Abstract Background While many risk models have been developed to predict prognosis in heart failure (HF), these models are rarely useful for the clinical practitioner as they include multiple variables that might be time-consuming to obtain, they are usually difficult to calculate, and they may suffer from statistical overfitting. Objectives To investigate whether a simpler model, namely the ACEF-MDRD score, could be used for predicting one-year mortality in HF patients. Methods 748 cases within the SELFIE-HF registry had complete data to calculate the ACEF-MDRD score. Patients were grouped into tertiles for analyses. For all tests, a p-value <0.05 was accepted as significant. Results Significantly more patients within the ACEF-MDRD high tertile (30.0%) died within one year, as compared to other tertiles (10.8% and 16.1%, respectively, for ACEF-MDRD low and ACEF-MDRD med , p<0.001 for both comparisons). There was a stepwise decrease in one-year survival as the ACEF-MDRD score increased (log-rank p<0.001). ACEF-MDRD was an independent predictor of survival after adjusting for other variables (OR: 1.14, 95%CI:1.04 – 1.24, p=0.006). ACEF-MDRD score offered similar accuracy to the GWTG-HF score for predicting one-year mortality (p=0.14). Conclusions ACEF-MDRD is a predictor of mortality in patients with HF, and its usefulness is comparable to similar yet more complicated models.

Resumo Fundamento Embora muitos modelos de risco tenham sido desenvolvidos para prever o prognóstico na insuficiência cardíaca (IC), esses modelos raramente são úteis para o clínico, pois incluem múltiplas variáveis que podem ser demoradas para serem obtidas, são geralmente difíceis de calcular e podem sofrer de overfitting estatístico. Objetivos Investigar se um modelo mais simples, nomeadamente o escore ACEF-MDRD, poderia ser usado para prever a mortalidade em um ano em pacientes com IC. Métodos 748 casos do registro SELFIE-HF tinham dados completos para calcular o escore ACEF-MDRD. Os pacientes foram agrupados em tercis para análise. Para todos os testes, um valor de p <0,05 foi aceito como significativo. Resultados Significativamente mais pacientes dentro do tercil ACEF-MDRD alto (30,0%) morreram dentro de um ano, em comparação com outros tercis (10,8% e 16,1%, respectivamente, para ACEF-MDRD baixo e ACEF-MDRD med , p<0,001 para ambas as comparações). Houve uma diminuição gradual na sobrevida em um ano à medida que o escore ACEF-MDRD aumentou (log-rank p<0,001). ACEF-MDRD foi preditor independente de sobrevida após ajuste para outras variáveis (OR: 1,14, IC95%:1,04 – 1,24, p=0,006). O escore ACEF-MDRD ofereceu precisão semelhante ao escore GWTG-HF para prever a mortalidade em um ano (p=0,14). Conclusões ACEF-MDRD é um preditor de mortalidade em pacientes com IC e sua utilidade é comparável a modelos semelhantes, porém mais complicados.

Abstract Background: Inflammation, which is associated with an unhealthy lifestyle, plays a critical role in the development of both cardiometabolic diseases (CMD) and cancer. Carcinoembryonic antigen (CEA) is a tumor marker which also has proinflammatory properties. Recent studies have reported CEA to be associated with atherosclerosis, metabolic syndrome, and visceral adiposity. Epicardial adipose tissue (EAT) can exhibit highly inflammatory and pathogenic properties, and is a known risk factor for CMD. However, its relationship with CEA is still unknown. Objectives: This study aimed to investigate the possible association of CEA with EAT. Methods: A total of 134 Caucasian (males = 56, females = 78) individuals, aged (22-83 years), who were admitted for routine health control, were enrolled in this cross-sectional study. CEA was measured with chemiluminescent microparticle immunoassay (CMIA). EAT was measured by transthoracic echocardiography, and the visceral fat rating (VFR) was assessed by a body composition analyzing machine. The p-value <0.05 was considered statistically significant. Results: CEA levels were categorized as tertiles: T1, 0.5-1.04; T2, 1.06–1.69; and T3, ≥1.7 ng/ml. The mean age, weight, VFR, EAT, and fasting glucose, as well as the median of systolic blood pressure (SBP), creatinine, and AST increased with the increasing CEA tertiles. CEA was significantly associated with EAT (r = 0.55, P<0.001) and VFR (r = 0.36, P<0.001). Multivariate linear regression analysis confirmed that gender, age, and EAT were the significant independent variables associated with CEA. Conclusion: Individuals with increased EAT have higher levels of CEA, suggesting that this biomarker is most likely produced by EAT; however, additional investigations are required to improve the present work.

