Differentiating the impact of fine and coarse particulate matter on cause-specific cerebrovascular mortality: An individual-level, case-crossover study.

BACKGROUND AND OBJECTIVES: Many studies suggested that short-term exposure to fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) was linked to elevated risk of cerebrovascular disease. However, little is known about the potentially differential effects of PM2.5 and PM2.5-10 on various types of cerebrovascular disease. METHODS: We collected individual cerebrovascular death records for all residents in Shanghai, China from 2005 to 2021. Residential daily air pollution data were predicted from a satellite model. The associations between particulate matters (PM) and cerebrovascular mortality were investigated by an individual-level, time-stratified, case-crossover design. The data was analyzed by the conditional logistic regression combined with the distributed lag model with a maximum lag of 7 days. Furthermore, we explored the effect modifications by sex, age and season. RESULTS: A total of 388,823 cerebrovascular deaths were included. Monotonous increases were observed for mortality of all cerebrovascular diseases except for hemorrhagic stroke. A 10 µg/m3 rise in PM2.5 was related to rises of 1.35% [95% confidence interval (CI): 1.04%, 1.66%] in mortality of all cerebrovascular diseases, 1.84% (95% CI: 1.25%, 2.44%) in ischemic stroke, 1.53% (95% CI: 1.07%, 1.99%) in cerebrovascular sequelae and 1.56% (95% CI: 1.08%, 2.05%) in ischemic stroke sequelae. The excess risk estimates per each 10 µg/m3 rise in PM2.5-10 were 1.47% (95% CI: 1.10%, 1.84%), 1.53% (95% CI: 0.83%, 2.24%), 1.93% (95% CI: 1.38%, 2.49%) and 2.22% (95% CI: 1.64%, 2.81%), respectively. The associations of both pollutants with all cerebrovascular outcomes were robust after controlling for co-pollutants. The associations were greater in females, individuals > 80 years, and during the warm season. CONCLUSIONS: Short-term exposures to both PM2.5 and PM2.5-10 may independently increase the mortality risk of cerebrovascular diseases, particularly of ischemic stroke and stroke sequelae.

Vasculopatías cerebrales por consumo de drogas de abuso en pacientes adultos: a propósito de un caso / Cerebral vasculopathies due to drug abuse in adult patients: a case report

INTRODUCCIÓN: La enfermedad de moyamoya es una enfermedad cerebrovascular que se caracteriza por la estenosis progresiva de las arterias del polígono de Willis, desarrollando una red vascular compensatoria anómala, denominada vasos moyamoya. Dichas áreas son más susceptibles de sufrir isquemia o hemorragia. CASO CLÍNICO: Varón de 47 años con clínica de debilidad en miembro superior izquierdo y torpeza en la marcha en miembro inferior izquierdo, de 5 días de evolución, en relación con consumo de cocaína. En arteriografía, red colateral compatible con patrón de moyamoya. DISCUSIÓN: El consumo crónico de cocaína produce aumento brusco de la presión arterial, vasoconstricción cerebral, vasculitis y trombosis aguda, con el consecuente desarrollo de vasos moyamoya como mecanismo fisiológico compensatorio

INTRODUCTION: Moyamoya disease is a cerebrovascular disease characterized by progressive stenosis of the arteries of the circle of Willis, conditioning the appearance of an anomalous compensatory vascular network, the moyamoya vessels. These areas are more susceptible to suffering ischemia or haemorrhage. CASE REPORT: A 47-year-old man with symptoms of weakness in the left upper limb and clumsy walk because of left leg, of 5 days' evolution, in relation to cocaine consumption. In arteriography, extensive collateral network compatible with the moyamoya pattern. DISCUSSION: The chronic consumption of cocaine produces abrupt increase in blood pressure, cerebral vasoconstriction, vasculitis and acute thrombosis, with the consequent development of moyamoya vessels as a compensatory physiological mechanism

Mecanismos de los efectos nocivos para la salud de la contaminación atmosférica proveniente de incendios forestales / Mechanisms of noxious effects of wildfire air pollution over human health

Los incendios forestales representan un problema creciente de la salud pública a nivel mundial, especialmente para la población más vulnerable (niños, ancianos, embarazadas y portadores de enfermedades cardiovasculares o respiratorias crónicas) expuesta al humo y a otros contaminantes aéreos. A diferencia de la contaminación atmosférica habitual de grandes urbes, aquella derivada de los incendios forestales tiene una composición diferente y su ocurrencia es esporádica y difícil de prever. La exposición a contaminantes atmosféricos derivados de incendios forestales se asocia a aumento de la morbilidad respiratoria y cardiovascular, mediada por una respuesta inflamatoria pulmonar y sistémica, estrés oxidativo y disfunción endotelial. En sujetos expuestos a humo de incendios forestales se ha observado un aumento en la producción de citoquinas pro-inflamatorias, activación endotelial y disfunción del sistema nervioso autónomo, que produce daño tisular, aumento de los mecanismos protrombóticos, aumento de la presión arterial y cambios en el ritmo cardiaco. Esta revisión analiza los mecanismos que han sido involucrados en generar efectos nocivos para la salud de seres humanos expuestos a material particulado y gases emanados de incendios forestales.

