É inquestionável o modelo patriarcal, branco e com privilégios financeiros que, aliados a uma visão do “homem detentor da razão e a mulher detentora da emoção”,2 ajudaram a construir o modelo de ciência que, de maneira equivocada, afastou as mulheres do campo científico.George Eliot e George Sand, romancistas do século XIX, eram pseudônimos de Mary Ann Evans e Amandine Aurore Lucile Dupin, respectivamente. Em comum, duas mulheres que para atingirem reconhecimento por seus textos, utilizavam nomes masculinos em suas obras, como bem relata Nodari em seu artigo publicado em 2021.3 As mulheres dispensam duas vezes mais tempo aos afazeres domésticos por semana em relação aos homens da mesma faixa etária , têm menor remuneração que seus pares do sexo masculino (77% da renda masculina), e naquelas com idade entre 25 e 49 anos que convivem no mesmo domicílio que uma criança de até três anos, o percentual de inserção no mercado de trabalho é menor que o dos homens na mesma situação .3Pensar este modelo como algo pertencente ao passado não é adequado. Dados da Pesquisa Nacional por Amostra de Domicílios (PNAD), do Instituto Brasileiro de Geografia e Estatística (IBGE) de 2019, expõe uma realidade social que apresenta reflexos na formação da cientista.5 Em 2020, a relação homem/mulher era 2,21, ao contrário de outras especialidades como dermatologia, pediatria e endocrinologia, com relações inferiores a 1.4 Este padrão observado no Brasil também é encontrado nos Estado Unidos6 e na Europa,7 com baixa representatividade global feminina na cardiologia ou em posições de liderança dentro da especialidade.Apesar do número crescente de mulheres na medicina e da formação universitária generalista mais jovem, a cardiologia ainda é uma especialidade com predominância masculina.3 Este dado é, na prática, refletido no estudo de Oliveira-Ciabati et al., que demonstrou que mais de 60% da composição docente da Universidade de São Paulo é do sexo masculino, o que também contribui para o aumento da disparidade de gênero nas publicações.2Após a especialização, o caminho segue em direção à pós-graduação para a formação docente com a consequente e natural liderança em áreas de pesquisa. Novamente, o cenário não sofre alterações e as mulheres representam 46% do corpo docente superior.8 Nele, os autores abordam de maneira bastante elucidativa a disparidade de gênero nas publicações das revistas Arquivos Brasileiros de Cardiologia (ABC Cardiol) e International Journal of Cardiovascular Sciences (IJCS), de 2000 a 2019.Neste contexto, o estudo publicado nos Arquivos Brasileiros de Cardiologia é fundamental para o entendimento do meio acadêmico brasileiro.8 De maneira geral, sabe-se que a primeira autoria reflete o principal responsável pelo artigo em questão, enquanto o último autor, ou sênior, reflete o líder da linha de pesquisa responsável pelo trabalho mais abrangente, capaz de gerar outras publicações.Entre os 1555 artigos publicados nas revistas que representam as maiores fontes de estudos na cardiologia do país, os autores observaram que as mulheres apresentaram predominância apenas na primeira autoria e apenas na revista IJCS (53%), enquanto homens predominaram na primeira autoria nos ABC Cardiol (58%) e como autores seniores em ambas (75% no ABC Cardiol e 59% no IJCS).8Outra observação feita pelos autores refere-se à evolução temporal da predominância de gênero nos campos autorais. Apesar de estarem sub-representadas nas revistas, entre 2000 e 2019, no ABC Cardiol, houve aumento na primeira autoria feminina dos artigos, de 12% para 44%. Enquanto última autoria, e, portanto, autoras seniores, o aumento foi mais modesto, de 16% em 2000 para 27% em 2019, na mesma revista.8 Embora o primeiro possa ser inconsciente e o segundo inerente ao gênero, ambos devem ser considerados na discussão sobre disparidade nas publicações cientificas e nenhum dos dois, isoladamente é consistente com os resultados observados.Entre os fatores ressaltados pelos autores que podem contribuir para esta disparidade de gênero, estão a visão estereotipada de que apenas o homem representa o cientista de sucesso, e a maternidade.8 não é exclusivo das publicações nacionais,7 e pode ser observado também em ensaios clínicos randomizados na cardiologia indexados no PubMed entre 2011 e 2020,9 e em diretrizes do Colégio Americano (American College of Cardiology/American Heart Association – ACC/AHA), da Sociedade de Canadense (Canadian Cardiovascular Society – CCS), e da Sociedade Europeia de Cardiologia (European Society of Cardiology – ESC), entre 2006 e 2020.10 Em ambos os estudos que avaliaram as publicações mencionadas, a sub-representatividade das mulheres se mantém, seja na autoria principal, seja como líder de pesquisa.O padrão notado no estudo8 é essencial. O caminho em direção a equidade é longo, mas o primeiro passo foi dado.8Por fim, a desigualdade de gênero encontrada nas publicações científicas tem origem multifatorial e inter-relações complexas, refletindo provavelmente o comportamento da sociedade. Iniquidades existentes anteriores à formação no ensino superior, desigualdades de renda e oportunidades devido à estereótipos inconsistentes, maternidade, dupla jornada de trabalho e sexismo estrutural, são apenas alguns entraves no sinuoso caminho da mulher até a autoria ou liderança científica. Para mudar este cenário, é preciso reconhecer o problema, e desta forma, a contribuição do estudo 1 Far beyond historical knowledge, analyzing gender disparity in scientific production transcends literature and must be understood as the result of a process of formation and development of society. The patriarchal, white model with financial privileges is unquestionable, which, combined with a vision of the “man with reason and the woman with emotion”,2 helped to build the model of science that, in a wrong way, kept women away from the scientific field.George Eliot and George Sand, 19th-century novelists, were pen names for Mary Ann Evans and Amandine Aurore Lucile Dupin, respectively. In common, two women who, to achieve recognition for their texts, used male names in their works, as portrayed by Nodari in his article published in 2021.3 Women spend twice as much time on housework per week compared to men of the same age group (21.4 versus 11 hours), earn less than their male peers , and in those aged between 25 and 49 years old who live in the same household with a child up to three years old, the percentage of insertion in the labor market is lower than that of men in the same situation (59.6% versus 89.2%).3To think of this model as something belonging to the past is inadequate. Data from the National Household Sample Survey (PNAD) from the Brazilian Institute of Geography and Statistics (IBGE) in 2019 exposes a social reality that reflects on the formation of the scientist.5 In 2020, the male/female ratio was 2.21, unlike other specialties such as dermatology, pediatrics and endocrinology, with ratios lower than 1.4 This pattern observed in Brazil is also found in the United States6 and Europe,7 with low global female representation in cardiology or leadership positions within the specialty.Despite the growing number of women in medicine and the younger generalist university education, cardiology is still a specialty with a male predominance.3 This data is, in practice, reflected in the study by Oliveira-Ciabati et al., which showed that more than 60% of the professors at the University of São Paulo are male, which also contributes to the increase in gender disparity in schools publications.2After the specialization, the path goes towards the postgraduate course for teacher training with the consequent and natural leadership in research areas. Again, the scenario does not change; women represent 46% of the superior faculty.Arquivos Brasileiros de Cardiologia is fundamental for understanding the Brazilian academic environment.8 In it, the authors approach in a very elucidative way the gender disparity in the publications of Arquivos Brasileiros de Cardiologia (ABC Cardiol) and the International Journal of Cardiovascular Sciences (IJCS) from 2000 to 2019.In this context, the study published by 8 Generally, it is known that the first author reflects the main responsible for the article in question, while the last author, or senior, reflects the leader of the research line responsible for the most comprehensive work, capable of generating other publications.Among the 1555 articles published in journals that represent the largest sources of studies in cardiology in the country, the authors observed that women predominated only in the first authorship and only in the IJCS journal (53%), while men predominated in the first authorship in the ABC Cardiol (58%) and as senior authors in both (75% in ABC Cardiol and 59% in IJCS).8Another observation made by the authors refers to the temporal evolution of gender predominance in authorship fields. Despite being underrepresented in magazines, between 2000 and 2019, in ABC, there was an increase in the first female authorship of articles, from 12% to 44%. As the last author, and therefore senior authors, the increase was more modest, from 16% in 2000 to 27% in 2019, in the same jornal.8 Although the first may be unconscious and the second inherent to the genre, both must be considered in the discussion about the disparity in scientific publications and neither, in isolation, is consistent with the observed results.Among the factors highlighted by the authors that may contribute to this gender disparity are the stereotyped view that only men represent the successful scientist and motherhood.8 is not unique to national publications.7 It can also be observed in randomized clinical trials in cardiology indexed in PubMed between 2011 and 20209 and in the American College of Cardiology/American Heart guidelines Association – ACC/AHA), the Canadian Cardiovascular Society (CCS), and the European Society of Cardiology (ESC), between 2006 and 2020.10 In both studies that evaluated the publications mentioned, the underrepresentation of women remains in the main authorship or as a research leader.The pattern noted in the study8 is essential. The path toward equity is long, but the first step has been taken.8Finally, the gender inequality found in scientific publications has a multifactorial origin and complex interrelationships, probably reflecting the behavior of society. Existing inequities prior to higher education training, inequalities in income and opportunities due to inconsistent stereotypes, motherhood, double shifts and structural sexism are just a few obstacles on women’s winding path to scientific authorship or leadership. To change this scenario, it is necessary to recognize the problem, and in this way, the contribution of the study


