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Resumo Fundamento A angiotomografia coronária (ATC) tem sido usada para avaliação de dor torácica principalmente em pacientes de baixo risco, e poucos dados existem com pacientes em risco intermediário. Objetivo Avaliar o desempenho de medidas seriadas de troponinas sensíveis e de ATC em pacientes de risco intermediário. Métodos Um total de 100 pacientes com dor torácica, TIMI score 3 ou 4 e troponina negativa foram prospectivamente incluídos. Todos os pacientes foram submetidos à ATC, e aqueles com obstruções ≥ 50% foram encaminhados à cineangiocoronariografia. Pacientes com lesões < 50% recebiam alta hospitalar, receberam alta e foram contatados 30 dias depois por telefonema para avaliação dos desfechos clínicos. Os desfechos foram hospitalização, morte, e infarto agudo do miocárdio em 30 dias. A comparação entre os métodos foi realizada pelo teste de concordância kappa. O desempenho das medidas de troponina e da ATC na detecção de lesões coronárias significativas e desfechos clínicos foi calculado. Os resultados foram considerados estatisticamente significativos quando p

1. Introducao A pandemia pelo novo coronavirus (SARS-CoV-2) vem gerando debates a respeito do melhor tratamento para a doenca e suas complicacoes. Publicacoes recentes demonstraram que as doencas cardiovasculares (DCV) estao entre os principais fatores de risco para evolucao desfavoravel da doenca, incluindo hipertensao arterial e diabetes mellitus. – Foi demonstrado que pacientes com infeccao pelo novo coronavirus (COVID-19) apresentam mecanismos pro-tromboticos distintamente ativados, com maior possibilidade de eventos tromboticos ocorrerem. Sindrome coronariana aguda (SCA) com e sem supradesnivelamento do [...]

Background: Low concentrations of high-density lipoprotein cholesterol (HDL-C) represent a well-established cardiovascular risk factor. Paradoxically, extremely high HDL-C levels are equally associated with elevated cardiovascular risk, resulting in the U-shape relationship of HDL-C with cardiovascular disease. Mechanisms underlying this association are presently unknown. We hypothesised that the capacity of high-density lipoprotein (HDL) to acquire free cholesterol upon triglyceride-rich lipoprotein (TGRL) lipolysis by lipoprotein lipase underlies the non-linear relationship between HDL-C and cardiovascular risk. Methods: To assess our hypothesis, we developed a novel assay to evaluate the capacity of HDL to acquire free cholesterol (as fluorescent TopFluor® cholesterol) from TGRL upon in vitro lipolysis by lipoprotein lipase. Results: When the assay was applied to several populations markedly differing in plasma HDL-C levels, transfer of free cholesterol was significantly decreased in low HDL-C patients with acute myocardial infarction (−45%) and type 2 diabetes (–25%), and in subjects with extremely high HDL-C of >2.59 mmol/L (>100 mg/dL) (−20%) versus healthy normolipidaemic controls. When these data were combined and plotted against HDL-C concentrations, an inverse U-shape relationship was observed. Consistent with these findings, animal studies revealed that the capacity of HDL to acquire cholesterol upon lipolysis was reduced in low HDL-C apolipoprotein A-I knock-out mice and was negatively correlated with aortic accumulation of [3H]-cholesterol after oral gavage, attesting this functional characteristic as a negative metric of postprandial atherosclerosis. Conclusions: Free cholesterol transfer to HDL upon TGRL lipolysis may underlie the U-shape relationship between HDL-C and cardiovascular disease, linking HDL-C to triglyceride metabolism and atherosclerosis. Fil: Feng, Ma. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Darabi, Maryam. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Tubeuf, Emilie. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Canicio, Aurélie. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Lhomme, Marie. Institute Of Cardiometabolism And Nutrition; Francia Fil: Frisdal, Eric. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Lanfranchi Lebreton, Sandrine. Université Pierre et Marie Curie; Francia Fil: Matheron, Lucrèce. Université Pierre et Marie Curie; Francia Fil: Rached, Fabiana. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Ponnaiah, Maharajah. Institute Of Cardiometabolism And Nutrition; Francia Fil: Serrano, Carlos V.. Instituto Do Coracao Do Hospital Das Clinicas; Brasil Fil: Santos, Raul D.. Instituto Do Coracao Do Hospital Das Clinicas; Brasil Fil: Brites, Fernando Daniel. Universidad de Buenos Aires; Argentina. Instituto Do Coracao Do Hospital Das Clinicas; Brasil Fil: Bolbach, Gerard. Université Pierre et Marie Curie; Francia Fil: Gautier, Emmanuel. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Huby, Thierry. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Carrie, Alain. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Bruckert, Eric. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Guerin, Maryse. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Couvert, Philippe. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Giral, Philippe. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Lesnik, Philippe. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Le Goff, Wilfried. Université Pierre et Marie Curie; Francia. Inserm; Francia Fil: Guillas, Isabelle. Inserm; Francia. Université Pierre et Marie Curie; Francia Fil: Kontush, Anatol. Inserm; Francia. Université Pierre et Marie Curie; Francia