Resumo Fundamentos A determinação precisa do colesterol de lipoproteína de baixa densidade (LDL-C) é importante para se alcançar concentrações de LDL-C recomendadas por diretrizes e para reduzir resultados cardiovasculares adversos em pacientes diabéticos. A equação de Friedewald comumente usada (LDL-Cf) produz resultados imprecisos em pacientes diabéticos devido a dislipidemia diabética associada. Recentemente, duas novas equações – Martin/Hopkins (LDL-CMH) e Sampson (LDL-Cs) – foram desenvolvidas para melhorar a precisão da estimativa de LDL-C, mas os dados são insuficientes para sugerir a superioridade de uma equação sobre a outra. Objetivos O presente estudo comparou a precisão e a utilidade clínica das novas equações de Martin/Hopkins e Sampson em pacientes diabéticos. Método Foram incluídos no estudo quatrocentos e dois (402) pacientes com diabetes. O risco cardiovascular dos pacientes e as metas de LDL-C foram calculadas por diretrizes europeias. As concentrações de LDL-Cmh, LDL-Cs, e LDL-Cf calculadas foram comparadas à concentração de LDL-C direto (LDL-Cd) para testar a concordância entre essas equações e LDL-Cd. Um P valor <0,05 foi aceito como estatisticamente significativo. Resultados A LDL-CMH e a LDL-Cs tiveram concordância melhor com o LDL-Cd em comparação com a LDL-Cf, mas não houve diferenças estatísticas entre as novas equações para concordância com o LDL-Cd (Alfa de Cronbach de 0,955 para ambos, p=1). Da mesma forma, a LDL-CMH e a LDL-Cs tinham um grau semelhante de concordância com o LDL-Cd para determinar se o paciente estava dentro da meta de LDL-C (96,3% para LDL-Cmh e 96,0% para LDL-Cs), que eram ligeiramente melhores que a LDL-Cf (94,6%). Em pacientes com uma concentração de triglicérides >400 mg/dl, a concordância com o LDL-Cd foi ruim, independentemente do método usado. Conclusão As equações de Martin/Hopkins e Sampson mostram uma precisão similar para o cálculo de concentrações de LDL-C nos pacientes com diabetes, e ambas as equações são ligeiramente melhores que a equação de Friedewald.

Abstract Background The accurate determination of low-density lipoprotein cholesterol (LDL-C) is important to reach guideline-recommended LDL-C concentrations and to reduce adverse cardiovascular outcomes in diabetic patients. The commonly used Friedewald equation (LDL-Cf), gives inaccurate results in diabetic patients due to accompanying diabetic dyslipidemia. Recently two new equations – Martin/Hopkins (LDL-Cmh) and Sampson (LDL-Cs) – were developed to improve the accuracy of LDL-C estimation, but data are insufficient to suggest the superiority of one equation over the other one. Objective The present study compared the accuracy and clinical usefulness of novel Martin/Hopkins and Sampson equations in diabetic patients. Methods This study included 402 patients with diabetes. Patients’ cardiovascular risk and LDL-C targets were calculated per European guidelines. Calculated LDL-Cmh, LDL-Cs, and LDL-Cf concentrations were compared with direct LDL-C concentration (LDL-Cd) to test agreement between these equations and LDL-Cd. A p-value <0.05 was accepted as statistically significant. Results Both LDL-Cmh and LDL-Cs had a better agreement with LDL-Cd as compared to LDL-Cf, but no statistical differences were found among novel equations for agreement with LDL-Cd (Cronbach’s alpha 0.955 for both, p=1). Likewise, LDL-Cmh and LDL-Cs showed a similar degree of agreement with LDL-Cd in determining whether a patient was in a guideline-recommended LDL-C target (96.3% for LDL-Cmh and 96.0% for LDL-Cs), which were marginally better than LDL-Cf (94.6%). In patients with a triglyceride concentration >400 mg/dl, agreement with LDL-Cd was poor, regardless of the method used. Conclusion Martin/Hopkins and Sampson’s equations show a similar accuracy for calculating LDL-C concentrations in patients with diabetes, and both equations were marginally better than the Friedewald equation.