ECs), vascular smooth muscle cells (VSMCs), macrophages, endothelial progenitor cells (EPCs), and adipose‐derived mesenchymal stem cells (AMSCs) contributes to atherosclerosis. Cellular senescence and atherosclerosis share various causative stimuli, in which dyslipidemia has attracted much attention. Dyslipidemia, mainly referred to elevated plasma levels of atherogenic lipids or lipoproteins, or functional impairment of anti‐atherogenic lipids or lipoproteins, plays a pivotal role both in cellular senescence and atherosclerosis. In this review, we summarize the current evidence for dyslipidemia‐induced cellular senescence during atherosclerosis, with a focus on low‐density lipoprotein (LDL) and its modifications, hydrolysate of triglyceride‐rich lipoproteins (TRLs), and high‐density lipoprotein (HDL), respectively. Furthermore, we describe the underlying mechanisms linking dyslipidemia‐induced cellular senescence and atherosclerosis. Finally, we discuss the senescence‐related therapeutic strategies for atherosclerosis, with special attention given to the anti‐atherosclerotic effects of promising geroprotectors as well as anti‐senescence effects of current lipid‐lowering drugs.Atherosclerosis, characterized by lipid‐rich plaques in the arterial wall, is an age‐related disorder and a leading cause of mortality worldwide. However, the specific mechanisms remain complex. Recently, emerging evidence has demonstrated that senescence of various types of cells, such as endothelial cells ( I.et al., et al., intima leads to the structural destruction and functional impairment of endothelial cells (ECs), which results in the recruitment and migration of monocytes across the endothelial barrier et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., ECs are essential to maintain the structural integrity and homeostasis of blood vessels et al., et al., in vivo and in vitro , mainly microRNAs  and long non‐coding RNAs (lncRNAs), promote vascular cell senescence  and the downregulation of human telomerase reverse transcriptase (hTERT). These alterations resulted in EC senescence through the ROS/ataxia‐telangiectasia mutated (ATM)/checkpoint kinase 2 (CHK2)/p53 pathway et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., It has been known that hypertriglyceridemia, which is caused by elevated levels of circulating TRLs, including chylomicron (CM), very‐low density lipoprotein (VLDL) and their remnants, aggravates atherosclerosis and is related to cardiovascular diseases  content meal promoted inflammation and ROS production in ECs, while a meal containing high monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs), especially n‐3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), exerted the opposite effects  and the downstream c‐Jun N‐terminal kinase (JNK), which resulted in decreased activity of silent information regulator 1 (SIRT1) ‐induced DNA damage, ROS production and cellular senescence in ECs through enhancing the Nrf2‐mediated antioxidant response , accompanied by decreased ROS production, cellular senescence and apoptosis in ECs (Yubero‐Serrano (4)et al., et al., et al., et al., et al., Although compelling evidence has demonstrated inverse associations between HDL cholesterol level and cardiovascular outcomes, therapeutic interventions that increase HDL cholesterol level such as cholesteryl ester transfer protein (CETP) inhibitors, have not been shown to reduce the risk of cardiovascular events et al., et al., et al., et al., et al., +KDR+ EPCs, which manifests as an impaired migratory response and vascularization. Furthermore, the number and migratory ability of EPCs in CAD patients was inversely correlated with cardiovascular risk factors, such as hypertension, diabetes and LDL‐cholesterol level  and CD133 (Fadini (2)et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al.  generation , which accelerated atherosclerosis in CKD patients et al., et al., et al., et al., As mentioned above, RLPs are hydrolysed from TRLs and are thought to be as atherogenic as LDL et al., et al., et al., et al., et al., via activating the Rho‐associated kinase (ROCK) pathway but inhibiting the PI3K/AKT/eNOS pathway media, are critical for maintaining vascular homeostasis through regulating vessel contraction and relaxation, and producing the extracellular matrix (ECM) , alkaline phosphatase (ALP), OPN, osteoprotegerin (OPG), and bone morphogenetic protein 2 (BMP‐2) (Nakano‐Kurimoto (2)via LOX‐1, CD36 and toll‐like receptors (TLRs) is closely linked to atherosclerosis et al., et al., et al., et al., et al., Unlike the well‐investigated roles of TRLs on ECs, there is little known about the effects of TRLs on VSMCs. It has been demonstrated that CM remnants, rather than CM itself, significantly increase monocyte chemotactic protein (MCP‐1) expression in VSMCs in a p38 MAPK‐dependent manner, suggesting a pro‐atherogenic role of CM remnants through pro‐inflammatory effects intima triggers the secretion of monocyte recruitment factors by ECs, which drives the infiltration and activation of immune cells. The activated monocytes mediate the internalization of oxidized LDL via several scavenger receptors such as LOX‐1, SR‐A, SR‐B1, CD36 and TLRs et al., et al., et al., et al., et al. et al., et al., et al., et al., It has been suggested that TRL uptake by monocytes leads to lipid accumulation, which in turn augments foam cell formation and inflammation. In addition to the extensively studied scavenger receptors SR‐A, SR‐B1 and CD36, other types of receptors such as the apolipoprotein B48 receptor, VLDL receptor, LDL receptor and LRP1 also mediate the internalization of TRLs in macrophages et al., et al., et al., et al., et al., Adipose tissue represents the largest energy reservoir in the body, and is classified as subcutaneous white adipose tissue (sWAT) or visceral white adipose tissue (vWAT) according to anatomical site. In addition to its main function of storing energy, there is growing recognition that WAT is a major endocrine organ that produces a variety of bioactive factors essential for the maintenance of systemic metabolic homeostasis et al., et al., et al., et al., The amounts and functions of sWAT deteriorate with advanced age, related to the reduced proliferation and differentiation capacities of preadipocytes et al., et al., et al., et al., et al., et al., et al., et al., et al., As mentioned above, obesity is a crucial factor for WAT and AMSC senescence (Minamino VII.(1)et al., et al., et al., et al., A key initial finding on slowing aging was the observation that caloric restriction (CR) in rodents had beneficial effects on the lifespan  and nicotinamide mononucleotide (NMN) have been investigated et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., et al., Currently available lipid‐lowering drugs, especially statins (Gong VIII.(1) Accumulating evidence suggests that dyslipidemia, especially elevated LDL and its modified products, elevated TRL and its hydrolysate, and dysfunctional HDL is involved in the occurrence and development of atherosclerosis. The contributory effects of cellular senescence to atherosclerosis has received much interest due to common causative stimuli and consequences.via several classical signalling pathways. Nevertheless, n‐3 PUFA and functional HDL may provide new insights into atherosclerosis due to their anti‐senescence effects on ECs.(2) Dyslipidemia‐induced EC senescence impairs the endothelium barrier and facilitates lipid deposition, resulting in EC dysfunction and atherosclerosis. The potential mechanisms are involved not only in oxidative stress, but also in inflammation, autophagy and some novel ncRNAs (3) EPC senescence induced by various types of lipoproteins and FAs contributes to the pathogenic mechanisms of atherosclerosis. Since a relatively small number of studies have focused on specific FAs and HDL other than oxidized LDL, further in‐depth research is needed to clarify the underlying molecular mechanisms.(4) Dyslipidemia‐induced VSMC senescence or calcification leads to VSMC dysfunction and fibrous cap thinning, which contributes to atherosclerotic plaque vulnerability. The effects of different types of FAs on VSMC senescence need to be explored in future studies.(5) Macrophage senescence induced by oxidized LDL also has an important role in atherosclerosis. In addition to the key link between dyslipidemia and inflammation that plays a vital role in macrophage senescence, oxidative stress, autophagy and apoptosis are also involved in this process. Further studies investigating the role of TRLs and the main types of FAs carried in TRLs on macrophage senescence are required.(6) Senescent AMSCs and WAT display impaired capacities in lipid metabolism, insulin resistance and aberrant secretion of adipocytokines, which can interfere with the normal function of distal tissues through SASP and participate in atherogenesis. TRLs derived from a high‐calorie diet could induce AMSC senescence with increased inflammation and intercellular ROS.


