Effects of PM10 Airborne Particles from Different Regions of a Megacity on In Vitro Secretion of Cytokines by a Monocyte Line during Different Seasons.

Several epidemiological studies have demonstrated that particulate matter (PM) in air pollution can be involved in the genesis or aggravation of different cardiovascular, respiratory, perinatal, and cancer diseases. This study assessed the in vitro effects of PM10 on the secretion of cytokines by a human monocytic cell line (THP-1). We compared the chemotactic, pro-inflammatory, and anti-inflammatory cytokines induced by PM10 collected for two years during three different seasons in five different Mexico City locations. MIP-1α, IP-10, MCP-1, TNF-α, and VEGF were the main secretion products after stimulation with 80 µg/mL of PM10 for 24 h. The THP-1 cells showed a differential response to PM10 obtained in the different sites of Mexico City. The PM10 from the north and the central city areas induced a higher pro-inflammatory cytokine response than those from the south. Seasonal pro-inflammatory cytokine secretion always exceeded anti-inflammatory secretion. The rainy-season-derived particles caused the lowest pro-inflammatory effects. We concluded that toxicological assessment of airborne particles provides evidence supporting their potential role in the chronic exacerbation of local or systemic inflammatory responses that may worsen the evolution of some chronic diseases.

Childhood Leukemia in Small Geographical Areas and Proximity to Industrial Sources of Air Pollutants in Three Colombian Cities.

Acute leukemia is the most common childhood cancer and has been associated with exposure to environmental carcinogens. This study aimed to identify clusters of acute childhood leukemia (ACL) cases and analyze their relationship with proximity to industrial sources of air pollution in three capital cities in Colombia during 2000-2015. Incident ACL cases were obtained from the population cancer registries for the cities of Bucaramanga, Cali, and Medellín. The inventory of industrial sources of emissions to the air was obtained from the regional environmental authorities and industrial conglomerates were identified. The Kulldorf's circular scan test was used to detect city clusters and to identify clusters around industrial conglomerates. Multivariable spatial modeling assessed the effect of distance and direction from the industrial conglomerates controlling for socioeconomic status. We identified industrials sectors within a buffer of 1 km around industrial conglomerates related to the ACL clusters. Incidence rates showed geographical heterogeneity with low spatial autocorrelation within cities. The spatio-temporal tests identified one cluster in each city. The industries located within 1 km around the ACL clusters identified in the three cities represent different sectors. Exposure to air pollution from industrial sources might be contributing to the incidence of ACL cases in urban settings in Colombia.

Proinflammatory effects of dust storm and thermal inversion particulate matter (PM10) on human peripheral blood mononuclear cells (PBMCs) in vitro: a comparative approach and analysis.

Particulate matter (PM) as the carcinogenic air pollutants can lead to aggravated health outcomes. Epidemiological studies demonstrated that PM can be engaged in different diseases such as cardiovascular, respiratory and cancer. The in vitro secretion of proinflammatory cytokines by human peripheral blood mononuclear cells (PBMCs) has been used to assess the effects of PM with an aerodynamic diameter < 10 µm (PM10). This study compared the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and interleukin 1-beta (IL1-ß) secretions of PBMCs exposed to PM10 of dust storm and inversion. We collected PM10 samples during the spring and autumn seasons in two locations. Isolated PBMCs were exposed separately to 50, 150, and 300 µg/ml of different type of PM10 for 4 and 24 h. The mean concentrations of TNF-α for the PM of dust storm and inversion were 6305.61 ± 2421 and 6651.74 ± 2820, respectively. Also the mean concentrations of IL1-ß for the PM of dust storm and inversion were 556.86 ± 162 and 656.35 ± 196, respectively. Furthermore, these values for the production of IL-6 were 12,655 ± 5661 and 16,685 ± 8069, respectively. Although no significant difference was observed between the PM of dust storm and that of inversion with regard to PBMCs, the results showed a significant increase in the proinflammatory cytokine secretion of both PMs compared with the controls. Moreover, TNF-α, IL1-ß, and IL-6 secreted in cells exposed to PM10 of dust storm were about 10 times more than the controls, these values for cells exposed to PM10 of inversion were around 10, 12, and 14 times more than the controls, respectively. It can be concluded that the PM10 of both dust storm and inversion can play a significant role in proinflammatory cytokine secretion due to its harmful effect on human health. Graphical abstractThis picture shows the Proinflammatory cytokine producing potential of PM10 with two sources (dust storm and urban air pollution) in exposure with human PBMCs in vitro.

