The Changing Landscape for Stroke\ua0Prevention in AF: Findings From the GLORIA-AF Registry Phase 2

Background GLORIA-AF (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation) is a prospective, global registry program describing antithrombotic treatment patterns in patients with newly diagnosed nonvalvular atrial fibrillation at risk of stroke. Phase 2 began when dabigatran, the first non\u2013vitamin K antagonist oral anticoagulant (NOAC), became available. Objectives This study sought to describe phase 2 baseline data and compare these with the pre-NOAC era collected during phase 1. Methods During phase 2, 15,641 consenting patients were enrolled (November 2011 to December 2014); 15,092 were eligible. This pre-specified cross-sectional analysis describes eligible patients\u2019 baseline characteristics. Atrial fibrillation disease characteristics, medical outcomes, and concomitant diseases and medications were collected. Data were analyzed using descriptive statistics. Results Of the total patients, 45.5% were female; median age was 71 (interquartile range: 64, 78) years. Patients were from Europe (47.1%), North America (22.5%), Asia (20.3%), Latin America (6.0%), and the Middle East/Africa (4.0%). Most had high stroke risk (CHA2DS2-VASc [Congestive heart failure, Hypertension, Age  6575 years, Diabetes mellitus, previous Stroke, Vascular disease, Age 65 to 74 years, Sex category] score  652; 86.1%); 13.9% had moderate risk (CHA2DS2-VASc = 1). Overall, 79.9% received oral anticoagulants, of whom 47.6% received NOAC and 32.3% vitamin K antagonists (VKA); 12.1% received antiplatelet agents; 7.8% received no antithrombotic treatment. For comparison, the proportion of phase 1 patients (of N = 1,063 all eligible) prescribed VKA was 32.8%, acetylsalicylic acid 41.7%, and no therapy 20.2%. In Europe in phase 2, treatment with NOAC was more common than VKA (52.3% and 37.8%, respectively); 6.0% of patients received antiplatelet treatment; and 3.8% received no antithrombotic treatment. In North America, 52.1%, 26.2%, and 14.0% of patients received NOAC, VKA, and antiplatelet drugs, respectively; 7.5% received no antithrombotic treatment. NOAC use was less common in Asia (27.7%), where 27.5% of patients received VKA, 25.0% antiplatelet drugs, and 19.8% no antithrombotic treatment. Conclusions The baseline data from GLORIA-AF phase 2 demonstrate that in newly diagnosed nonvalvular atrial fibrillation patients, NOAC have been highly adopted into practice, becoming more frequently prescribed than VKA in Europe and North America. Worldwide, however, a large proportion of patients remain undertreated, particularly in Asia and North America. (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation [GLORIA-AF]; NCT01468701

Agrandamiento gingival inducido por nifedipino

Revista Ciencias Biomédicas Vol.5, Núm. 1 (2014) Pag 144 - 147Introducción: el agrandamiento gingival es el aumento del tamaño de la encía causado por diversos factores, entre los cuales se encuentran medicamentos, principalmente antihipertensivos, inmunosupresores y anticonvulsivantes. Entre los primeros, el nifedipino, un antagonista del calcio, es uno de los más frecuentemente señalados. Caso clínico: paciente masculino de 62 años, con hipertensión arterial tratada con nifedipino por más de quince años, quien presentó agrandamiento gingival crónico en la zona de los incisivos laterales y caninos del maxilar superior. Se realizó gingivectomía a bisel externo, con electro bisturí, con evolución adecuada y buena cicatrización. Conclusión: el agrandamiento gingival segundario a nifedipino, amerita tratamiento, que incluye suspensión del medicamento e higiene oral. En algunas circunstancias se debe realizar gingivectomía

The pandemic: virtuality in education

Revista Ciencias Biomédicas Vol.9, Núm.2 (2020) Pag. 147 - 15

Eriptosis: mecanismos moleculares y su implicación en la enfermedad aterotrombótica