Scientific Reports 10.1038/s41598-021-93603-z, published online 09 July 2021Correction to: The Funding section in the original version of this Article was omitted. The Funding section now reads:“This publication was made possible by Federal Emergency Management Agency (FEMA), Grant/Award Number: EMW – 2017 – FP – 00445 (author DLS), Fundação de Apoio à Pesquisa do Distrito Federal, Grant/Award Number: 3/2016 (author LGGP) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Finance Code 001: EMKVKS was supported by a CAPES scholarship (author EMKVKS).”The original Article has been corrected.


A disfunção hepática é uma variável postulada de prognóstico desfavorável na cardiomiopatia dilatada (CMD).Este estudo teve como objetivo investigar o valor prognóstico do escore albumina-bilirrubina (ALBI), um modelo relativamente novo para a avaliação da função hepática, em pacientes com CMD idiopática.Um total de 1.025 pacientes com CMD idiopática foram incluídos retrospectivamente e divididos em três grupos com base nos escores de ALBI: grau 1 , grau 2  e grau 3 . Foi analisada a associação do escore ALBI com eventos clínicos adversos maiores (ECAM) intra-hospitalares e mortalidade a longo prazo. Valor de p inferior a 0,05 foi considerado estatisticamente significativo.odds ratio ajustada = 2,80, IC 95%: 1,63 – 4,80, p < 0,001). Após seguimento mediano de 27 meses, 146  pacientes morreram. A curva de Kaplan-Meier indicou que a taxa cumulativa de sobrevida a longo prazo foi significativamente menor em pacientes com grau mais alto de ALBI . O escore ALBI foi independentemente associado à mortalidade a longo prazo .A taxa de ECAM intra-hospitalares foi significativamente maior nos pacientes com grau 3 . A análise multivariada mostrou que o escore ALBI foi um preditor independente para ECAM intra-hospitalares (O escore ALBI, como modelo de risco simples, pode ser considerado uma ferramenta de estratificação de risco para pacientes com CMD idiopática. Em estudos anteriores, o escore ALBI tem sido amplamente utilizado em pacientes com hepatopatias, incluindo carcinoma hepatocelular, cirrose hepática e insuficiência hepática.8 Além disso, Matsue e colaboradores indicaram que o escore ALBI está associado à sobrecarga hídrica e ao prognóstico de pacientes com insuficiência cardíaca aguda.9 No entanto, ainda não está claro se esse escore pode ser considerado uma ferramenta de estratificação de risco em pacientes com CMD idiopática. Portanto, o presente estudo foi realizado para investigar a associação do escore ALBI e desfechos adversos na CMD idiopática.A lesão hepática é comum em pacientes com insuficiência cardíaca por causa da perfusão prejudicada e da congestão sistêmica devido a alterações hemodinâmicas.10 Os critérios de exclusão foram os seguintes: 1) idade < 18 anos; 2) presença de tumor maligno; 3) gravidez; 4) doença autoimune; 5) histórico de terapia de sincronização cardíaca ou transplante cardíaco; e 6) CMD com etiologia definida, como cardiopatia hipertensiva, doença arterial coronariana (> 50% de lesão obstrutiva em um ou mais vasos epicárdicos), valvopatia, cardiopatia congênita, desencadeantes de miocardite, cardiomiopatia alcoólica, cardiomiopatia periparto, cardiomiopatia causada por distúrbio endócrino, não compactação do miocárdio ventricular e cardiomiopatia induzida por arritmia. Além disso, também excluímos pacientes sem registros de albumina ou bilirrubina sérica de admissão. Foram incluídos um total de 1.025 pacientes com CMD idiopática. O presente estudo foi aprovado pelo comitê de ética do Hospital Popular da Província de Guangdong, com dispensa de consentimento informado.Trata-se de um estudo de coorte retrospectivo realizado no Hospital Popular da Província de Guangdong. Pacientes diagnosticados com CMD idiopática foram incluídos consecutivamente entre janeiro de 2010 e novembro de 2015. O diagnóstico de CMD estava de acordo com a declaração do grupo de trabalho de doenças miocárdicas e pericárdicas da Sociedade Europeia de Cardiologia.11Foram coletadas amostras de sangue venoso para medir as concentrações de albumina e bilirrubina pela manhã após pernoite. Os níveis séricos de albumina e bilirrubina foram detectados em um analisador bioquímico automatizado . O ecocardiograma transtorácico foi realizado rotineiramente dentro de 24 horas da admissão. Foram medidos diâmetro do átrio esquerdo (DAE), diâmetro diastólico final do ventrículo esquerdo (DDFVE), fração de ejeção do ventrículo esquerdo (FEVE) e outros índices de ecocardiograma de acordo com as recomendações da Sociedade Americana de Ecocardiografia.2) foi calculada usando a equação Chronic Kidney Disease Epidemiology Collaboration equation.12 O escore ALBI foi calculado usando a fórmula seguinte: .As variáveis clínicas foram coletadas do prontuário eletrônico por um pesquisador e verificadas aleatoriamente por outro. A taxa de filtração glomerular estimada  intra-hospitalares, como morte, acidente vascular cerebral, diálise e insuficiência cardíaca aguda durante a hospitalização.Os pacientes incluídos foram divididos em 3 grupos com base na pontuação ALBI: grau 1 ; grau 2 ; e grau 3 . A distribuição das variáveis foi avaliada pelo teste de Kolmogorov-Smirnov. As variáveis contínuas com distribuição normal são apresentadas como média ± desvio padrão e as variáveis contínuas com distribuição não normal são apresentadas como mediana e intervalo interquartil. As variáveis categóricas são apresentadas em números e percentuais. As variáveis contínuas foram comparadas usando ANOVA de uma via quando normalmente distribuídas e o teste Kruskal-Wallis H quando não normalmente distribuídas. O teste do qui-quadrado foi realizado para as variáveis categóricas. A análise da curva característica de operação do receptor (ROC) foi usada para determinar os níveis de corte ideais do escore ALBI para predizer eventos adversos. Foram usadas a regressão logística e a análise de sobrevivência de Cox para avaliar o efeito do escore ALBI em ECAM intra-hospitalares e mortalidade a longo prazo, respectivamente. Variáveis significativas na análise univariada (exceto os elementos do ALBI) foram incluídas na análise multivariada. Além disso, curvas de Kaplan-Meier foram elaboradas e comparadas pelo teste log-rank entre os grupos. Para todas as análises, p < 0,05 foi considerado como indicativo de significância estatística. Todas as análises foram realizadas no software SPSS .Em total, foram incluídos 1.025 pacientes nesta análise. As características basais entre os grupos são apresentadas na 2, lgALT(log10ALT), bilirrubina total, DAE, DDFVE, FEVE, e uso de betabloqueador foram associados aos ECAM intra-hospitalares  foram a óbito; 48  apresentaram insuficiência cardíaca aguda; 23  necessitaram de diálise renal e 23  apresentaram acidente vascular cerebral. A taxa de ECAM intra-hospitalar foi significativamente maior em pacientes com grau 3 do que naqueles com graus 1 e 2 . Outras variáveis significativas incluíram idade, classe funcional da NYHA, anemia, TFGe < 60 mL/min/1,73 m2, lgALT, hipoproteinemia, bilirrubina total, DAE, DDFVE, FEVE, e uso de betabloqueador e digoxina. Esses fatores de risco significativos, exceto os componentes do escore ALBI, foram incluídos no modelo multivariado de sobrevivência de Cox, que revelou que o escore ALBI permaneceu um preditor independente para mortalidade a longo prazo  pacientes foram a óbito. A curva de Kaplan-Meier indicou que a taxa cumulativa de sobrevida a longo prazo foi significativamente menor em pacientes com grau mais alto de ALBI , one of the leading causes of heart failure, is characterized by ventricular dilation and systolic dysfunction.4 Hepatic dysfunction has been identified as one of the risk factors for poor outcomes in patients with DCM.5 The albumin-bilirubin (ALBI) score is a simple and objective method to assess liver function. In previous studies, ALBI score has been widely used in patients with liver diseases, including hepatocellular carcinoma, liver cirrhosis, and liver failure.8 In addition, Matsue et al indicated that the ALBI score is associated with fluid overload and the prognosis of patients with acute heart failure.9 However, it is yet unclear whether this score can be considered a risk-stratifying tool in patients with idiopathic DCM. Hence, this study was conducted to investigate the association of the ALBI score and adverse outcomes in idiopathic DCM.Liver injury is common in patients with heart failure owing to impaired perfusion and systemic congestion due to hemodynamic changes.10 The exclusion criteria were as follows: 1) age < 18 years; 2) presence of malignant tumor; 3) pregnancy; 4) autoimmune disease; 5) previous cardiac synchronization therapy or heart transplantation; and 6) DCM with definite etiology such as hypertensive heart disease, coronary artery disease , valvular heart disease, congenital heart disease, myocarditis triggers, alcoholic