1. Epidemiologia da Parada Cardiorrespiratoria e Apresentacao da Diretriz […] Atualizacao da Diretriz de Ressuscitacao Cardiopulmonar e Cuidados Cardiovasculares de Emergencia da Sociedade Brasileira de Cardiologia – 2019

Introduction: Despite having higher sensitivity as compared to conventional troponins, sensitive troponins have lower specificity, mainly in patients with renal failure. Objective: Study aimed at assessing the sensitive troponin I levels in patients with chest pain, and relating them to the existence of significant coronary lesions. Methods: Retrospective, single-center, observational. This study included 991 patients divided into two groups: with (N = 681) and without (N = 310) significant coronary lesion. For posterior analysis, the patients were divided into two other groups: with (N = 184) and without (N = 807) chronic renal failure. The commercial ADVIA Centaur® TnI-Ultra assay (Siemens Healthcare Diagnostics) was used. The ROC curve analysis was performed to identify the sensitivity and specificity of the best cutoff point of troponin as a discriminator of the probability of significant coronary lesion. The associations were considered significant when p < 0.05. Results: The median age was 63 years, and 52% of the patients were of the male sex. The area under the ROC curve between the troponin levels and significant coronary lesions was 0.685 (95% CI: 0.65 - 0.72). In patients with or without renal failure, the areas under the ROC curve were 0.703 (95% CI: 0.66 - 0.74) and 0.608 (95% CI: 0.52 - 0.70), respectively. The best cutoff points to discriminate the presence of significant coronary lesion were: in the general population, 0.605 ng/dL (sensitivity, 63.4%; specificity, 67%); in patients without renal failure, 0.605 ng/dL (sensitivity, 62.7%; specificity, 71%); and in patients with chronic renal failure, 0.515 ng/dL (sensitivity, 80.6%; specificity, 42%). Conclusion: In patients with chest pain, sensitive troponin I showed a good correlation with significant coronary lesions when its level was greater than 0.605 ng/dL. In patients with chronic renal failure, a significant decrease in specificity was observed in the correlation of troponin levels and severe coronary lesions.

FUNDAMENTO: Alguns estudos têm sugerido redução da atividade do clopidogrel sobre a ativação e adesão plaquetárias em pacientes em uso de estatinas. OBJETIVO: Avaliar se a ativação e agregação plaquetárias diminuem com clopidogrel, e se ocorre redução da ação do clopidogrel quando associado à atorvastatina ou à sinvastatina. MÉTODOS: Estudo prospectivo que incluiu 68 pacientes com angina estável em uso prévio de sinvastatina, atorvastatina, ou nenhuma estatina (grupo controle), com indicação prévia eletiva de realização de intervenção coronária percutânea. Foi analisada a ativação plaquetária através do número de plaquetas, níveis de P-selectina e glucoproteína IIb/IIIa (com e sem estímulo de ADP) através de citometria de fluxo. Os resultados foram analisados antes e após a intervenção coronária percutânea e da administração de clopidogrel. RESULTADOS: Observamos redução da atividade plaquetária com uso de clopidogrel. Além disso, não houve diferenças entre as variáveis analisadas que comprovassem redução da atividade do clopidogrel quando associado à estatinas. Observou-se níveis de p-selectina (pré-angioplastia: 14,23±7,52 x 11,45±8,83 x 7,65±7,09; pós angioplastia: 21,49±23,82 x 4,37±2,71 x 4,82±4,47, ρ

The balance between different immunological stimuli is essential in the progression and stabilization of atherosclerotic plaques. Immune regulation has been suggested as potential target for the treatment of atherosclerotic disease. We sought to determine whether treatment with pentoxifylline, a phosphodiesterase inhibitor with immunomodulating properties, could reduce the pro-inflammatory response observed in patients with acute coronary syndromes (ACS) and increase anti-inflammatory activity. In a double-blind, prospective, placebo-controlled study, 64 patients with ACS were randomized to receive pentoxifylline 400mg TID or placebo for 6 months. Analysis of the pro-inflammatory markers, C-reactive protein (CRP), interleukin (IL)-6, IL-12, interferon-gamma and tumor necrosis factor (TNF)-alpha and the anti-inflammatory cytokines, transforming growth factor (TGF)-beta1 and IL-10 were done at baseline, 1 and 6 months. Pentoxifylline treatment significantly reduced the adjusted levels of CRP and TNF-alpha compared to placebo after 6 months (P=0.04 and P