Wildfires represent a growing global public health issue, especially to the most vulnerable segment of the population (children, old people, pregnant women, patients with cardiovascular or respiratory diseases) exposed to smoke and other air borne contaminants generated from these events. In contrast to great cities ' usual atmospheric pollution, that derives from forest fires differ in composition and its occurrence is sporadic and usually unpredictable. Exposure to atmospheric pollutants derived from forest fires has been associated to increased respiratory and cardiovascular morbidity, mediated by an inflammatory systemic response, oxidative stress and endothelial dysfunction. In people exposed to forest fire smoke an increased production of pro-inflammatory cytokines, endothelial activation and autonomic nervous system dysfunction has been observed, that leads to tissue injury, increased prothrombotic response, increased blood pressure and changes in heart rhythm. This review analyzes the mechanisms that have been involved in generating harmful health effects in humans exposed to inhaled particulate matter and gases steaming from wildfires.

Complicaciones neurológicas por cocaína / Neurological damages due to cocaine abuse

La información sobre los riesgos del uso de cocaína no llega a calar entre los usuarios, la población general, ni siquiera entre los profesionales sanitarios. En el presente trabajo hemos hecho una breve revisión bibliográfica sobre los aspectos en que la cocaína afecta neurológicamente. Además de los daños tóxicos y estructurales por la cocaína y sus metabolitos, debemos tener presente la acción sobre el sistema cardiovascular y los posibles accidentes que pueden padecerse. Entre esos aspectos debemos mencionar: los accidentes cerebrovasculares (hemorragias, infartos) por la acción vasoconstrictora y los efectos activadores sobre corazón. Otros daños y alteraciones son las crisis convulsivas debidas a fenómenos toxicometabólicos y por incremento de catecolaminas. Fenómenos de repetición por la intoxicación cocaínica son las cefaleas provocadas por diferentes causas desde las hemorragias e infartos cerebrales, hipertensión arterial, etc. También están las crisis de agitación que pueden aparecer en el transcurso de la intoxicación. Se han podido detectar procesos catatónicos o distónicos atribuibles al uso de cocaína. La hipertermia es otro fenómeno frecuente entre los consumidores de cocaína, sobre todo cuando se consume en espacios que pueden producir incremento de temperatura. Además se han descrito daños de tipo neuropsicofarmacológico como el síndrome serotoninérgico Los efectos desmielinizantes son por el efecto tóxico y actúan sobre la sustancia blanca La rabdomiolisis son daños musculares por la hipertermia, la hiperestimulación simpática, vasoconstricción, etc

The information about the risks of the use of cocaine doesn't end up soaking among the users, the general population, not even among the sanitary professionals. In the present work we have made a brief bibliographical revision on the aspects in that the cocaine affects neurologically. Besides the toxic and structural damages for the cocaine and their metabolites, we would have present the action on the cardiovascular system and the possible accidents that they can be suffered. Among those aspects we must present and mention: the cerebrovascular accidents (haemorrhage, coronaries) due the vasoconstrictive action and the activator effects of cocaine on heart. Other damages and alterations are the due spastic crises for toxic and metabolic phenomena and for catecholamine increment. Repetition phenomena due the cocaine intoxication are the migraines caused by different problems from the haemorrhages and cerebral coronaries, arterial hypertension, etc. the crises of agitation (seizures) that can appear also in the course of the intoxication. They have been able to detect catatonic processes or dystonia attributable to the use of cocaine. The hyperthermia is another frequent phenomenon among the consumers of cocaine, mainly when wastes away in spaces that can produce increment of temperature. Also we can found neuropsycopharmacological damages like the serotoninergic syndrome. The demyelation effects have been described due the toxic effect and the rabdomiolisis on the white substance, as muscular damages for the hyperthermia, the sympathetic hyperestimulation, vasoconstrictive phenomena, etc

A multinational case-control study of cardiovascular disease and steroid hormone contraceptives: description and validation of methods

A hospital-based, case-control study of the association between current usage of oral contraceptives and first-time cases of acute myocardial infarction, stroke, or a venous thromboembolic event (deep vein thrombiosis or pulmonary embolus) was carried out in 17 countries from four regions (Africa, Europe, Asia, and Latin America, [including Jamaica]). A total of 3792 cases and 10,281 hospitalised controls matched for age were recruited during a 4-year period, ending June 1993. The study was designed to have sufficient power to detect a relative risk of 2 for developing each of the three study diseases, associated with current oral contraceptive use in each of the four regions, with the exception of acute myocardial infarction (for which all non European regions were combined) and for venous thromboembolic events in Asia, where these disorders are rare. This report describes the background, pilot study, methods, and the analyses carried out to validate the methods used in the study. (Au)

Anticonceptivos orales y morbilidad de enfermedades cardiovasculares / Oral contraceptives and cardiovascular diseases morbility

Se estudió asociación entre ciertas enfermedades cardiovasculares no reumáticas y el uso de anticonceptivos orales den mujeres de 20 a 44 años de edad hospitalizadas en unudades de segundo y tercer nivel de atención médica del Instituto Mexicano del Seguro Social en el Valle de México, de 1979 a 1984. Se analizaron los datos de 201 casos y 606 testigos apareados por edad, paridad y nivel de educación. Se encontró que el riesgo relativo de desarrollar cardiopatía isquémica, accidente cerebrovascular, tromboembolia pulmonar y trombosis venosa aumentó en forma estadísticamente significativa para las mujeres que estaban usando o habían usado alguna vez anticonceptivos orales. En el análisis conjunto de estas enfermedades, el riesgo se presenta desde los primeros meses de uso, con el empleo de anticonceptivos que contienen 40 µg o menos de estrógeno y se incrementa conforme es mayor la edad de la mujer