cardiomyopathy, peripartum cardiomyopathy, cardiomyopathy caused by endocrine disorder, noncompaction of the ventricular myocardium, and arrhythmia-induced cardiomyopathy. Furthermore, we also excluded patients without admission serum albumin or bilirubin records. A total of 1025 idiopathic DCM patients were enrolled. The present study was approved by the ethics committee of Guangdong Provincial People's Hospital, with a waiver of informed consent.This was a retrospective cohort study conducted at Guangdong Provincial People's Hospital. Patients diagnosed with idiopathic DCM were consecutively enrolled between January 2010 and November 2015. The diagnosis of DCM was in agreement with the statement of the European Society of Cardiology working group on myocardial and pericardial diseases.11Venous blood samples were collected for measurement of albumin and bilirubin concentrations in the morning after an overnight stay. Serum albumin and bilirubin levels were detected on an automated biochemical analyzer . Transthoracic echocardiography was routinely performed within 24 hours of admission. Left atrial diameter (LAD), left ventricular end diastolic diameter (LVEDD), left ventricular ejection fraction (LVEF), and other echocardiogram indices were measured according to the recommendations of the American Society of Echocardiography.2) was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation.12 The ALBI score was calculated using the following formula: 0.66× log10 bilirubin-0.085×albumin.6Clinical variables were collected from the electronic case report form by one researcher and randomly checked by another. Estimated glomerular filtration rate  such as death, stroke, dialysis, and acute heart failure during hospitalization.Included patients were divided into three groups based on ALBI score: grade 1 ; grade 2 ; and grade 3 . The distribution of variables was assessed by the Kolmogorov-Smirnov test. Normally distributed continuous variables are presented as mean ± standard deviation, and non-normally distributed continuous variables are presented as median and interquartile range. Categorical variables are presented as numbers and percentage. Continuous variables were compared using one-way ANOVA when normally distributed or the Kruskal-Wallis H test when not normally distributed. The chi-square test was performed for categorical variables. Receiver operating characteristic (ROC) curve analysis was used to determine the optimum cut-off levels of ALBI score for predicting adverse events. Logistic regression and Cox survival analysis were used to assess the effect of ALBI score on in-hospital MACEs and long-term mortality, respectively. Significant variables in univariate analysis (except the elements of ALBI) were included into the multivariate analysis. In addition, Kaplan–Meier curves were drawn and compared using the log-rank test among groups. For all analyses, p < 0.05 was considered to indicate statistical significance. All analyses were conducted using SPSS software .In all, 1025 patients were included in this analysis. Baseline characteristics among the groups are displayed in 2, lgALT(log10ALT), total bilirubin, LAD, LVEDD, LVEF, and β-blocker usage were associated with in-hospital MACEs  died; 48 (4.7%) suffered from acute heart failure; 23 (2.2%) required renal dialysis, and 23 (2.2%) suffered a stroke. The in-hospital MACE rate was significantly higher in patients with grade 3 than in those with grades 1 and 2  patients died. The Kaplan–Meier curve indicated that the cumulative rate of long-term survival rate was significantly lower in patients with higher ALBI grade (log-rank test = 45.50, p < 0.001, ROC curve analysis indicated that the area under the curve of ALBI score, serum albumin, and total bilirubin for predicting long-term death were 0.684 (95% CI: 0.654 – 0.714, To our knowledge, this is the first study to evaluate the prognostic role of ALBI score in patients with idiopathic DCM. The results showed that ALBI score was an independent risk factor for in-hospital MACEs and long-term mortality. In addition, ALBI score exhibited better predictive ability for long-term death than serum albumin and total bilirubin. The ALBI score can be easily measured and would be useful in identifying idiopathic DCM patients who are at a high risk of poor outcomes.14 In addition, right ventricular dysfunction is prevalent in patients with DCM, 15 and it has been demonstrated to influence the course and prognosis of DCM.16 Progression of right ventricular dysfunction can lead to systemic congestion, resulting in sinusoidal congestion and peri-sinusoidal edema, which impair delivery of oxygen and nutrients to hepatocytes.19 In addition, decreased cardiac output and inadequate liver perfusion may trigger hypoxic injury. This injury of hepatocytes can manifest as decreased serum albumin and elevated bilirubin.DCM is characterized by ventricular remodeling which can gradually develop into left heart failure and even global heart failure.20 We found that hypoalbuminemia was related to adverse outcome in patients with idiopathic DCM. This could be explained by several theories. First, in addition to being a marker of liver injury, hypoalbuminemia is frequently associated with renal dysfunction.21 Albumin is restricted by the normal glomerular barrier, and filtered albumin can be reabsorbed by proximal tubular cells.22 However, increased protein urine discharge can be found in renal insufficiency, which results in hypoalbuminemia. Therefore, hypoalbuminemia might reflect the concurrent renal dysfunction and portend poor outcomes. Second, hypoalbuminemia results in lower serum osmotic pressure and can exacerbate pulmonary edema and pleural effusion, precipitating refractory heart failure in patients with DCM.21 Third, serum albumin and prealbumin levels have been shown to reflect nutritional status.24 Malnutrition at times may progress to cardiac cachexia, which is characterized by protein-calorie malnutrition with muscle wasting and peripheral edema, leading to poor quality of life and increased mortality.24Albumin, which reflects the synthetic function of the liver, has multiple physiological roles, such as counterbalancing hydrostatic pressure, antioxidant and anti-inflammatory functions, and transporting molecules and drugs.16 In addition, hyperbilirubinemia reflects poor latent cardiac status in chronic heart failure.25 Lang et al. indicated that bilirubin had adverse effects on erythrocytes, inducing suicidal death of erythrocytes. Excessive damage to erythrocytes leads to severe anemia and further affects the prognosis.26 These pieces of evidence support our finding that hyperbilirubinemia is a risk factor for patients with idiopathic DCM.Similarly, in patients with advanced DCM, several metabolic processes of bilirubin in the liver, including uptake, conjugation, and secretion, are attenuated by hepatocellular hypoxia and congestion, leading to greater increase in serum total bilirubin. Although bilirubin has antioxidant and anti-inflammatory properties, extremely elevated bilirubin levels represent impaired hemodynamics caused by right ventricular dysfunction, which has an adverse prognostic effect on patients with DCM.27 To the best of our knowledge, no study yet has evaluated the prognostic value of ALBI score in patients with idiopathic DCM. The present study demonstrated that ALBI score was independently associated with in-hospital and long-term adverse outcomes. The ALBI score consists of only two variables, and it is a simple risk-stratifying tool in patients with idiopathic DCM. Based on the current study, the clinical application of the ALBI score might be extended from hepatic diseases to idiopathic DCM.Both hypoalbuminemia and hyperbilirubinemia were risk factors for poor prognosis in patients with idiopathic DCM. The ALBI score, combining these two effects, has been extensively tested as an objective, simple, and distinguishing method for assessing liver function.Our study has some limitations. First, this was a retrospective cohort study; therefore, some admission bilirubin and albumin levels were missing, which may affect the results. Second, bilirubin and albumin were not dynamically detected. The relationship between prognosis and ALBI score at different time points is unknown. Finally, as our included study population did not represent patients with idiopathic DCM in different settings, such as in western countries, the study results should be validated in different idiopathic DCM cohorts.This study showed that the ALBI score was independently associated with increased risk of in-hospital MACEs and long-term mortality in patients with idiopathic DCM. Moreover, compared to bilirubin and albumin, the ALBI score exhibited relatively superior predictive ability for long-term mortality, which might identify more patients at high risk of poor outcomes.