Introduction: A recently published study raised doubts about the need for percutaneous treatment of nonculprit lesions in patients with acute coronary syndromes (ACS). Methods: Retrospective, unicentric, observational study. Objective: To analyze the long-term outcomes in patients undergoing treatment of the culprit artery, comparing those who remained with significant residual lesions in nonculprit arteries (group I) versus those without residual lesions in other coronary artery beds (group II). The study included 580 patients (284 in group I and 296 in group II) between May 2010 and May 2013. We obtained demographic and clinical data, as well as information regarding the coronary treatment administered to the patients. In the statistical analysis, the primary outcome included combined events (reinfarction/angina, death, heart failure, and need for reintervention). The comparison between groups was performed using the chi-square test and ANOVA. The long-term analysis was conducted with the Kaplan-Meier method, with a mean follow-up of 9.86 months. Results: The mean ages were 63 years in group I and 62 years in group II. On long-term follow-up, there was no significant difference in combined events in groups I and II (31.9% versus 35.6%, respectively, p = 0.76). Conclusion: The strategy of treating the culprit artery alone seems safe. In this study, no long-term differences in combined endpoints were observed between patients who remained with significant lesions compared with those without other obstructions. Resumo Fundamento: Um estudo publicado recentemente levantou dúvidas sobre a necessidade de abordagem percutânea de lesões não culpadas em pacientes com síndromes coronarianas agudas (SCA). Métodos: Estudo retrospectivo, unicêntrico e observacional. Objetivo: Comparar desfechos a longo prazo entre pacientes submetidos à abordagem da artéria culpada, comparando os que permaneceram com lesões residuais significativas em artérias não culpadas (grupo I) versus aqueles sem lesões residuais em outros leitos coronarianos (grupo II). Foram incluídos 580 pacientes (284 no grupo I e 296 no grupo II) entre maio de 2010 e maio de 2013. Foram obtidos dados demográficos e clínicos, além de informações sobre o tratamento coronariano administrado aos pacientes. Na análise estatística, o desfecho primário incluiu eventos combinados (reinfarto/angina, morte, insuficiência cardíaca e necessidade de reintervenção). A comparação entre grupos foi realizada através do teste do qui-quadrado e ANOVA. A análise a longo prazo foi realizada pelo método de Kaplan-Meier, com seguimento médio de 9,86 meses. Resultados: As médias das idades foram de 63 anos no grupo I e 62 anos no grupo II. O seguimento a longo prazo não mostrou diferença significativa em eventos combinados nos grupos I e II (31,9% versus 35,6%, respectivamente, p = 0,76). Conclusão: A estratégia de tratar somente a artéria considerada culpada parece segura. Neste estudo, não houve diferenças a longo prazo em desfechos combinados entre pacientes que permaneceram com lesões significativas comparativamente àqueles sem outras obstruções.

OBJETIVO: Os marcadores da ativacao plaquetaria em geral se apresentam elevados na doenca arterial coronariana. Desse modo, procuramos identificar a presenca e as potenciais associacoes de diferentes marcadores da ativacao plaquetaria. METODOS: Estudamos pacientes com angina instavel (n=28), pacientes com angina estavel (n=36) e pacientes sem doenca arterial coronariana (n=30); sexo e idade foram estratificados. Os niveis sanguineos da molecula de adesao P-selectina, do thromboxane B2 e de serotonina foram medidos por imunoensaios enzimaticos. RESULTADOS: Quando comparamos os grupos, os resultados foram: a P-selectina, o thromboxane B2 e os niveis do serotonina apresentaram-se significativamente mais elevados nos pacientes com angina instavel do que nos pacientes com angina estavel. CONCLUSAO: Estes marcadores da ativacao plaquetaria podem, portanto, identificar formas instaveis de doenca arterial coronariana.

