factores de satisfacción: atención hospitalaria, cirugía ambulatoria y seguimiento postcirugía, controlando las variables socio demográficas intervinientes. Resultados: El 98% de los pacientes consideró la información previa a la cirugía como buena (18%) o muy buena (82%). El trato (..) (AU)

Introduction: Quality of care is closely related to patient satisfaction. This satisfaction has special relevance in patients treated for ambulatory surgery because they stay at the hospital for a short time. Health expectations of users are focused on the services they receive from the health professionals, so nursing personnel is a key piece in providing care and the user's perception of it. Objectives: To determine the degree of satisfaction of patients operated in a department of major ambulatory surgery (MAS). To know which aspects of the care process generates greater satisfaction or dissatisfaction and thus make improvements. Material and methods: A descriptive observational study of patients operated in the department of MAS of our hospital was conducted. By telephone interviews two months after surgery, we studied the opinion of patients through a validated questionnaire of14 items, which determined three satisfaction factors: hospital care, ambulatory surgery and postsurgical follow-up, controlling the social demographic variables involved. Results: 98% of the patients found the information prior to surgery good (18%) or very good (82%) (..) (AU)

Long-term prognosis of first myocardial infarction according to the electrocardiographic pattern (ST elevation myocardial infarction, non-ST elevation myocardial infarction and non-classified myocardial infarction) and revascularization procedures.

The aim of this study was to describe differences in the characteristics and short- and long-term prognoses of patients with first acute myocardial infarction (MI) according to the presence of ST-segment elevation or non-ST-segment elevation. From 2001 and 2003, 2,048 patients with first MI were consecutively admitted to 6 participating Spanish hospitals and categorized as having ST-segment elevation MI (STEMI), non-ST-segment elevation MI (NSTEMI), or unclassified MI (pacemaker or left bundle branch block) according to electrocardiographic results at admission. The proportions of female gender, hypercholesterolemia, hypertension, and diabetes were higher among NSTEMI patients than in the STEMI group. NSTEMI 28-day case fatality was lower (2.99% vs 5.26%, p = 0.02). On multivariate analysis, the odds ratio of 28-day case fatality was 2.23 for STEMI patients compared to NSTEMI patients (95% confidence interval 1.29 to 3.83, p = 0.004). The multivariate adjusted 7-year mortality for 28-day survivors was higher in NSTEMI than in STEMI patients (hazard ratio 1.31, 95% confidence interval 1.02 to 1.68, p = 0.035). However, patients with unclassified MI presented the highest short- and long-term mortality (11.8% and 35.4%, respectively). The excess of short-term mortality in unclassified and STEMI patients was mainly observed in those patients not treated with revascularization procedures. In conclusion, patients with first NSTEMI were older and showed a higher proportion of previous coronary risk factors than STEMI patients. NSTEMI patients had lower 28-day case fatality but a worse 7-year mortality rate than STEMI patients. Unclassified MI presented the worst short- and long-term prognosis. These results support the invasive management of patients with acute coronary syndromes to reduce short-term case fatality.

Análisis de los tiempos de atención en pacientes con infarto agudo de miocardio tratados con angioplastia primaria según su procedencia y según el horario de realización del procedimiento / Analysis of reperfusion delay in patients with acute myocardial infarction treated with primary angioplasty based on first medical contact and time of presentation

Introducción y objetivos. En la angioplastia primaria se recomienda un tiempo inferior a 120 min entre el primer contacto médico (PCM) y la reperfusión. El retraso hasta la reperfusión varía según dónde se realice el PCM. Estudios recientes señalan peores tiempos en horario de guardia. El objetivo es el análisis de distintos intervalos de tiempo hasta la reperfusión según dónde se produce el PCM y el horario de presentación. Métodos. Estudio prospectivo observacional de pacientes con infarto tratados con angioplastia primaria (febrero de 2007-mayo de 2009). Según el PCM, se diferenció: grupo Hospital (hospital con angioplastia primaria), grupo Traslado (hospital sin angioplastia primaria) y grupo SEM (sistema de emergencias médicas, atención extrahospitalaria). Para cada grupo se registró: retraso prehospitalario, retraso diagnóstico, retraso en activación y/o traslado y retraso en el procedimiento. Resultados. Se realizó angioplastia primaria a 457 pacientes, 155 en el grupo Hospital, 228 en el grupo Traslado y 72 en el grupo SEM. Las medianas [intervalo intercuartílico] del tiempo PCM-reperfusión fueron 80 [63-107], 148 [118-189] y 81 [66-98] min respectivamente (p<0,0001). El grupo Traslado presentó mayor retraso diagnóstico (p<0,0001) y retraso en activación y/o traslado (p<0,0001). El grupo SEM presentó el tiempo total más corto por tener un retraso prehospitalario menor (p=0,001). No se encontró diferencia según el horario de realización (p=0,42). Conclusiones. A los pacientes del grupo Traslado se los reperfundió más tardíamente y a los del grupo SEM, más precozmente. No hubo diferencias según el horario. La identificación de demoras injustificadas debe permitir adoptar medidas que mejoren la eficiencia del tratamiento (AU)