Aeroparticles, Composition, and Lung Diseases.

Urban air pollution is a serious worldwide problem due to its impact on human health. In the past 60 years, growing evidence established a correlation between exposure to air pollutants and the developing of severe respiratory diseases. Recently particulate matter (PM) is drawing more public attention to various aspects including historical backgrounds, physicochemical characteristics, and its pathological role. Therefore, this review is focused on these aspects. The most famous air pollution disaster happened in London on December 1952; it has been calculated that more than 4,000 deaths occurred during this event. Air pollution is a complex mix of gases and particles. Gaseous pollutants disseminate deeply into the alveoli, allowing its diffusion through the blood-air barrier to several organs. Meanwhile, PM is a mix of solid or liquid particles suspended in the air. PM is deposited at different levels of the respiratory tract, depending on its size: coarse particles (PM10) in upper airways and fine particles (PM2.5) can be accumulated in the lung parenchyma, inducing several respiratory diseases. Additionally to size, the composition of PM has been associated with different toxicological outcomes on clinical and epidemiological, as well as in vivo and in vitro animal and human studies. PM can be constituted by organic, inorganic, and biological compounds. All these compounds are capable of modifying several biological activities, including alterations in cytokine production, coagulation factors balance, pulmonary function, respiratory symptoms, and cardiac function. It can also generate different modifications during its passage through the airways, like inflammatory cells recruitment, with the release of cytokines and reactive oxygen species (ROS). These inflammatory mediators can activate different pathways, such as MAP kinases, NF-κB, and Stat-1, or induce DNA adducts. All these alterations can mediate obstructive or restrictive respiratory diseases like asthma, COPD, pulmonary fibrosis, and even cancer. In 2013, outdoor air pollution was classified as Group 1 by IARC based on all research studies data about air pollution effects. Therefore, it is important to understand how PM composition can generate several pulmonary pathologies.

TNFα and IL-6 Responses to Particulate Matter in Vitro: Variation According to PM Size, Season, and Polycyclic Aromatic Hydrocarbon and Soil Content.

BACKGROUND: Observed seasonal differences in particulate matter (PM) associations with human health may be due to their composition and to toxicity-related seasonal interactions. OBJECTIVES: We assessed seasonality in PM composition and in vitro PM pro-inflammatory potential using multiple PM samples. METHODS: We collected 90 weekly PM10 and PM2.5 samples during the rainy-warm and dry-cold seasons in five urban areas with different pollution sources. The elements, polycyclic aromatic hydrocarbons (PAHs), and endotoxins identified in the samples were subjected to principal component analysis (PCA). We tested the potential of the PM to induce tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) secretion in cultured human monocytes (THP-1), and we modeled pro-inflammatory responses using the component scores. RESULTS: PM composition varied by size and by season. PCA identified two main components that varied by season. Combustion-related constituents (e.g., vanadium, benzo[a]pyrene, benzo[a]anthracene) mainly comprised component 1 (C1). Soil-related constituents (e.g., endotoxins, silicon, aluminum) mainly comprised component 2 (C2). PM from the rainy-warm season was high in C2. PM (particularly PM2.5) from the dry-cold season was rich in C1. Elevated levels of cytokine production were associated with PM10 and C2 (rainy-warm season), whereas reduced levels of cytokine production were associated with PM2.5 and C1 (dry-cold season). TNFα secretion was increased following exposure to PM with high (vs. low) C2 content, but TNFα secretion in response to PM was decreased following exposure to samples containing ≥ 0.1% of C1-related PAHs, regardless of C2 content. The results of the IL-6 assays suggested more complex interactions between PM components and particle size. CONCLUSIONS: Variations in PM soil and PAH content underlie seasonal and PM size-related patterns in TNFα secretion. These results suggest that the mixture of components in PM explains some seasonal differences in associations between health outcomes and PM in epidemiologic studies. CITATION: Manzano-León N, Serrano-Lomelin J, Sánchez BN, Quintana-Belmares R, Vega E, Vázquez-López I, Rojas-Bracho L, López-Villegas MT, Vadillo-Ortega F, De Vizcaya-Ruiz A, Rosas Perez I, O'Neill MS, Osornio-Vargas AR. 2016. TNFα and IL-6 responses to particulate matter in vitro: variation according to PM size, season, and polycyclic aromatic hydrocarbon and soil content. Environ Health Perspect 124:406-412; http://dx.doi.org/10.1289/ehp.1409287.