Reduction in cardiovascular events with statins has been in part attributed to their anti-inflammatory properties.Evaluate the effects of atorvastatin on levels of inflammatory markers, such as tumor necrosis factor-alpha (TNF), interleukins (IL-1 and IL-6), soluble intercellular adhesion molecule-1 (sICAM-1) and C-reactive protein (CRP) in hypercholesterolemic patients (LDL-cholesterol160 mg/dL).Two lipid-lowering regimens were taken for 8 weeks. One set of patients (n=45, 26 men, average 50 +/- 2 years of age) was subjected to atorvastatin treatment (20-40 mg/day), plus diet recommendation. Another set of patients (n=23, 12 men, average 53 +/- 3 years of age) went through diet recommendation alone. Both groups were recommended to perform standard physical activity. Plasma samples were collected after overnight fasting at baseline and after 8 weeks for ELISA. The use of atorvastatin when compared to diet alone, resulted in significant (P0.0001) reductions for: LDL-cholesterol (39.9% versus 4.4%), TNF (21.4% versus 2.9%), IL-6 (22.1% versus 2.0%), IL-1 (16.4% versus 2.7%) and sICAM-1 (9.6% versus 0.1%), respectively. The percentage of patients with CRP levels3 mg/dL in the atorvastatin group fell from 25.0 to 6.7% (P0.0001) while in the diet group the reduction was not significant.In hypercholesterolemic patients, atorvastatin, compared to diet alone resulted in significant reductions in levels of proinflammatory cytokines (TNF, IL-1 and IL-6) as well as in sICAM-1 and CRP. Thus, statin-induced inhibition of inflammatory markers may play an important role in the pharmacological and clinical effects of statins seen in cardiovascular diseases.

Background: The prevalence and clinical outcomes of heart failure with preserved left ventricular ejection fraction after acute myocardial infarction have not been well elucidated. Objective: To analyze the prevalence of heart failure with preserved left ventricular ejection fraction in acute myocardial infarction and its association with mortality. Methods: Patients with acute myocardial infarction (n = 1,474) were prospectively included. Patients without heart failure (Killip score = 1), with heart failure with preserved left ventricular ejection fraction (Killip score > 1 and left ventricle ejection fraction ≥ 50%), and with systolic dysfunction (Killip score > 1 and left ventricle ejection fraction < 50%) on admission were compared. The association between systolic dysfunction with preserved left ventricular ejection fraction and in-hospital mortality was tested in adjusted models. Results: Among the patients included, 1,256 (85.2%) were admitted without heart failure (72% men, 67 ± 15 years), 78 (5.3%) with heart failure with preserved left ventricular ejection fraction (59% men, 76 ± 14 years), and 140 (9.5%) with systolic dysfunction (69% men, 76 ± 14 years), with mortality rates of 4.3%, 17.9%, and 27.1%, respectively (p < 0.001). Logistic regression (adjusted for sex, age, troponin, diabetes, and body mass index) demonstrated that heart failure with preserved left ventricular ejection fraction (OR 2.91; 95% CI 1.35–6.27; p = 0.006) and systolic dysfunction (OR 5.38; 95% CI 3.10 to 9.32; p < 0.001) were associated with in-hospital mortality. Conclusion: One-third of patients with acute myocardial infarction admitted with heart failure had preserved left ventricular ejection fraction. Although this subgroup exhibited more favorable outcomes than those with systolic dysfunction, this condition presented a three-fold higher risk of death than the group without heart failure. Patients with acute myocardial infarction and heart failure with preserved left ventricular ejection fraction encounter elevated short-term risk and require special attention and monitoring during hospitalization. Resumo Fundamento: A prevalência e os desfechos clínicos em pacientes com insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada pós-infarto agudo do miocárdio ainda não foram bem elucidados. Objetivo: Analisar a prevalência de insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada no infarto agudo do miocárdio e sua associação com a mortalidade. Métodos: Pacientes com infarto agudo do miocárdio (n = 1.474) foram incluídos prospectivamente. Pacientes admitidos sem insuficiência cardíaca (Killip = 1), com insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada (Killip > 1 e fração de ejeção do ventrículo esquerdo ≥ 50%) e com insuficiência cardíaca sistólica (Killip > 1 e fração de ejeção do ventrículo esquerdo < 50%) foram comparados. A associação entre insuficiência cardíaca sistólica e com fração de ejeção do ventrículo esquerdo preservada, com a mortalidade hospitalar foi testada em modelos ajustados. Resultados: Dentre os incluídos, 1.256 (85,2%) pacientes foram admitidos sem insuficiência cardíaca (72% homens, 67 ± 15 anos), 78 (5,3%) com insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada (59% homens, 76 ± 14 anos) e 140 (9,5%) com insuficiência cardíaca sistólica (69% homens, 76 ± 14 anos), com mortalidade, respectivamente, de 4,3; 17,9 e 27,1% (p < 0,001). A regressão logística (ajustada para sexo, idade, troponina, diabetes e índice de massa corporal) demonstrou que insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada (odds ratio de 2,91; intervalo de confiança de 95% de 1,35-6,27; p = 0,006) e insuficiência cardíaca sistólica (odds ratio de 5,38; intervalo de confiança de 95% de 3,10-9,32; p < 0,001) se associaram à mortalidade intra-hospitalar. Conclusão: Um terço dos pacientes com infarto agudo do miocárdio admitidos com insuficiência cardíaca apresentou fração de ejeção do ventrículo esquerdo preservada. Apesar de esse subgrupo ter evolução mais favorável que os pacientes com insuficiência cardíaca sistólica, ele apresentou risco de morte três vezes maior do que o grupo sem insuficiência cardíaca. Pacientes com infarto agudo do miocárdio e insuficiência cardíaca com fração de ejeção do ventrículo esquerdo preservada apresentaram elevado risco em curto prazo e mereceram especial atenção e monitorização durante a internação hospitalar.