Estudos mostraram uma redução em hospitalizações e um aumento em mortalidade por DCV durante o surto de COVID-19 em muitos países. 8 Contudo, a maioria desses estudos envolveram pacientes com síndrome coronariana aguda (SCA) em países desenvolvidos, com poucos dados sobre admissões por insuficiência cardíaca (IC), e as causas para o aumento na mortalidade não foram bem esclarecidas. Nós avaliamos as mudanças na gravidade, causas de descompensação da IC, e mortalidade em 30 dias de pacientes admitidos por IC em hospitais públicos incluídos no programa Boas Práticas Clínicas (BPC) em Cardiologia no Brasil durante a pandemia da COVID-19 e comparadas com períodos prévios.O Brasil é um dos principais países afetados pela pandemia causada pelo novo coronavírus (COVID-19), com mais de meio milhão de mortes em junho de 2021, o segundo maior número de mortes no mundo. Get With The Guidelines , para melhorar a qualidade do cuidado cardiovascular e desfechos dos pacientes no Brasil. O delineamento, racional e procedimentos do estudo foram previamente publicados. 9 Incluímos pacientes consecutivos, com idade igual ou superior a 18 anos, admitidos com IC descompensada em hospitais públicos terciários afiliados ao Sistema Único de Saúde (SUS) durante a pandemia por COVID-19 entre 12 de março de 2020 a 31 de outubro de 2020 (semanas epidemiológicas 11 a 44). Os pacientes foram comparados com pacientes admitidos nos mesmos hospitais durante as mesmas semanas epidemiológicas em 2019 e 2018.Realizamos um estudo do tipo coorte usando dados do programa BPC, o qual encontra-se em andamento, e consiste em uma adaptação da iniciativa Acute Decompensated Heart Failure National Registry (ADHERE) – usando uma abordagem do tipo stepwise de acordo com medidas de pressão arterial, creatinina, e nitrogênio ureico sanguíneo, para estratificar pacientes com IC em risco baixo, intermediário e alto. 11 O desfecho foi mortalidade por todas as causas em um seguimento de 30 dias. Óbito e data de óbito foram verificados por meio de prontuários médicos, descendentes e atestados de óbito.Características basais específicas à IC foram coletadas prospectivamente durante a hospitalização, por investigadores locais treinados, usando prontuários médicos e entrevistas estruturadas com o paciente. Calculou-se o escore do algoritmo do registro ADHERE – Consentimento informado foi obtido de cada paciente, e o estudo foi aprovado pelo comitê de ética do centro coordenador do estudo (no. 48561715.5.1001.0060).As variáveis contínuas foram avaliadas quanto à distribuição normal usando a forma, simetria e curtose da distribuição, e o teste de Kolmogorov-Smirnov se necessário. Nós comparamos características clínicas, medidas de gravidade e tratamento entre os períodos de tratamento usando o teste t não pareado para variáveis com distribuição normal, apresentadas como média ± desvio padrão, e o teste de Mann-Whitney para variáveis sem distribuição normal, apresentadas como mediana (percentis 25 e 75). Os dados categóricos foram apresentados como proporções e comparados usando o teste do qui-quadrado. Para avaliar a associação entre os períodos do estudo e os desfechos, nós calculamos estimativas de Kaplan-Meier e comparamos a probabilidade de mortalidade por todas as causas usando o teste de log-rank. Realizou-se análise de regressão (riscos proporcionais) de Cox ajustado por idade, sexo, etiologia da IC , fração de ejeção do ventrículo esquerdo (FEVE), terapia de ressincronização cardíaca (TRC), cardioversor desfibrilador implantável (CDI), e nível educacional, e estratificado por renda, doença renal crônica (DRC) e IC prévia. A suposição de risco proporcional foi testada com base nos resíduos de Schoenfeld, sem violação da suposição de risco proporcional para os grupos estudados. Valores de p<0,05 foram considerados estatisticamente significativos. As análises foram realizadas usando o programa Stata versão 15.1 .Durante as semanas epidemiológicas 11 a 44 nos anos 2018, 2019 e 2020, um total de 1084 pacientes foram admitidos com IC em sete centros elegíveis, representando seis estados  no Brasil. Desses pacientes, nós excluímos 218 por ausência de medidas de pressão arterial sistólica (n=86), creatinina (n=43), ureia no sangue (n=20) ou perda de seguimento (n=69). A análise final foi realizada em 866 pacientes admitidos por IC.vs . 11,6 ± 3,0 antes da pandemia).Em comparação aos dois anos anteriores, observamos uma redução de 20% no número de pacientes admitidos com IC durante a pandemia de COVID-19, principalmente nos primeiros quatro meses , em comparação aos dois anos anteriores.Mortalidade por todas as causas de pacientes internados por IC aumentou significativamente durante o surto da COVID-19   . No perUma baixa adesão às recomendações de tratamento medicamentoso ou dietético, e doença renal aguda foram mais comumente relatados como fatores desencadeantes de descompensação de IC durante o surto de COVID-19, em comparação ao período anterior   . A freqNeste grande registro de hospitalizações por IC no Brasil, nossos principais achados foram: 1) a mortalidade em 30 dias aumentou aproximadamente duas vezes durante o surto de COVID-19 em comparação a antes da pandemia; 2) pacientes com IC eram mais propensos a desenvolverem IC descompensada por baixa adesão ao tratamento e por doença renal aguda; e 3) os pacientes foram admitidos em condições piores, como indicado por um pior escore de risco ADHERE. Esses achados ajudam a entender o impacto da pandemia em pacientes com IC no Brasil, afetando o comportamento dos pacientes, interrompendo a prestação de serviços de saúde, e aumentando o risco de morte por IC aguda.5 Tal fato indica que pacientes com DCV foram afetados em graus diferentes, dependendo do nível de resposta de cada país à pandemia. Nosso estudo mostrou um aumento na mortalidade por IC aguda em um país amplamente afetado, e que tal impacto teve duração mais longa que os primeiros meses da pandemia.Até o momento, existem poucos relatados do impacto da pandemia da COVID-19 sobre pacientes com IC. Similar a nossos achados, estudos da Alemanha e da Inglaterra descreveram que a mortalidade em curto prazo aumentou significativamente entre pacientes admitidos por IC durante o início da pandemia, o que não foi descrito em estudos posteriores conduzidos na Dinamarca. insights sobre os mecanismos para esses piores desfechos. O tratamento da IC é complexo, e geralmente requer uma abordagem multidisciplinar centrado no paciente para melhorar a adesão ao tratamento em longo prazo. 12 Os piores desfechos da IC aguda pode refletir uma ruptura na prestação do cuidado no ambiente ambulatorial. Os serviços ambulatoriais foram interrompidos, e as equipes de cardiologia foram reorganizadas e transferidas para a prestação de cuidado da COVID-19 em muitos centros, alterando o foco das medidas efetivas essenciais para reduzir mortalidade dessa população. Além disso, a perda do apoio social devido ao isolamento social pode ter afetado a continuidade do tratamento, particularmente entre indivíduos vulneráveis.As causas para uma maior mortalidade são multifatoriais. A não adesão ao tratamento dietético e medicamentoso como fatores desencadeantes de IC descompensada durante a pandemia da COVID-19 pode fornecer 13 Políticas de saúde visando essa população, incluindo estratégias para se manter a prestação de cuidado no ambulatório, tais como telemedicina e monitoramento remoto, pode ajudar a reduzir a mortalidade durante a pandemia.Vale notar que as orientações para o manejo de DCV durante a pandemia da COVID-19 focaram principalmente SCA, mas pacientes com IC também foram muito afetados pela pandemia. Esforços são necessários para continuar a prover cuidado adequado a esses pacientes. Nosso estudo tem limitações: incluímos somente hospitais públicos, a maioria hospitais universitários. Ainda, todos os hospitais em nosso estudo participavam do programa BPC, cujo objetivo é melhorar a qualidade do cuidado de DCV e desfechos dos pacientes, de modo que as internações no estudo podem não refletir as internações por IC em todos os hospitais públicos no Brasil. Finalmente, nossos resultados não representam os pacientes que não foram internados ou aqueles que não vieram ao hospital.Neste grande registro de pacientes admitidos com IC em hospitais públicos incluídos no programa BPC no Brasil, um dos países mais afetados pela pandemia da COVID-19, a baixa adesão ao tratamento e doença renal aguda foram as principais causas da descompensação da insuficiência cardíaca, e a mortalidade em 30 dias aumentaram duas vezes durante o surto da COVID-19 em comparação a períodos anteriores. Estratégias de saúde pública em resposta à pandemia deveria garantir manutenção do cuidado a pacientes com IC, particularmente nos países mais afetados. 