Variation in the composition and in vitro proinflammatory effect of urban particulate matter from different sites.

Spatial variation in particulate matter-related health and toxicological outcomes is partly due to its composition. We studied spatial variability in particle composition and induced cellular responses in Mexico City to complement an ongoing epidemiologic study. We measured elements, endotoxins, and polycyclic aromatic hydrocarbons in two particle size fractions collected in five sites. We compared the in vitro proinflammatory response of J774A.1 and THP-1 cells after exposure to particles, measuring subsequent TNFα and IL-6 secretion. Particle composition varied by site and size. Particle constituents were subjected to principal component analysis, identifying three components: C(1) (Si, Sr, Mg, Ca, Al, Fe, Mn, endotoxin), C(2) (polycyclic aromatic hydrocarbons), and C(3) (Zn, S, Sb, Ni, Cu, Pb). Induced TNFα levels were higher and more heterogeneous than IL-6 levels. Cytokines produced by both cell lines only correlated with C(1) , suggesting that constituents associated with soil induced the inflammatory response and explain observed spatial differences.

Air pollution: An environmental factor contributing to intestinal disease.

The health impacts of air pollution have received much attention and have recently been subject to extensive study. Exposure to air pollutants such as particulate matter (PM) has been linked to lung and cardiovascular disease and increases in both hospital admissions and mortality. However, little attention has been given to the effects of air pollution on the intestine. The recent discovery of genes linked to susceptibility to inflammatory bowel diseases (IBD) explains only a fraction of the hereditary variance for these diseases. This, together with evidence of increases in incidence of IBD in the past few decades of enhanced industrialization, suggests that environmental factors could contribute to disease pathogenesis. Despite this, little research has examined the potential contribution of air pollution and its components to intestinal disease. Exposure of the bowel to air pollutants occurs via mucociliary clearance of PM from the lungs as well as ingestion via food and water sources. Gaseous pollutants may also induce systemic effects. Plausible mechanisms mediating the effects of air pollutants on the bowel could include direct effects on epithelial cells, systemic inflammation and immune activation, and modulation of the intestinal microbiota. Although there is limited epidemiologic evidence to confirm this, we suggest that a link between air pollution and intestinal disease exists and warrants further study. This link may explain, at least in part, how environmental factors impact on IBD epidemiology and disease pathogenesis.

Ambient particulate matter induces interleukin-8 expression through an alternative NF-κB (nuclear factor-kappa B) mechanism in human airway epithelial cells.

BACKGROUND: Exposure to ambient air particulate matter (PM) has been shown to increase rates of cardiopulmonary morbidity and mortality, but the underlying mechanisms are still not well understood. OBJECTIVE: We examined signaling events involved in the expression of the inflammatory gene interleukin-8 (IL-8) in human airway epithelial cells (HAECs) exposed to ambient PM collected in an urban area of Mexicali, Mexico. METHODS: We studied IL-8 expression and regulatory signaling pathways in cultured HAECs exposed to Mexicali PM suspended in media for 0-4 hr. RESULTS: Exposure resulted in a dose-dependent, 2- to 8-fold increase in IL-8 mRNA expression relative to controls. PM exposure induced IL-8 transcriptional activity in BEAS-2B cells that was dependent on the nuclear factor-kappa B (NF-κB) response element in the IL-8 promoter. Chromatin immunoprecipitation (ChIP) assays showed a 3-fold increase in binding of the p65 (RelA) NF-κB isoform to the IL-8 promoter sequence in HAECs exposed to PM. Western blot analyses showed elevated levels of phosphorylation of p65 but no changes in IκBα phosphorylation or degradation. IL-8 expression was blunted in a dose-dependent manner in BEAS-2B cells transduced with a lentivirus encoding a dominant negative p65 mutant in which phosphorylation sites were inactivated. CONCLUSION: Taken together, these findings show that the increase in IL-8 mRNA expression in HAECs exposed to PM10 (PM ≤ 10 µm in aerodynamic diameter) is mediated through an NF-κB-dependent signaling mechanism that occurs through a pathway involving direct phosphorylation of the transcription factor p65 in the absence of IκBα degradation. These data show that exposure to PM10 in ambient air can induce inflammatory responses by activating specific signaling mechanisms in HAECs.