Background Assuming that coronary interventions, both coronary bypass surgery (CABG) and percutaneous coronary intervention (PCI), are directed to preserve left ventricular function, it is not known whether medical therapy alone (MT) can achieve this protection. Thus, we evaluated the evolution of LV ejection fraction (LVEF) in patients with stable coronary artery disease (CAD) treated by CABG, PCI, or MT as a post hoc analysis of a randomized controlled trial with a follow-up of 10 years. Methods Left ventricle ejection fraction was assessed with transthoracic echocardiography in patients with multivessel CAD, participants of the MASS II trial before randomization to CABG, PCI, or MT, and re-evaluated after 10 years of follow-up. Results Of the 611 patients, 422 were alive after 10.32 ± 1.43 years. Three hundred and fifty had LVEF reassessed: 108 patients from MT, 111 from CABG, and 131 from PCI. There was no difference in LVEF at the beginning (0.61 ± 0.07, 0.61 ± 0.08, 0.61 ± 0.09, respectively, for PCI, CABG, and MT, P = 0.675) or at the end of follow-up (0.56 ± 0.11, 0.55 ± 0.11, 0.55 ± 0.12, P = 0.675), or in the decline of LVEF (reduction delta of −7.2 ± 17.13, −9.08 ± 18.77, and −7.54 ± 22.74). Acute myocardial infarction (AMI) during the follow-up was associated with greater reduction in LVEF. The presence of previous AMI (OR: 2.50, 95% CI: 1.40–4.45; P = 0.0007) and during the follow-up (OR: 2.73, 95% CI: 1.25–5.92; P = 0.005) was associated with development of LVEF

FUNDAMENTO: A ocorrencia de sangramento aumenta a mortalidade intra-hospitalar em pacientes com sindromes coronarianas agudas (SCAs), e ha uma boa correlacao entre os escores de risco de sangramento e a incidencia de eventos hemorragicos. No entanto, o papel dos escores de risco de sangramento como fatores preditivos de mortalidade e pouco estudado. OBJETIVO: Analisar o papel do escore de risco de sangramento como fator preditivo de mortalidade intra-hospitalar numa coorte de pacientes com SCA tratados num centro terciario de cardiologia. METODOS: Dos 1.655 pacientes com SCA (547 com SCA com supra de ST e 1.118 com SCA sem supra de ST), calculou-se o escore de risco de sangramento ACUITY/HORIZONS prospectivamente em 249 pacientes e retrospectivamente nos demais 1.416. Informacoes sobre mortalidade e complicacoes hemorragicas tambem foram obtidas. RESULTADOS: A idade media da populacao estudada foi 64,3 ± 12,6 anos e o escore de risco de sangramento medio foi 18 ± 7,7. A correlacao entre sangramento e mortalidade foi altamente significativa (p < 0,001; OR = 5,29), assim como a correlacao entre escore de sangramento e hemorragia intra-hospitalar (p < 0,001; OR = 1,058), e entre escore de sangramento e mortalidade intra-hospitalar (OR ajustado = 1,121, p < 0,001, area sob a curva ROC 0,753; p < 0,001). O OR ajustado e a area sob a curva ROC para a populacao com SCA com supra de ST foram 1,046 (p = 0,046) e 0,686 ± 0,040 (p < 0,001), respectivamente, e para SCA sem supra de ST foram 1,150 (p < 0,001) e 0,769 ± 0,036 (p < 0,001), respectivamente. CONCLUSAO: O escore de risco de sangramento e um fator preditivo muito util e altamente confiavel para mortalidade intra-hospitalar em uma grande variedade de pacientes com SCAs, especialmente aqueles com angina instavel ou infarto agudo do miocardio sem supra de ST.