1 It has been reported that the COVID-19 outbreak has affected the delivery of care of patients without COVID-19 (non-COVID-19 patients), particularly patients with cardiovascular (CV) diseases, increasing the death toll from the pandemic. Studies have shown a reduction in hospitalizations in tandem with an increase mortality from CV diseases during the outbreak in many countries.8 However, most of these reports focused on patients with acute coronary syndrome (ACS ) in developed countries, with few data on heart failure (HF) admissions, and the reasons for the worse mortality are not well understood. We evaluated the changes in severity, reasons for decompensation and 30-day mortality of patients admitted for HF in public hospitals included in the Best Practices in Cardiology (BPC) program in Brazil during the COVID-19 outbreak and compared with previous periods.Brazil is one of the most hit countries by the pandemic caused by the novel coronavirus , with more than half million deaths in June, 2021, the world’s second-highest number of deaths.9 We included consecutive patients aged 18 years or older admitted with decompensated HF in tertiary public hospitals affiliated to the Brazilian Unified Health System (SUS) during the COVID-19 outbreak from March 12th, 2020 to October 31st, 2020  and compared them with patients admitted in the same hospitals during the same epidemiological weeks in 2019 and 2018.We performed a cohort study using data from the BPC program, which is an ongoing program adapted from the Get With The Guidelines initiative, to improve quality of cardiovascular care and patients’ outcomes in Brazil. The study design, rationale and procedures have been previously published.11 The outcome was all-cause death in a 30-day follow up. Death and date of death were ascertained through medical records, next of kin and death certificates.Baseline HF-specific characteristics were prospectively collected during hospitalization, by trained local investigators, using medical charts and structured interviews with the patient. The Acute Decompensated Heart Failure National Registry (ADHERE) algorithm score was calculated using a stepwise approach according to systolic blood pressure, creatinine and urea nitrogen blood levels to stratify HF patients into low, intermediate and high risk.Informed consent was obtained from every patient and this study was approved by the Coordinating Center’s Institutional Review Board (# 48561715.5.1001.0060).Continuous variables were evaluated for the normal distribution using the shape, skewness, and kurtosis of distribution, and Kolmogorov-Smirnov test if needed. We compared clinical characteristics, measures of severity and treatment between study periods using the unpaired t test for normally distributed variables, which were presented as mean ± standard deviation, and the Mann-Whitney U test for non-normally distributed variables, presented as median . Categorical data was presented as proportions and compared using the chi-square test. To assess the association between study periods and the outcomes, we calculated Kaplan-Meier estimates and compared the probability of all-cause mortality using the log-rank test. A Cox  regression analysis adjusted for age, sex, etiology of HF , left ventricular ejection fraction (LVEF), cardiac resynchronization therapy (CRT), implantable cardioverter defibrillator (ICD), and education levels, and stratified by income levels, chronic kidney disease (CKD) and previous HF was performed; the proportional hazard assumption was tested based on Schoenfeld residuals, with no violation for the proportional hazard assumption for the studied groups. P-values<0.05 were considered statistically significant. Analyses were performed using Stata version 15.1 .Alagoas, Bahia, Ceará, Minas Gerais, Pará and São Paulo ) in Brazil. From these, we excluded 218 patients due to missing systolic blood pressure (n=86), creatinine (n=43), blood urea levels (n=20) or loss to follow-up (n=69). The final analysis was performed in 866 patients admitted for HF.During the epidemiological weeks 11 to 44 in the years of 2018, 2019 and 2020, 1,084 patients were admitted for HF in seven eligible centers, representing six states .Compared with the previous two years, we observed a 20% reduction in the number of patients admitted for HF during the COVID-19 outbreak, particularly in the first four months , as compared with the two previous years.All-cause mortality of patients hospitalized for HF significantly increased during the COVID-19 outbreak   . In thePoor compliance to either dietary and medication treatment recommendations, and acute kidney disease were more commonly reported as factors triggering HF decompensation during the COVID-19 outbreak, as compared with the previous period   . InfectIn this large registry of HF hospitalizations in Brazil, our main findings were: 1) the 30-day mortality increased roughly twice during the COVID-19 outbreak compared with before the pandemic; 2) patients with HF were more likely to decompensate due to poor treatment compliance and acute kidney disease; and 3) they were admitted in worse condition, as indicated by a worse ADHERE risk score. These findings help understand the impact of the pandemic in patients with HF in Brazil, affecting patients’ behavior, disrupting the delivery of healthcare, and increasing the risk of dying from acute HF.5 This indicates that patients with CV diseases have been differently affected depending on the country-level response to the pandemic. Our study showed an increase in mortality from acute HF in a largely affected country, and that this impact has lasted longer than the first few months of the outbreak.So far, there are few reports of the impact of the COVID-19 pandemic on HF patients. Similar to our findings, studies from Germany and England found that the short-term mortality significantly increased among patients admitted for HF during the beginning of the COVID pandemic, but this was not found in later studies from Denmark.12 The worse outcomes from acute HF may reflect a disruption in the delivery of care in the outpatient setting. Ambulatory services were interrupted, and cardiology teams were rearranged and transitioned to the care of COVID-19 in many centers, shifting the focus from effective measures that are essential to reduce mortality of this population. Moreover, loss of social support due to social isolation may have hampered continuity of treatment, particularly among vulnerable individuals.The reasons for the higher mortality are multifactorial. Non-adherence to dietary and drug treatment as factors triggering HF decompensation during the COVID-19 pandemic may provide insights on the mechanisms for these worse outcomes. Treatment of HF is complex, and it often requires a patient-centered multidisciplinary approach to improve long-term treatment compliance.13 Healthcare policies targeted to this population, including strategies to maintain delivery of outpatient care, such as telemedicine and remote monitoring, may help reduce mortality during the pandemic.It should be noticed that guidance to manage CV diseases during the COVID-19 pandemic have mainly focused on ACS, but patients with HF have also been largely affected by the pandemic. Efforts should be made to continue providing adequate care for these patients.Our study has limitations: we included only public hospitals, most of them university hospitals. Also, all hospitals in our study participated in the BPC program, which aims to improve quality of cardiovascular care and patients’ outcomes, and this may not reflect HF admissions in all public hospitals in Brazil. Finally, our results do not represent those patients who were not admitted or who did not to come to the hospital.In this large registry of patients admitted for HF in public hospitals included in the BPC program in Brazil, one of the most-affected countries by the COVID-19 pandemic, poor treatment compliance and acute kidney disease were the most common reasons for HF decompensation, and the 30-day mortality increased twice during the COVID-19 outbreak, as compared with previous periods. Public health strategies in response to the pandemic should ensure maintenance of care to HF patients, particularly in the most affected countries.