Abstract In the last decades, ferroptosis and its relationship with Parkinson’s disease have gained significant attention. Compounds that affect ferroptosis and iron-dependent pathways in particular, have possible candidates for study in this context.Sinapic acid is an iron-chelator and high antioxidant bioactive phenolic acid. Its neuroprotective action, due to the antioxidant capacity, has been shown in several experimental models.However, the relationship between iron and antioxidant actions is still misunderstood and therefore, in the current study, we tried to investigate the effects of sinapic acid in rotenone-induced Parkinson’s disease with the aspect of ferroptosis and iron-dependent alterations.The Parkinson’s disease model was induced by a single dose intrastriatal and intrategmental rotenone (5µg/µl) injection.Sinapic acid (30mg/ kg) was orally administered during a 28-day period after the Parkinson’s disease model was validated.Our results demonstrated that sinapic acid treatment attenuated rotenone-induced increase of serum transferrin and iron levels.Furthermore, sinapic acid inhibited rotenone-induced heme oxygenase-1(HO-1) increase and decrease of glutathione peroxidase-4 (GPx-4) levels in brain tissue. Also, sinapic acid treatment decreased motor impairment, likely as a result of the ameliorative effects on the tyrosine hydroxylase immunoreactivity loss after the rotenone insult.Our study suggests that the iron regulatory role of sinapic acid possibly plays a role in the protective effect on rotenone-induced neuronal damage.

FUNDAMENTO: A extensão da doença arterial coronariana aterosclerótica em pacientes com angina estável tem importantes implicações prognósticas e terapêuticas. Em modelos atuais de evolução de placas, os trombócitos desempenham um papel importante no crescimento de placas. O volume plaquetário médio é um marcador facilmente determinado, com evidência de correlação com a agregabilidade plaquetária in vitro, além de valores comprovadamente maiores após eventos vasculares agudos. OBJETIVO: No presente estudo, investigou-se a relação entre o volume plaquetário médio e a extensão angiográfica da doença arterial coronariana em pacientes com angina estável. MÉTODOS: Foram analisados prontuários, hemograma completo e dados angiográficos anteriores de 267 pacientes elegíveis com angina estável. A extensão angiográfica da doença arterial coronariana foi avaliada à luz de dados angiográficos, com o uso por um especialista do escore de Gensini em uma cardiologia invasiva. Os valores para o volume plaquetário médio foram obtidos a partir de hemogramas completos, obtidos um dia antes da angiografia. Com relação ao intervalo populacional para o volume plaquetário médio, os pacientes foram agrupados dentro (n = 176) e abaixo (n = 62) do referido intervalo. Foi realizada uma comparação entre grupos e uma análise correlacional. RESULTADOS: Não houve correlação linear entre o escore de Gensini total e o volume plaquetário médio (p = 0,29), ao passo que a contagem total de trombócitos apresentou correlação inversa com o volume plaquetário médio (p < 0,001, r = 0,41). Os pacientes com volume plaquetário médio abaixo do normal apresentaram um escore de Gensini (36,73 ± 32,5 vs. 45,63 ± 32,63; p = 0,023) e doença coronariana triarterial (18% VS. 36%; p = 0,007) significativamente inferiores se comparados com aqueles apresentando valores de volume plaquetário médio dentro dos intervalos populacionais. CONCLUSÃO: Nossas constatações não demonstraram nenhuma relação linear entre o volume plaquetário médio e a extensão da doença arterial coronariana, ao passo que os pacientes com volume plaquetário médio abaixo do normal apresentaram uma extensão reduzida da doença arterial coronariana.

BACKGROUND: Extent of atherosclerotic coronary artery disease in patients with stable angina has important prognostic and therapeutic implications. In current models of plaque evolution, thrombocytes play an important role in plaque growth. Mean platelet volume is a readily obtainable marker that was shown to correlate with platelet aggregability in vitro and increased values were demonstrated after acute vascular events. OBJECTIVE: In this study, we investigated the relationship of mean platelet volume and angiographic extent of coronary artery disease in patients with stable angina. METHODS: Past medical records, complete blood count and angiographic data of 267 eligible stable angina patients were reviewed. Angiographic extent of coronary artery disease was evaluated form angiographic data using Gensini score by an expert in invasive cardiology. Mean platelet volume values were obtained from complete blood counts that obtained one day before angiography. Patients were grouped as those within (n = 176) and lower than (n = 62) population-based range for mean platelet volume. Comparison between groups and correlation analysis was performed. RESULTS: There were no linear correlation between total Gensini score and mean platelet volume (p = 0.29), while total thrombocyte count was inversely correlated with mean platelet volume (p < 0.001; r = 0.41). Patients with lower than normal mean platelet volume had significantly lower Gensini score (36.73 ± 32.5 vs. 45.63 ± 32.63; p = 0.023) and three-vessel disease (18% vs. 36%; p = 0.007) compared with those mean platelet volume values within population-based ranges. CONCLUSION: Our findings show no linear relationship exists between mean platelet volume and extent of coronary artery disease, while patients with lower than normal mean platelet volume had reduced extent of coronary artery disease.