PM(10) impairs the antioxidant defense system and exacerbates oxidative stress driven cell death.

The aim of this study was to investigate the effect of airborne particulate matter with a mean aerodynamic diameter of < or =10microm (PM(10)) on oxidative stress markers and antioxidant enzymatic activity and its relevance in the face of acute oxidative challenge in a human lung epithelial cell line (A549). PM(10)-induced reactive oxygen species (ROS) generation and oxidative damage with no changes in cellular viability. In addition, PM(10) decreased glutathione (GSH) levels (54.9%) and the activity of the antioxidant enzymes superoxide dismutase (65%), catalase (31.2%), glutathione reductase (61.5%) and glutathione-S-transferase (42.39%). Trolox, a scavenger of reactive species, prevented the increase of ROS generation and the decrease in GSH levels but partially prevented PM(10)-induced oxidative damage. Interestingly, it was unable to avoid the decrease in the activity of antioxidant enzymes. Finally, the survival of the cells previously exposed to PM(10) and challenged with hydrogen peroxide was significantly lower. We conclude that the impairment in the antioxidant defense system induced by PM(10) weaken ROS detoxification which exacerbates cell death when these cells are exposed to an acute oxidative challenge.

DNA damage response of A549 cells treated with particulate matter (PM10) of urban air pollutants.

We describe the events triggered by a sub-lethal concentration of airborne particulate matter (PM(10)) in A549 cells, which include the formation DNA double-strand breaks, gammaH2A.X generation, and 53BP1 recruitment. To protect the genome, cells activated ATM/ATR/Chk1/Chk2/p53 pathway but, after 48 h, cells turned into a senescence-like state. Trolox, an antioxidant, was able to prevent most of the alterations observed after particulate matter exposure, demonstrating the important role of ROS as mediator of PM(10)-induced genotoxicity and suggesting that DNA damage could be the mechanisms by which particulate matter augment the risk of lung cancer.

Trends in childhood cancer incidence: review of environmental linkages.

Cancer in children is rare and accounts for about 1% of all malignancies. In the developed world, however, it is the commonest cause of disease-related deaths in childhood, carrying with it a great economic and emotional cost. Cancers are assumed to be multivariate, multifactorial diseases that occur when a complex and prolonged process involving genetic and environmental factors interact in a multistage sequence. This article explores the available evidence for this process, primarily from the environmental linkages perspective but including some evidence of the genetic factors.

Relations between PM10 composition and cell toxicity: a multivariate and graphical approach.

Previous studies have used particle mass and size as metrics to link airborne particles with deleterious health effects. Recent evidence suggests that particle composition can play an important role in PM-toxicity; however, little is known about the specific participation of components (individually or acting in groups) present in such a complex mixture that accounts for toxicity. This work explores relationships among PM(10) components in order to identify their covariant structure and how they vary in three sites in Mexico City. Relationships between PM(10) with cell toxicity and geographical location were also explored. PM(10) was analyzed for elemental composition, organic and elemental carbon, endotoxins and the induction of inhibition of cell proliferation, IL-6, TNFalpha and p53. PM(10) variables were evaluated with principal component analysis and one-way ANOVA. The inhibition of cell proliferation, IL-6 and TNFalpha were evaluated with factorial ANOVA and p53 with the Welch test. The results indicate that there is heterogeneity in particle mass, composition and toxicity in samples collected at different sites. Multivariate analysis identified three major groups: (1) S/K/Ca/Ti/Mn/Fe/Zn/Pb; (2) Cl/Cr/Ni/Cu; and (3) endotoxins, organic and elemental carbon. Groups 1 and 3 showed significant differences among sites. Factorial ANOVA modeling indicated that cell proliferation was affected by PM concentration; TNFalpha and IL-6 by the interaction of concentration and site, and p53 was different by site. Radial plots suggest the existence of complex interactions between components, resulting in characteristic patterns of toxicity by site. We conclude that interactions of PM(10) components determine specific cellular outcomes.