ResumenIntroducciónLa eriptosis se ha descrito como el proceso de muerte celular programada en el eritrocito antes de la senectud. Puede desencadenarse en situaciones como: el estrés osmótico, el estrés oxidativo, la exposición a metales pesados, entre otros factores. Diversos estudios sugieren que los eritrocitos pueden desempeñar un papel activo en la hemostasia normal o anormal en ciertas condiciones en las que se produce perturbación de la membrana de estas células.ObjetivoDescribir los mecanismos involucrados en la eriptosis y su estrecha relación con los procesos de adhesión a la pared vascular que conllevan a la enfermedad trombótica.MétodoSe hizo una revisión narrativa a partir de la literatura encontrada en las bases de datos PubMed y Science Direct utilizando las palabras claves. Se seleccionaron 51 artículos originales, 20 revisiones de la literatura y un estudio de casos, que se ajustaban a las exigencias del objetivo. Se revisaron los resúmenes de forma separada e independiente. Seguidamente se buscaron las publicaciones en el texto completo para la revisión.ConclusionesLa eriptosis se caracteriza por la disminución del volumen celular, la vesiculación y la translocación del fosfatidil serina hacia la superficie externa de la membrana plasmática. Las alteraciones en la distribución de los fosfolípidos favorecen los procesos de adhesión celular a la pared vascular, conllevando al deterioro de la microcirculación, lo cual puede ocasionar importantes trastornos a nivel cardiovascular. La comprensión y el esclarecimiento de la eriptosis pueden ser esenciales para la búsqueda de nuevas dianas terapéuticas, encaminadas a ofrecer otras alternativas farmacológicas en el tratamiento de la enfermedad cardiovascular.AbstractIntroductionEryptosis has been described as programmed process of cellular death in erythrocytes before old age. It can be triggered, among other factors, by situations such as osmotic stress, oxidative stress or exposure to heavy metals. Several studies suggest that erythrocytes can play an active role in normal or abnormal haemostasis in certain conditions where the membrane of these cells is perturbed.ObjetiveTo describe the mechanisms involved in eryptosis and their close relationship with the processes of adhesion to the vascular wall that entail the thrombotic disease.MethodsA narrative review was carried out from the literature found in data base PubMed and Science Direct by using the key words. 51 original articles, 20 literature reviews and one case study complying with the requirements were selected. Abstracts were reviewed separately and independently. Complete publications were then located for review.ConclusionsEryptosis is characterised by the decrease in cell volume, the vesiculation and the translocation of phosphatidylserine towards the outer surface of the plasma membrane. Disorders in the distribution of the phospholipids favour processes of cell adhesion to the vascular wall, causing impairment of microcirculation, which can result in important cardiovascular diseases. Understanding and clarifying eryptosis could be essential for finding new therapeutic targets, aimed at offering other pharmacological alternatives for the treatment of cardiovascular diseases

News on angiotensin II and atrial fibrillation : from the molecular to the pathophysiological.

Revista Ciencias Biomédicas Vol.10, Núm.2 (2021) Pag. 109-119Introduction: atrial fibrillation is the most prevalent arrhythmia in the world, having high morbidity and mortality rates. Numerous studies have shown the involvement of the angiotensin renin system in the pathogenesis of atrial fibrillation, and in several of these, the underlying mechanism involving a process of atrial tissue remodeling is speculated. Objective: present literature related to the pathophysiological mechanisms of Atrial Fibrillation, its impact on cardiovascular risk, and related aspects between angiotensin II and atrial fibrillation. Methods: a non-systematic review of the available literature was conducted using key terms such as "Atrial Fibrillation" and "Angiotensin II", in addition to synonyms, which were combined with the "AND" and "OR" connectors, both in English and Spanish, in the PubMed, ScienceDirect, Embase, EBSCO, and MEDLINE databases. Results: atrial fibrosis is a structural alteration that facilitates the maintenance of atrial fibrillation, Angiotensin II contributes to this process extensively by stimulating inflammatory processes, decreasing the activity of collagenase, increased expression of MAPK, and changes in cardiac electrophysiological properties through binding to the AT1 receptor. Conclusions: getting to know the pathophysiology of atrial fibrillation at the molecular level, allows to further elucidate the context and possible complications of affected patients, facilitating the generation of hypotheses that contribute to the timely, accurate and effective diagnosis, the development of new therapeutic targets, as well as a better approach in the clinical area