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.

Air pollution and children's respiratory health: a scoping review of socioeconomic status as an effect modifier.

OBJECTIVES: Air pollution is a leading environmental risk, and socioeconomic status (SES) is postulated as an effect modifier, especially in children. There is a growing interest in exploring this modifier. The present manuscript reviews SES as an effect modifier in children's respiratory health. METHODS: A search in the PubMed and SCOPUS databases was conducted in September 2017 to identify studies with the inclusion criteria of being centred on children, respiratory outcomes, air pollutants and SES measurement. RESULTS: A total of 17 studies were included. Twelve used single SES variables, and the remaining studies included composite SES indices. Household income (9) and parental education (8) were frequently evaluated. The significance of the effect modifier was found in nine studies that demonstrated a higher risk for individuals living in a lower SES. Sources of heterogeneity included SES measurement, health outcomes and geographical aggregation. CONCLUSIONS: The results suggest a higher modification in the effect of SES, generally indicating greater risk for children in lower SES. Children's characteristics need to be more carefully theorized and measured in this area, including the use of transdisciplinary approaches.

Land use regression models to assess air pollution exposure in Mexico City using finer spatial and temporal input parameters.

The Mexico City Metropolitan Area (MCMA) is one of the largest and most populated urban environments in the world and experiences high air pollution levels. To develop models that estimate pollutant concentrations at fine spatiotemporal scales and provide improved air pollution exposure assessments for health studies in Mexico City. We developed finer spatiotemporal land use regression (LUR) models for PM2.5, PM10, O3, NO2, CO and SO2 using mixed effect models with the Least Absolute Shrinkage and Selection Operator (LASSO). Hourly traffic density was included as a temporal variable besides meteorological and holiday variables. Models of hourly, daily, monthly, 6-monthly and annual averages were developed and evaluated using traditional and novel indices. The developed spatiotemporal LUR models yielded predicted concentrations with good spatial and temporal agreements with measured pollutant levels except for the hourly PM2.5, PM10 and SO2. Most of the LUR models met performance goals based on the standardized indices. LUR models with temporal scales greater than one hour were successfully developed using mixed effect models with LASSO and showed superior model performance compared to earlier LUR models, especially for time scales of a day or longer. The newly developed LUR models will be further refined with ongoing Mexico City air pollution sampling campaigns to improve personal exposure assessments.

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.

The oxidative potential and biological effects induced by PM10 obtained in Mexico City and at a receptor site during the MILAGRO Campaign.

As part of a field campaign that studied the impact of Mexico City pollution plume at the local, sub-regional and regional levels, we studied transport-related changes in PM(10) composition, oxidative potential and in vitro toxicological patterns (hemolysis, DNA degradation). We collected PM(10) in Mexico City (T(0)) and at a suburban-receptor site (T(1)), pooled according to two observed ventilation patterns (T(0) → T(1) influence and non-influence). T(0) samples contained more Cu, Zn, and carbon whereas; T(1) samples contained more of Al, Si, P, S, and K (p < 0.05). Only SO(4)(-2) increased in T(1) during the influence periods. Oxidative potential correlated with Cu/Zn content (r = 0.74; p < 0.05) but not with biological effects. T(1) PM(10) induced greater hemolysis and T(0) PM(10) induced greater DNA degradation. Influence/non-influence did not affect oxidative potential nor biological effects. Results indicate that ventilation patterns had little effect on intrinsic PM(10) composition and toxicological potential, which suggests a significant involvement of local sources.

In vitro biological effects of airborne PM2.5 and PM10 from a semi-desert city on the Mexico-US border.