Todos os pacientes consecutivos foram selecionados e aqueles com FA ou FA prévia foram excluídos. Acompanhamos esses pacientes por 8 a 10 anos, observamos a incidência de FA e avaliamos os preditores clínicos, eletrocardiográficos e ecocardiográficos de FA de início recente.6Atividade ectópica supraventricular excessiva (AESVE) foi definida como ≥ 500 contrações atriais prematuras por 24 horas ou qualquer episódio de taquicardia supraventricular sustentada.A análise estatística foi realizada no IBM SPSS Statistics versão 25. As variáveis categóricas foram comparadas pelo teste do chi-quadrado, e as diferenças foram consideradas estatisticamente significativas quando o valor de p < 0,05.No total, foram incluídos 104 pacientes; 79,5% tiveram AVC e 20,5% tiveram AIT; 45,7% eram do sexo feminino; a média de idade foi de 63,8 ± 14,7 anos na época do evento . Em relaEm um seguimento de 8-10 anos, a FA de início recente foi detectada em 11,5% dos pacientes; estes tiveram mortalidade semelhante aos em ritmo sinusal sustentado . A ingestão de álcool, fator de risco estabelecido para o desenvolvimento de FA, foi associada a um aumento não significativo da FA , enquanto fatores de risco cardiovascular, aumento do átrio esquerdo, insuficiência mitral não foram associados com desenvolvimento de FA. Em relação às contrações atriais prematuras (CAPs), a documentação de AESVE na apresentação mostrou-se significativamente associada ao novo início de FA no seguimento . A AESVE também parece estar relacionada à maior mortalidade no seguimento de longo prazo, embora essa diferença não tenha sido estatisticamente significativa  .8 O Copenhagen Holter Study mostrou que CAPs excessivos foram associados a um risco aumentado de morte, acidente vascular cerebral e internações por FA em um acompanhamento médio de 6,3 anos.7 A mesma coorte foi acompanhada por 15 anos, e os pacientes com ≥ 30 CAPs/hora ou com qualquer execução de ≥ 20 CAPs tiveram um risco aumentado de AVC isquêmico além de desenvolver FA. Nesse estudo, o AVC foi mais frequentemente a primeira apresentação clínica do que a FA.8 Todos esses relatos e o presente estudo lançaram a questão se os pacientes com ESVEA se beneficiam da anticoagulação. De facto, a atribuição da fibrilação auricular como causa do AVC altera totalmente a terapêutica do doente, pelo que é da maior importância não só identificar os doentes com FA paroxística, mas também reconhecer quais são os que têm mais risco de ter episódios ocultos de FA. O Holter de 24 horas permite a detecção de FA paroxística, mas aparentemente com baixa eficácia. Em nosso estudo, apenas 1,9% dos pacientes foram identificados com FA imediatamente após AVC ou AIT, enquanto 11,5% apresentaram FA no seguimento de longo prazo.Nosso estudo corrobora relatos anteriores sugerindo que CAPs excessivos aumentaram o risco de morte e FA.Nosso estudo mostrou que a AESVE é um forte preditor de FA de início recente, destacando a importância do monitoramento de ECG. Esse achado, combinado com outros fatores de risco, como acidente vascular cerebral embólico de origem desconhecida, pode ser usado para identificar pacientes com maior risco de desenvolver FA que se beneficiam de um monitoramento de ECG de longo prazo ou de um acompanhamento mais regular. 2 On the other hand, the diagnosis of AF as the cause of ischaemic stroke shifts the therapeutic approach with a major prognostic impact.4 Detection of previously unknown AF after stroke is crucial, and several studies have established the effectiveness of ECG monitoring for post-stroke AF detection.1 According to ESO Guidelines for managing ischaemic stroke and transient ischaemic attack (TIA), after the acute phase, a 24-hour Holter ECG monitoring should be performed.5 New ESC Guidelines recommend short-term ECG recording for at least the first 24 h and continuous ECG monitoring for at least 72 h whenever possible in cryptogenic stroke.1Atrial fibrillation (AF) is a major risk factor for thromboembolic events, increasing five times the risk of stroke; it is also associated with more severe events and a higher risk of stroke recurrence. We conducted a retrospective study in a single tertiary center in patients who suffered an ischaemic stroke or TIA and performed Holter monitoring between October 2009 and October 2011. All consecutive patients were selected, and those with AF or previous AF were excluded. We followed these patients for 8 to 10 years, observed the incidence of AF and evaluated the clinical, electrocardiographic and echocardiographic predictors of new-onset AF.6Excessive supraventricular ectopic activity (ESVEA) was defined as ≥ 500 premature atrial contractions per 24 hours or any sustained supraventricular tachycardia episode.Statistical analysis was performed in IBM SPSS Statistics version 25. Categorical variables were compared using the chi-square test, and differences were considered statistically significant when the p-value < 0.05.In total, 104 patients were included; 79.5% had a stroke, and 20.5% had a TIA; 45.7% were female; the mean age was 63.8 ± 14.7-year-old at the time of the event . ConcernAt a follow-up of 8-10 years, new-onset AF was detected in 11.5% of patients; these had similar mortality compared to those in sustained sinus rhythm . Alcohol intake, an established risk factor for the development of AF, was associated with a non-significant increase in AF , while cardiovascular risk factors, left atrium enlargement, mitral regurgitation was not associated with AF development. Regarding premature atrial contractions (PACs), documentation of ESVEA at presentation showed to be significatively associated with new-onset of AF at follow-up . ESVEA also seems to be related to higher mortality at a long-term follow-up, although this difference was not statistically significant  .8 Copenhagen Holter Study showed that excessive PACs were associated with an increased risk of death, stroke, and admissions for AF at a median follow-up 6.3 years.7 The same cohort was followed for 15 years, and the patients with ≥ 30 PACs/hour or with any runs of ≥ 20 PACs had an increased risk of ischemic stroke beyond developing AF. In that study, stroke was often the first clinical presentation than AF.8 All these reports and the present study released whether patients with ESVEA benefit from anticoagulation. In fact, the assignment of atrial fibrillation as the cause of stroke totally changes patient’s therapy, so it is of major importance to identify patients with paroxysmal AF and recognize which ones have more risk of having occult episodes of AF. 24-hour Holter monitoring allows the detection of paroxysmal AF, but apparently with low effectiveness. In our study, only 1.9% of patients were identified with AF promptly after stroke or TIA, while 11.5% exhibited AF in long-term follow-up.Our study corroborates previous reports suggesting that excessive PACs increased the risk of death and AF.Our study showed that ESVEA is a strong predictor of new-onset AF, highlighting the importance of ECG monitoring. This finding, combined with other risk factors such as embolic stroke of unknown source, can be used to identify patients at higher risk of developing AF who benefit from a long-term ECG monitoring or a more regular follow-up.