An urban survey of paediatric environmental health concerns: Perceptions of parents, guardians and health care professionals.

OBJECTIVES: To conduct a survey in Edmonton, Alberta, to gather information regarding concerns about the influence of environmental factors on children's health and to use the information to set an agenda for the resources of the Paediatric Environmental Health Specialty Unit at Misericordia Hospital (Edmonton, Alberta). METHODS: Two questionnaires with 28 closed-ended questions were developed to examine parents', guardians' and health care professionals' concerns. They comprised items about six environmental factors (air, water and food quality; household supplies; radiation; and waste disposal). Health care professionals were also asked four questions about their knowledge of and their needs in Paediatric Environmental Health. Parents and guardians attending the public health centres and nurses working therein received questionnaires. Physicians were surveyed by e-mail. RESULTS: After verification, the questionnaire data from 400 parents or guardians and 152 health care professionals were used for analyses. Results from contingency table, Hotelling's T² and effect size analyses revealed similarities in the levels of concern in both groups, and the results were combined. The greatest concern of both groups was with environmental tobacco smoke, followed by pesticides in water. Concerns about six additional environmental elements were also expressed. The health care professionals showed a high level of concern about the need for resources, specific training and public education regarding paediatric environmental health. CONCLUSION: A significant level of concern was consistently found between the two groups studied, regardless of professional training. The highest level of concern was with a well-documented topic (ie, environmental tobacco smoke). Less concern associated with decreased documentation calls for increasing the knowledge of society, including health care professionals, to address the adverse effects of environmental factors on children.

Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.

Exposure to urban airborne particulate matter (PM) is associated with adverse health effects. We previously reported that the cytotoxic and proinflammatory effects of Mexico City PM10 (less than or equal to 10 micro m mean aerodynamic diameter) are determined by transition metals and endotoxins associated with these particles. However, PM2.5 (less than or equal to 2.5 micro m mean aerodynamic diameter) could be more important as a human health risk because this smaller PM has the potential to reach the distal lung after inhalation. In this study, we compared the cytotoxic and proinflammatory effects of Mexico City PM10 with those of PM2.5 using the murine monocytic J774A.1 cell line in vitro. PMs were collected from the northern zone or the southeastern zone of Mexico City. Elemental composition and bacterial endotoxin on PMs were measured. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production by J774A.1 cells was measured in the presence or absence of recombinant endotoxin-neutralizing protein (rENP). Both northern and southeastern PMs contained endotoxin and a variety of transition metals. Southeastern PM10 contained the highest endotoxin levels, 2-fold higher than that in northern PM10. Northern and southeastern PM2.5 contained the lowest endotoxin levels. Accordingly, southeastern PM10 was the most potent in causing secretion of the proinflammatory cytokines TNF-alpha and IL-6. All PM2.5 and PM10 samples caused cytotoxicity, but northern PMs were the most toxic. Cytokine secretion induced by southeastern PM10 was reduced 50-75% by rENP. These results indicate major differences in PM10 and PM2.5. PM2.5 induces cytotoxicity in vitro through an endotoxin-independent mechanism that is likely mediated by transition metals. In contrast, PM10 with relatively high levels of endotoxin induces proinflammatory cytokine release via an endotoxin-dependent mechanism.

Biologic effects induced in vitro by PM10 from three different zones of Mexico City.