Introducao Arterite de Takayasu (AT) e uma arterite inflamatoria cronica de etiologia desconhecida que acomete grandes vasos, principalmente aorta e seus principais ramos, vasos pulmonares e coronarias1. Devido a raridade dos casos a monitoracao da atividade da doenca e o melhor esquema terapeutico ainda tem sido um desafio para todos os que tratam esses pacientes. Especificamente em casos de sindromes coronarias agudas (SCA), a melhor forma de tratamento intervencionista mantem-se indefinido. Algumas series de casos apresentam sua experiencia com angioplastia coronaria (ATC) e/ou cirurgia de revascularizacao miocardica (CRM), porem com pouca consistencia1. Nesse contexto, o relato da evolucao de uma mesma paciente submetida a implante de stent coronario convencional e, posteriormente, farmacologico de forma consecutiva, associado a estenose coronaria intrastent nos dois procedimentos na ausencia de inflamacao, com subsequente realizacao de CRM, e unico e reforca a dificuldade de manejo de SCA nessa doenca.

Few studies have prospectively addressed the effects of exercise in the inflammatory activity of patients with coronary artery disease (CAD). We sought to evaluate the consequences of an acute bout of exercise on inflammatory markers and BNP in untrained CAD patients before and after randomization to a training program. 34 CAD patients underwent a 50-min acute exercise session on a cycle-ergometer at 65% peak oxygen uptake before and after blood sampling. They were then randomized to a 4-month chronic exercise program (15 patients) or general lifestyle recommendations (19 patients), undergoing a new acute session of exercise after that. In the overall population, acute exercise caused a significant increase in C-reactive protein [CRP; 1.79 (4.49) vs. 1.94 (4.89) mg/L, P

A obesidade vem se tornando uma epidemia global. Cerca de 1,1 bilhões de adultos e 10% das crianças do mundo são atualmente considerados portadores de sobrepeso ou obesos. Classicamente associada a fatores de risco para doença cardiovascular, como diabete melito e hipertensão arterial sistêmica, a obesidade vem sendo cada vez mais encarada como fator de risco independente para doença arterial coronariana (DAC). A aterosclerose coronariana compreende uma série de respostas inflamatórias em nível celular e molecular, cujas reações se encontram mais exacerbadas em pacientes obesos. Antes considerado mero depósito de gordura, o tecido adiposo é visto hoje em dia como órgão endócrino e parácrino ativo, produtor de diversas citocinas inflamatórias, como as adipocinas. Este artigo visa alertar para o grave problema de saúde pública em que a obesidade se tornou nas últimas décadas e correlacionar o processo inflamatório exacerbado nos indivíduos obesos com a maior incidência de DAC nessa população. Obesity is becoming a global epidemic. Around 1.1 billion adults and 10% of the world's children are currently overweight or considered obese. Generally associated with risk factors for cardiovascular disease, such as Diabetes Mellitus and systemic arterial high blood pressure, the obesity has been more and more seen as an independent risk factor for Coronary Artery Disease (CAD). Coronary arteriosclerosis comprises a series of inflammatory responses at cellular and molecular level, whose reactions are stronger in obese patients. In the past, the adipose tissue was regarded as a mere fat deposition. Now it is seen from a totally different standpoint, as an active endocrine and paracrine organ that produces several inflammatory cytokines, such as the adipokines. This article aims to raise awareness about obesity as an increasingly significant public health issue over the past decades, as well as to relate the intense inflammatory process in obese individuals with an increased tendency for this group of individuals to develop CAD. La obesidad se está tornando una epidemia global. Cerca de 1,1 billones de adultos y el 10% de los niños del mundo están considerados actualmente portadores de sobrepeso u obesos. Clásicamente asociada a factores de riesgo para enfermedad cardiovascular, como diabetes melitus e hipertensión arterial sistémica, la obesidad se está considerando cada vez más factor de riesgo independiente para enfermedad arterial coronaria (EAC). La aterosclerosis coronaria comprende una serie de respuestas inflamatorias a nivel celular y molecular, cuyas reacciones se encuentran más exacerbadas en pacientes obesos. Antes considerado mero depósito de grasa, el tejido adiposo está visto hoy en día como órgano endócrino y parácrino activo, productor de diversas citocinas inflamatorias, como las adipocinas. Este artículo apunta a alertar sobre el grave problema de salud pública en que se convirtió la obesidad en las últimas décadas y correlacionar el proceso inflamatorio exacerbado en los individuos obesos con la mayor incidencia de EAC en esta población.