Compelling evidence indicates that exposure to urban airborne particulate matter (PM) affects health. However, how PM components interact with PM-size to cause adverse health effects needs elucidation, especially when considering soil and anthropogenic sources. We studied PM from Mexicali, Mexico, where soil particles contribute importantly to air pollution, expecting to differentiate in vitro effects related to PM-size and composition. PM samples with mean aerodynamic diameters ≤2.5µm (PM(2.5)) and ≤10µm (PM(10)) were collected in Mexicali (October 2005-March 2006) from a semi-urban (expected larger participation of soil sources) and an urban (predominately combustion sources) site. Samples were pooled by site and size, analyzed for elemental composition (particle-induced X-ray emission) and tested in vitro for: induction of human erythrocytes membrane disruption (hemolysis) (colorimetrically); inhibition of cell proliferation (ICP) (crystal violet) and TNFα/IL-6 secretion (ELISA) using J774.A1 murine monocytic cells; and DNA degradation using Balb/c3T3 cell naked DNA (electrophoretically). Results of PM elemental composition principal component analysis were used in associating cellular effects. Sixteen elements identified in PM grouped in two principal components: Component(1) (C(1)): Mg, Al, Si, P, Cl, K, Ca, Ti, V, Cr, Fe, and Component(2) (C(2)): Cu, Zn. Hemolysis was predominately induced by semi-urban-PM(10) (p<0.05) and was associated with urban-PM(10)C(1) (r=0.62, p=0.003). Major ICP resulted with semi-urban PM(2.5) (p<0.05). TNFα was mainly induced by urban samples regardless of size (p<0.05) and associated with urban-PM(2.5)C(2) (r=0.48, p=0.02). Both PM(10) samples induced highest DNA degradation (p<0.05), regardless of location. We conclude that PM-size and PM-related soil or anthropogenic elements trigger specific biological-response patterns.

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.

E-Selectin expression in human endothelial cells exposed to PM10: the role of endotoxin and insoluble fraction.

Exposure to PM10 is associated with cardiovascular effects. We evaluated the effects of PM10 on E-Selectin expression and monocytic cell adhesion in human umbilical vein endothelial cells (HUVECs). HUVEC were exposed to PM10 (5-40 microg/cm2) for 6 h, following which surface E-Selectin expression was detected by fluorescence microscopy and flow cytometry. The effects of total particles, particles treated with polymixin-B to block the effects of endotoxin, and both soluble and insoluble fractions of particles, were assessed. Incubation with PM10 lead to a concentration-related increase of E-Selectin expression (>seven-fold increase at 40 microg/cm2). Particles pre-treated with polymixin-B inhibited E-Selectin expression to a level slightly higher than untreated particles. An increase in fluorescence was also observed with the insoluble fraction, while the soluble fraction had no significant effect. HUVEC exposed to PM10 were also evaluated for adhesivity of monocytic cells (U937). PM10 strongly increased the adhesion of U937 cells to HUVEC. In conclusion, PM10 induces endothelial cell activation, evidenced by enhanced E-Selectin expression. This activation is manifested functionally as an increase in monocytic cell adhesion. Insoluble components as well as endotoxins appear to be responsible for this activity.

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.

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

Signos eléctricos de la pericarditis experimental / Electric changes of experimental pericarditis

Se analizaron, en 25 corazones de perro, los cambios electrocardiográficos (directos y de superficie) así como los tensionales, inducidos por una solución al 7.5% de salicilato de metilo instilada en el saco pericárdico y por un derrame agudo provocado tardíamente (90 minutos) por la inyección de 50 ml de una mezcla de suero y sangre. Se tomaron presiones intracavitarias de aurícula derecha (AD), ventrículo derecho (VD), ventrículo izquierdo (VI), saco pericárdico, (P) y de la arteria femoral. Se obtuvieron muestras para microscopía de luz y electrónica en 11 corazones. Se concluye que la pericarditis aguda produce daño miocárdico de las primeras tres a seis hileras de miocitos y hemorragia del pericardio. Se encontró desnivel positivo de RST-T en todas las derivaciones directas y de superficie, pero de estas últimas sobre todo en D2, D3, aVF, de V4 a V6 y de V3R a V5R y abdominales altas. La lesión evolucionó a isquemia (ondas T negativas) en las mismas derivaciones incluyendo las torácicas derechas, excepto de V3R a V3, en las que persiste un ligero desnivel positivo de RST-T con muesca de T en V2-V3. Se encontró una muesca en la unión del QRS con el ST sugestiva de lesión auricular. No se modificó la velocidad de inscripción, ni el tiempo de la deflexión intrínseca ni de la intrinsecoide. Estos hechos, en conjunto con el RST-T hundido en aVR, en la AD y en la cavidad del ventrículo derecho, orientan el diagnóstico hacia el de pericarditis. La onda P se volvió + ou = en el lado derecho y bimodal en V3-V4 como manifestación de daño auricular (68%). Se concluye que el RST-T elevado en las torácicas derechas y abdominales altas no es concluyente de infarto del VD, en ausencia de modificaciones del QRS. Las presiones se modificaron sólo con el derrame agudo, con cifras promedio de PAD 20.6, Pericardio 20.6 y diastólica tardía de VD 13.2. En el VI sólo 5 casos tuvieron presiones diastólicas tardías superiores a 15 mmHg entre 20 y 24 mmHg