Exposure to urban airborne particles is associated with an increase in morbidity and mortality. There is little experimental evidence of the mechanisms involved and the role of particle composition. We assessed cytotoxicity (crystal violet assay), apoptosis [terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) or annexin V assay], DNA breakage (comet assay), and production of proinflammatory mediators [tumor necrosis factor Alpha (TNF-Alpha), interleukin 6 (IL-6), prostaglandin E2 (PGE2)] (enzyme-linked immunosorbent assay), and E-selectin (flow cytometry) in cell lines exposed to particulate matter < 10 microm in size (PM10) obtained from the northern, central, and southern zones of Mexico City. Particle concentrations ranged from 2.5 to 160 microg/cm(2). We used epithelial, endothelial, fibroblastic, and monocytic cells and assessed DNA damage in Balb-c cells, TNF-Alpha and IL-6 production in mouse monocytes, and PGE2 in rat lung fibroblasts. We determined the expression of E-selectin in human endothelial cells and evaluated the cytotoxic potential of the PM10 samples in all cell types. PM10 from all three zones of Mexico City caused cell death, DNA breakage, and apoptosis, with particles from the north and central zones being the most toxic. All of these PM10 samples induced secretion of proinflammatory molecules, and particles from the central zone were the most potent. Endothelial cells exposed to PM10 from the three zones expressed similar E-selectin levels. Mexico City PM10 induced biologic effects dependent on the zone of origin, which could be caused by differences in the mixture or size distribution within particle samples. Our data suggest that particle composition as well as particle size should be considered in assessing the adverse effects of airborne particulate pollution.

Prueba de coaglutinación para la detección de rotavirus humano en heces fecales: comparación con la prueba de Elisa / Coagulation test used for the detection of human rotavirus in feces: a comparison with Elisa test

Con objeto de encontrar una prueba sencilla y rápida que detecte la presencia de rotavirus (RV) en heces fecales de niños con diarrea asociada a este agente, se utilizó un método de diagnóstico directo en placa, que se basa en la aglutinación de Staphylococcus aureus rico en proteína A (previamente sensibilizado con suero anti-RV), ante la presencia del antígeno homólogo. La utilidad diagnóstico de la coaglutinación (COA), fue comparada con un método de ELISA en 64 muestras diarreicas positivas a esta prueba y en un grupo de 81 negativas, encontrándose una concordancia entre ambas del 82% (X = 94.60, p <0.001), lo cual sugiere que si no se cuenta con facilidades para practicar el análisis inmunoenzimático, la COA es una alternativa confiable para el diagnóstico de rutina de la diarrea asociada a RV, y su bajo costo, fácil ejecución y rapidez en la lectura, lo hacen accesible a cualquier laboratorio

Infarto experimental de aurícula izquierda / Experimental left atrial infarction

Los signos eléctricos del infarto experimental de la aurícula izquierda se estudiaron en 15 perros, anestesiados con pentobarbital sódico intravenoso, sometidos a intubación de la tráquea, esternotomía media y corazón expuesto con saco pericárdico cerrado. Fue infiltrado alcohol a 96- en la aurícula izquierda, con una aguja delgada introducida superficialmente en sentido paralelo al pericardio visceral. Los regsitros cercanos y directos demostraron una reducción importante de las fuerzas electromotrices correspondientes a la orejuela y porciones laterales de la aurícula izquierda, dando ondas P de tipo QS o QR mellados con ST a auricular elevado y activación tardía de las regiones circunvencinas cuando la porción izquierda de la banda interauricular fue dañada. Las ondas P son del tipo bimodal, anchas con o sin onda qp en las derivaciones V2-V4, asociadas a STa elevado en V4-V5, a VL y precordiales altas a nivel de la línea de V4. Las porciones finales de P en D2, D3 y a VF son negativas. El QTac se prolonga más en la aurícula derecha que en la izquierda, los que sugiere una recuperación más precoz de la aurícula izquierda como lo observado en los infartos de la aurícula derecha. Los signos descritos son útiles para el diagnóstico de infarto auricular o miocarditis con daño predominante en la aurícula izquierda

Repercusiones del infarto experimental de la aurícula derecha sobre P, Ta y QTa / Repercusions of experimental infarction of the right atrial in P, Ta and QTa