Muitas dessas mortes em excesso estão relacionadas à subnotificação devido à falta de testes ou a diagnósticos incorretos (mortes verdadeiras por COVID-19 atribuídas a outras condições). Outros eventos fatais foram por outras causas e de alguma forma indiretamente associados à pandemia, como as mortes por doenças não tratadas adequadamente devido ao sistema de saúde sobrecarregado. Considerando que as doenças cardiovasculares (DCV) são a principal causa de morte no Brasil,2 é crucial desvendar o impacto da COVID-19 nas estatísticas de DCV.No Brasil, a OMS estima 99 e 220 mortes em excesso associadas à pandemia de COVID-19 por 100.000 habitantes em 2020 e 2021, respectivamente.3 analisando dados de hospitais públicos no Brasil, relatam que o número de óbitos hospitalares por DCV em 2020 foi apenas 1,58% inferior ao esperado com base na média dos anos anteriores. No entanto, a taxa de letalidade hospitalar por DCV aumentou 13,3% em todo o ano e 18,8% de março a dezembro.3Nesse contexto, Armstrong et al.,10 É importante ressaltar que um achado repetidamente relatado é um aumento desconfortável nas mortes domiciliares.13 Portanto, agora está claro que a pandemia impactou substancialmente o cuidado com DCV no Brasil.Esses achados estão de acordo com outros estudos que relataram, durante a pandemia, redução no número de pacientes que procuram atendimento médico, diminuição das internações e procedimentos por DCV, pacientes hospitalizados mais graves e, consequentemente, aumento da letalidade hospitalar por DCV.Quais são os aprendizados deste diagnóstico? Em primeiro lugar, espera-se que os médicos tenham aprendido que há casos em que a investigação, intervenção ou hospitalização não podem ser adiadas. Em segundo lugar, há um grande espaço para educar os pacientes sobre os sinais de alerta de condições graves, como síndrome coronariana aguda e acidente vascular cerebral, minimizando as mortes em casa devidas ao medo do paciente de ir ao hospital. Terceiro, suavizar as consequências da pandemia só é possível com um sistema de saúde bem preparado que possa responder rapidamente às demandas do surto sem comprometer o atendimento de outras doenças mortais. O Brasil não está acostumado a desastres naturais ou pandemias, e muitos subestimaram os danos potenciais do vírus. Agora nós temos a oportunidade de aprender com a experiência, como os países asiáticos fizeram com a epidemia de SARS em 2003, e melhor nos prepararmos para futuros eventos catastróficos.Após a fase mais crítica, pré-vacinação, da pandemia, a atenção agora se volta para outra preocupação: até que ponto o cancelamento de consultas e procedimentos médicos forçados pela pandemia afetará as DCV? O controle inadequado dos fatores de risco e as intervenções realizadas tardiamente podem adicionar outra camada ao impacto da pandemia de COVID-19 nos desfechos das DCV. O monitoramento contínuo da situação é necessário e provavelmente será abordado por estudos futuros.14 encontraram um excesso de mortalidade de 26,3%  entre pretos/pardos no Brasil em 2020, enquanto esse número foi de 15,1%  em brancos.14 Em Belo Horizonte-MG, o excesso de mortalidade em 2020 aumentou à medida que o Índice de Vulnerabilidade à Saúde piorou.15 Além disso, Brant et al. relataram que o aumento de óbitos domiciliares por DCV em Belo Horizonte-MG em 2020 foi mais acentuado em indivíduos mais vulneráveis socialmente.13 Identificar os subgrupos mais afetados é estratégico para definir alvos prioritários para intervenções de saúde pública e evitar o perigoso caminho de aumento das desigualdades em saúde.Outro aspecto relevante é reconhecer que os efeitos da pandemia não são uniformes na comunidade. Marinho et al.,2 Ainda não está claro se a pandemia modificará substancialmente essa tendência. No entanto, a mudança no padrão de internações por DCV e o aumento inaceitável de óbitos domiciliares não podem ser assistidos passivamente sem perplexidade. É hora de aprender com os dados e agir para minimizar os impactos da pandemia nos desfechos das DCV.Nas últimas décadas, observamos um declínio contínuo da mortalidade por DCV ajustada por idade no Brasil, embora essa queda tenha se atenuado nos últimos anos. 1The World Health Organization (WHO) estimates nearly 15 million excess deaths associated with COVID-19 in the world in 2020 and 2021, defined as the difference between the total number of deaths  and the number of expected deaths if there was no pandemic.1 This would translate into around 680,000 excess deaths in the first two years of the pandemic, i.e., tens of thousands higher than the officially reported COVID-19 deaths in the period. Many of these excess deaths are related to sub notification due to lack of testing or misdiagnosis (true deaths from COVID-19 assigned to other conditions). Other fatal events were from other causes and somehow indirectly associated with the pandemic, such as the deaths from illnesses not properly treated due to the overwhelmed health system. Considering that cardiovascular disease (CVD) is the main cause of death in Brazil,2 it is crucial to unravel the impact of COVID-19 on CVD statistics.In Brazil, the WHO estimates 99 and 220 excess deaths associated with the COVID-19 pandemic per 100,000 inhabitants in 2020 and 2021, respectively.3 analyzing data from public hospitals in Brazil, report that the number of in-hospital deaths due to CVD in 2020 was only 1.58% lower than expected based on the average of previous years. However, the in-hospital case fatality rate due to CVD increased by 13.3% in the whole year and by 18.8% from March to December.3In this context, Armstrong et al.,10 Importantly, a repeatedly reported finding is an uncomfortable increase in home deaths.13 Therefore, it is now clear that the pandemic has substantially impacted CVD care in Brazil.These findings are in agreement with other studies that reported, during the pandemic, a reduction in the number of patients seeking medical care, a decrease in CVD hospitalizations and procedures, more severely diseased hospitalized patients, and consequently an increase in hospital lethality due to CVD.What are the takeaways from this diagnosis? First, physicians are expected to have learned that there are cases where the investigation, intervention, or hospitalization cannot be postponed. Second, there is a large room to educate patients about warning signs of severe conditions, such as acute coronary syndrome and stroke, minimizing the home deaths due to patient fear of going to the hospital. Third, smoothing the consequences of the pandemic is only possible with a well-prepared health system that can rapidly respond to the outbreak's demands while not compromising the care of other deadly diseases. Brazil is not used to natural disasters or pandemics, and many underestimated the potential damage of the virus. Now we have the opportunity to learn from the experience as Asian countries did from the SARS epidemic in 2003 and better prepare ourselves for future catastrophic events.After the most critical, pre-vaccination phase of the pandemic, the attention now shifts to another concern: to which extent will the cancellation of medical consultations and procedures forced by the pandemic affect CVD? Suboptimal risk factor control and interventions carried out late may add another layer to the impact of the COVID-19 pandemic on CVD outcomes. Continuous monitoring of the situation is needed and will probably be addressed by future studies.14 found an excess mortality rate of 26.3% (23.3%-29.3%) among blacks/browns in Brazil in 2020, while this number was 15.1% (14.1%-16.1%) in whites.14 In Belo Horizonte-MG, the excess mortality in 2020 increased as the Health Vulnerability Index worsened.15 Also, Brant et al. reported that the increase in CVD home deaths in Belo Horizonte-MG in 2020 was more pronounced in more socially vulnerable individuals.13 Identifying the most affected subgroups is strategic for defining priority targets for public health interventions and avoiding the dangerous path of increasing health inequalities.Another relevant aspect is to acknowledge that the effects of the pandemic are not uniform in the community. Marinho et al.2 It is not yet clear whether the pandemic will substantially modify this trend. Nevertheless, the change in the pattern of hospitalizations for CVD and the unacceptable increase in home deaths cannot be passively watched without perplexity. It is time to learn from the data and act to minimize the impacts of the pandemic on CVD outcomes.In the last decades, we have observed a continuous decline in the age-adjusted CVD mortality in Brazil, although this decrease has attenuated in the last years.