The association of plaques with outward arterial remodeling and acute coronary syndromes (ACS) has been mostly investigated by cross-sectional intravascular ultrasound studies. Magnetic resonance imaging (MRI) has made it possible to noninvasively assess the coronary vessels of patients with chronic coronary artery disease, but no study has been done in patients with ACS. We sought to serially investigate changes in coronary vessel walls of patients with ACS using noninvasive serial MRI.A total of 42 segments of coronary arteries from 22 patients presenting with non-ST-segment elevation ACS were studied at baseline in the acute phase and at 6 months after stabilization and optimization of medical therapy. Patients received routine medical treatment during this period with control of risk factors. Vessel wall area, maximum wall thickness, mean wall thickness, and lumen area were analyzed longitudinally using MRI.Vessel wall area (38.8 +/- 20.0 vs 27.7 +/- 10.4 mm2; P = .001), maximum wall thickness (2.9 +/- 0.7 vs 2.5 +/- 0.6 mm; P.001), and mean wall thickness (2.0 +/- 0.7 vs 1.6 +/- 0.5 mm; P.001) were significantly reduced at 6 months compared with baseline, whereas lumen area did not show significant changes (11.5 +/- 4.8 vs 10.9 +/- 5.0 mm2; P = .52). The wall/lumen ratio was significantly reduced from 3.7 +/- 1.7 to 2.9 +/- 1.3 (P = .01), suggesting a regression of outward remodeling.Patients with ACS have increased coronary vessel wall thickness and area that can regress with stabilization and medical therapy over the period of 6 months. Magnetic resonance imaging can detect and serially follow these changes, monitoring coronary vascular remodeling from the acute to the chronic phase of the disease.

OBJETIVO: Analisar a liberação intracoronariana de marcadores inflamatórios (MI) após intervenções coronarianas percutâneas (ICP) e comparar suas concentrações com relação ao tipo de ICP utilizada (rotablator vs angioplastia por balão). MÉTODOS: Foram randomizados 22 pacientes com média de idade de 60±11,9 anos, 12 do sexo masculino, portadores de síndromes coronarianas estáveis, submetidos ao tratamento eletivo de uma única lesão coronariana utilizando rotablator (N=11) ou pré-dilatação por balão (N=11) para implante de stents. As amostras foram colhidas na raiz da aorta e no seio coronariano, imediatamente antes e 15 minutos após as intervenções. Todas as dosagens foram feitas antes do implante do stent, sendo analisadas as citocinas TNF-a, IL-6 e IL-1 e as moléculas de adesão solúveis ICAM-1, E-selectina e P-selectina, utilizando o método ELISA. RESULTADOS: As concentrações de TNF-a e IL-6 aumentaram após as ICP, passando respectivamente de 9,5±1,5 pg/ml para 9,9±1,8 pg/ml (p=0,017) e de 6,0±2,4 pg/ml para 6,9±3,0 pg/ml (p

Edimar Alcides Bocchi, Fabio Vilas-Boas, Sergio Perrone, Angel G Caamano, Nadine Clausell, Maria da Consolacao VMoreira, Jorge Thierer, Hugo Omar Grancelli, Carlos Vicente Serrano Junior, Denilson Albuquerque, Dirceu Almeida,Fernando Bacal, Luis Felipe Moreira, Adonay Mendonza, Antonio Magana, Arturo Tejeda, Daniel Chafes, Efraim Gomez,Erick Bogantes, Estela Azeka, Evandro Tinoco Mesquita, Francisco Jose Farias B Reis, Hector Mora, Humberto Vilacorta,Jesus Sanches, Joao David de Souza Neto, Jose Luis Vuksovic, Juan Paes Moreno, Julio Aspe y Rosas, Lidia ZytynskiMoura, Luis Antonio de Almeida Campos, Luis Eduardo Rohde, Marcos Parioma Javier, Martin Garrido Garduno, MucioTavares, Pablo Castro Galvez, Raul Spinoza, Reynaldo Castro de Miranda, Ricardo Mourilhe Rocha, Roberto Paganini,Rodolfo Castano Guerra, Salvador Rassi, Sofia Lagudis, Solange Bordignon, Solon Navarette, Waldo Fernandes, AntonioCarlos Pereira Barretto, Victor Issa, Jorge Ilha Guimaraes.

Mulher de 67 anos de idade, apresentando estenose mitral grave, nao-reumatica, apos 18 anos da realizacao de miotomia/miectomia septal cirurgica para correcao de miocardiopatia hipertrofica septal assimetrica. A paciente foi submetida a troca da valva mitral por protese mecânica, tornando-se caso unico, em razao da combinacao das duas sindromes, extremamente rara e com grave prognostico