Se produjo infarto auricular derecho (AD) en 18 perros, mediante infiltración subepicárdica de alcohol en la cara anterolateral, orejuela derecha y porción derecha de la banda interauricular. Se tomaron múltiples registros con papel fotográfico (VR6) y de inscripción directa (Sanborn 150) de 4 canales a velocidad de 50 y 100mm/seg.: 5 unipolares directas y 19 de superficie, incluyendo torácicas derechas y abdominales MD, ME y MI en condiciones de control, después de la infiltración y 120 minutos más tarde. Al fin de experimento se produjeron extrasístoles en AD (EAD) y bloqueo A-V para determinar, con certeza, la duración del QTa y su fin en el ST ventricular. Hubo disminución de la frecuencia cardiaca, ligero ensanchamiento del P-R y de la onda P y ritmo auricular derecho bajo (4 casos). Los cambios más significativos se observaron el las derivaciones torácicas derechas y a veces hasta V4-V5. El vector de lesión apunta hacia adelante elevando el segmento P-R en las derivaciones mencionadas y en las direchas de AD. Apareció onda Qp o complejos en W en las mismas derivaciones y en D2, D3 y a VF. Los signos tienen más valor en las torácicas sea en ritmo sinusal o AD bajo. El vector de necrosis se aleja de la AD. La onda Ta isquémica se prolongó hasta la irregularidad del ST ventricular, la que también se observaba en los trazos directos y en D2 desde los registros de control. El QT auricular corregido (QTac) se encontró prolongado a VM mayor de + 0.04 seg, siendo más largo en la AD dañada, lo

Comparación del estudio anatómico postmortem y la ecocardiografía bidimensional en el infarto del miocardio / Comparison of postmortem anatomical study and two-dimensional echocardiography in myocardial infarction

Se estudiaron 10 pacientes, de 30 a 69 años, que habían sufrido un infarto del miocardio (IM) de más de 6 meses de evolución y que fallecieron. En todos se realizó autopsia y, en un lapso menor de 15 días antes de su muerte, ecocardiograma bidimensional (E 2-D) y cateterismo. Se correlacionó la localización y extensión del IM con el E 2-D respecto a movilidad segmentaria (MS), espesor diastólico final (EDF) y porcentaje de engrosamiento parietal sistólico (PEPS) de los 15 segmentos en que se dividió la pared ventricular izquierda. Se comparó también con la coronariografía. Se observó concordancia de la disinergia con la localización (P<0.01) y extensión (P<0.05) del área de necrosis, especialmente cuando era transmural. El espesor parietal postmortem de cada uno de los segmentos tuvo buena correlación con el EDF en el E 2-D (r=0.926). El EDF fue menor en los segmentos con necrosis, de 8.8 + ou - 1.8 mm, que en los segmentos sin esta alteración, de 14.1 + ou - 1.9 mm (P<0.05). En grado de adelgazamiento parietal fue mayor en los segmentos con IM transmural. El PEPS fue significativamente menor (P<0.01) en los segmentos con necrosis, de 12.1 + ou - 3% y de 24.1 + ou - 4.3% en los que no la presentaron. La alteración de la MS mostró relación con la obstrucción coronaria mayor del 75%, en especial cuando esta había determinado necrosis. El EDF fue menor en los segmentos con IM y obstrucción coronaria significativa, que en aquellos sin necrosis aunque la obstrucción coronaria fuera importante (P<0.01). El PEPS fue menor en los segmentos con necrosis, tanto con obstrucción coronaria significativa como moderada (11.3 + ou - 2.3%) que en aquellos con obstrucción coronaria pero sin necrosis (22.3 + ou - 4.2%), a su vez inferior al de los que no presentaron obstrucción coronaria ni necrosis (30.1 + ou - 2.2%), diferencia significativa (P<0.01). La medición por E 2-D del EDF y del PEPS segmentarios es útil para reconocer y diferenciar la necrosis de la isquemia parietal del ventrículo izquierdo en la enfermedad arterial coronaria

Diagnóstico con ecocardiografía bidimensional de un trombo libre en la aurícula izquierda / Diagnosis with bidimensional echocardiography of a free thrombus in the left atrial

La presencia de trombosis auricular izquierda en la valvulopatía mitral reumática constituye un importante factor de morbimortalidad en la evolución natural de esta enfermedad. Ello indica la importancia de efectuar un diagnóstico precoz, así como el estudio de aquellos pacientes que han tenido un accidente tromboembólico previo. Describimos el caso de una mujer en la sexta década de la vida con estenosis mitral pura y portadora de un trombo libre en la aurícula izquierda, muy claramente demostrado en el ecocardiograma. Hacemos énfasis en la sensibilidad y especialidad que tiene la ecocardiografía bidimensional para el diagnóstico de estos casos