RESUMO
Background: Frequent monitoring of patients declined during the COVID-19 pandemic, harming patients with chronic diseases who critically needed correct monitoring. We evaluated the impact of the COVID-19 pandemic in patients with non-valvular atrial fibrillation (NVAF) receiving treatment with vitamin K antagonists (VKA) or non-vitamin K antagonist oral anticoagulants (NOAC) in clinical practice in Spain. Methods: This observational, retrospective study analyzed prevalent patients treated with NOAC/VKA on 14/03/2019 (pre-COVID-19 period) and 14/03/2020 (COVID-19 period), who were followed up to 12 months. The study also considered incident patients who started treatment with NOAC/VKA between 15/03/2019 and 13/03/2020 (pre-COVID-19 period) and from 15/03/2020 to 13/03/2021 (COVID-19 period). Demographic characteristics, comorbidities, effectiveness, treatment patterns, and healthcare resource utilization were considered. Results: Prevalent patients amounted to 12,336 and 13,342 patients, whereas 1,612 and 1,602 incident patients were included in the pre-COVID-19 and COVID-19 periods, respectively. Prevalent patients treated with VKA had more strokes, thromboembolism, and major bleeding compared to those receiving NOAC, particularly during the COVID-19 period. NOAC patients had a 12 % lower risk of death than those on treatment with VKA (Hazard ratio = 0.88 [95 % CI: 0.81 - 0.95], p = 0.033). In addition, VKA patients were less persistent after 12 months than NOAC patients (pre-COVID-19 period: 52.1 % vs. 78.9 %, p < 0.001; COVID-19 period: 49.2 % vs. 80.3 %, p < 0.001), and required more healthcare visits and hospitalizations than those on treatment with NOAC. Conclusion: Compared to VKA, NOAC seems to have reduced the incidence of severe events and the use of healthcare resources for NVAF, particularly during the pandemic.
RESUMO
Anthracyclines are cytostatic antibiotics discovered almost half a century ago exerting their action through inhibition of topoisomerase II. The two most representative drugs are doxorubicin and daunorubicin and they have been proven as useful antineoplastics and are widely prescribed in daily oncology practice; unfortunately, cardiotoxicity has been a limiting factor when it comes to their use. Diverse mechanisms have been involved in anthracycline cardiotoxicity, none of which are capable of causing the whole clinical picture by itself. Traditionally, reactive oxygen species (ROS) have received more attention, although recently basic research has proven other factors to be as important as ROS. These factors mainly involve sarcomeric structure disruption, toxic accumulation of metabolites, iron metabolism, energetic alterations and inflammation. The role of genetics has been studied by some groups, although a clear genotype-response relationship is yet to be elucidated. With the improved survival from different oncologic diseases we are witnessing more cases of chemotherapy-induced cardiotoxicity and the advent of new anticancer drugs poses several challenges for the cardiologist, highlighting the importance of a deep knowledge of the main mechanisms inducing this toxicity.
Hace casi medio siglo se descubrieron las antraciclinas; estas son antibióticos citostáticos inhibidores de la topoisomerasa II. Los 2 fármacos más representativos de este grupo son la doxorrubicina y la daunorrubicina. Estos fármacos han demostrado ser eficaces antineoplásicos y han sido ampliamente utilizados en la práctica oncológica. Desafortunadamente, la cardiotoxicidad sigue siendo un elemento limitante para su uso. Los mecanismos mediante los cuales estos fármacos ocasionan cardiotoxicidad son múltiples pero ninguno de ellos de forma individual es capaz de explicar el cuadro clínico por completo. Casi siempre se ha considerado que la formación de especies reactivas de oxígeno era responsable de gran parte de la toxicidad, sin embargo la experimentación básica reciente ha demostrado que hay otros factores, entre los que destacan las alteraciones en la estructura sarcomérica, la acumulación de metabolitos tóxicos, las alteraciones del metabolismo del hierro o de los mecanismos energéticos, y la liberación de mediadores de inflamación. Por otra parte, diversos grupos han investigado la intervención que la genética podría tener en el desarrollo de esta enfermedad, si bien no se puede definir aún una clara correlación genotipo-respuesta. Con el aumento de la supervivencia por el tratamiento de diversas enfermedades oncológicas, se están detectando más casos de cardiotoxicidad mediada por quimioterapia; y con la aparición de nuevos fármacos quimioterápicos se añaden nuevos retos, con lo que se demuestra la importancia del estudio profundo de los mecanismos causales.