Introduction and objectives. In primary angioplasty, the interval between first medical contact (FMC) and reperfusion should be less than 120minutes. The time to reperfusion varies depending on where FMC is established. Recent studies suggest longer times in patients presenting in off-hours. The objective is to evaluate the time intervals between the onset of symptoms and reperfusion according to where the FMC occurs and time of day of patient presentation. Methods. Prospective observational study of acute myocardial infarction patients treated with primary angioplasty (February 2007 to May 2009). Depending on the FMC, patients were classified as belonging to the hospital group (hospital with primary angioplasty), the transfer group (hospital without primary angioplasty), or the emergency medical system (EMS) group (out-of-hospital care). For each group, the prehospital delay, diagnostic delay, delay in activation and/or transfer, and procedure delay were recorded. Results. Primary angioplasty was performed in 457 patients: 155 in the hospital group, 228 in the transfer group and 72 in the EMS group. The median [interquartile range] door-to-reperfusion times were 80 [63-107], 148 [118-189] and 81 [66-98] minutes, respectively (P <.0001). The transfer group showed a greater delay in diagnosis (P <.0001) and delayed activation and/or transfer (P <.0001). The EMS group had the shortest total time due to a reduced prehospital delay (P =.001). No difference was found with regard to the time of presentation (P =.42). Conclusions. Transfer group patients were treated later and EMS group patients much earlier. There were no differences in association with the time of presentation. The identification of inappropriate delays should enable the introduction of measures to improve the efficiency of treatment (AU)

[Analysis of reperfusion delay in patients with acute myocardial infarction treated with primary angioplasty based on first medical contact and time of presentation]. / Análisis de los tiempos de atención en pacientes con infarto agudo de miocardio tratados con angioplastia primaria según su procedencia y según el horario de realización del procedimiento.

INTRODUCTION AND OBJECTIVES: In primary angioplasty, the interval between first medical contact (FMC) and reperfusion should be less than 120 minutes. The time to reperfusion varies depending on where FMC is established. Recent studies suggest longer times in patients presenting in off-hours. The objective is to evaluate the time intervals between the onset of symptoms and reperfusion according to where the FMC occurs and time of day of patient presentation. METHODS: Prospective observational study of acute myocardial infarction patients treated with primary angioplasty (February 2007 to May 2009). Depending on the FMC, patients were classified as belonging to the hospital group (hospital with primary angioplasty), the transfer group (hospital without primary angioplasty), or the emergency medical system (EMS) group (out-of-hospital care). For each group, the prehospital delay, diagnostic delay, delay in activation and/or transfer, and procedure delay were recorded. RESULTS: Primary angioplasty was performed in 457 patients: 155 in the hospital group, 228 in the transfer group and 72 in the EMS group. The median [interquartile range] door-to-reperfusion times were 80 [63-107], 148 [118-189] and 81 [66-98] minutes, respectively (P<.0001). The transfer group showed a greater delay in diagnosis (P<.0001) and delayed activation and/or transfer (P<.0001). The EMS group had the shortest total time due to a reduced prehospital delay (P=.001). No difference was found with regard to the time of presentation (P=.42). CONCLUSIONS: Transfer group patients were treated later and EMS group patients much earlier. There were no differences in association with the time of presentation. The identification of inappropriate delays should enable the introduction of measures to improve the efficiency of treatment.

Consumo de cocaína en el síndrome coronario agudo / Cocaine use in acute coronary syndrome

No disponible