Increased monocyte adherence to the vessel wall is one of the earliest events in atherosclerosis. The mechanism by which hypercholesterolemia causes alterations in endothelial adhesiveness for monocytes is unclear. This study sought to determine if monocyte adhesion molecule expression is affected by low-density lipoprotein (LDL)-cholesterol levels. Patients with hypercholesterolemia and stable coronary artery disease were compared with those without major cardiovascular risk (control). Patients with hypercholesterolemia were treated with simvastatin 20--40 mg/day for 8--10 weeks. Blood samples were examined with flow cytometry assays at baseline and after cholesterol-lowering therapy. Monocyte CD11b and CD14 adhesion molecule expression, measured as fluorescence intensity, were significantly (P0.0001) higher in hypercholesterolemic patients before the study (176.9+/-9.8 and 138.0+/-4.8, respectively) when compared with that in control subjects (97.2+/-8.1 and 84.0+/-6.4, respectively). Both decreased markedly with treatment: to 118.8+/-6.9 and 103.1+/-3.9, respectively. Monocyte L-selectin expression was significantly lower in patients with hypercholesterolemia before treatment (43.0+/-3.0) when compared with control subjects (79.9+/-2.7), and it increased markedly with treatment (54.2+/-2.5). LDL levels correlated directly with both CD11b and CD14 expression and correlated inversely with L-selectin expression. These data show that hypercholesterolemia affects monocyte adhesion molecule expression which, in turn, decreases with statin-induced plasmatic cholesterol reduction. Such perturbations in monocyte function likely represent a proinflammatory response to hypercholesterolemia and may have a role in the early progression of atherogenesis.

Background Although the release of cardiac biomarkers after percutaneous (PCI) or surgical revascularization (CABG) is common, its prognostic significance is not known. Questions remain about the mechanisms and degree of correlation between the release, the volume of myocardial tissue loss, and the long-term significance. Delayed-enhancement of cardiac magnetic resonance (CMR) consistently quantifies areas of irreversible myocardial injury. To investigate the quantitative relationship between irreversible injury and cardiac biomarkers, we will evaluate the extent of irreversible injury in patients undergoing PCI and CABG and relate it to postprocedural modifications in cardiac biomarkers and long-term prognosis. Methods/Design The study will include 150 patients with multivessel coronary artery disease (CAD) with left ventricle ejection fraction (LVEF) and a formal indication for CABG; 50 patients will undergo CABG with cardiopulmonary bypass (CPB); 50 patients with the same arterial and ventricular condition indicated for myocardial revascularization will undergo CABG without CPB; and another 50 patients with CAD and preserved ventricular function will undergo PCI using stents. All patients will undergo CMR before and after surgery or PCI. We will also evaluate the release of cardiac markers of necrosis immediately before and after each procedure. Primary outcome considered is overall death in a 5-year follow-up. Secondary outcomes are levels of CK-MB isoenzyme and I-Troponin in association with presence of myocardial fibrosis and systolic left ventricle dysfunction assessed by CMR. Discussion The MASS-V Trial aims to establish reliable values for parameters of enzyme markers of myocardial necrosis in the absence of manifest myocardial infarction after mechanical interventions. The establishments of these indices have diagnostic value and clinical prognosis and therefore require relevant and different therapeutic measures. In daily practice, the inappropriate use of these necrosis markers has led to misdiagnosis and therefore wrong treatment. The appearance of a more sensitive tool such as CMR provides an unprecedented diagnostic accuracy of myocardial damage when correlated with necrosis enzyme markers. We aim to correlate laboratory data with imaging, thereby establishing more refined data on the presence or absence of irreversible myocardial injury after the procedure, either percutaneous or surgical, and this, with or without the use of cardiopulmonary bypass.

Depression and coronary artery disease (CAD) are both extremely prevalent diseases. In addition, compromised quality of life and life expectancy are characteristics of both situations. There are several conditions that aggravate depression and facilitate the development of CAD, as well as provoke a worse prognosis in patients with already established CAD: inferior adherence to medical orientations (medications and life style modifications), greater platelet activation and aggregation, endothelial dysfunction, and impaired autonomic dysfunction (lowered heart rate variability). Recent literature has shown that depression alone is becoming an independent risk factor for cardiac events both in primary and secondary prevention. As the diagnosis of depression in patients with heart disease is difficult, due to similarities of symptoms, the health professional should perform a careful evaluation to differentiate the clinical signs of depression from those related with general heart diseases. After a myocardial infarction, depression is an independent risk factor for mortality. Successful therapy of depression has been shown to improve patients' quality of life and cardiovascular outcome. However, multicentric clinical trials are needed to support this inference. A practical liaison between qualified professionals is necessary for the better management of depressed patients with excess risk in developing CAD. Accordingly, pathophysiological and clinical implications between depression and CAD are discussed in this article.

BACKGROUND Previous studies have demonstrated that polymorphonuclear leukocytes (PMNs) are locally activated in reperfused myocardium and contribute to the myocardial cell injury associated with reperfusion. It has been suggested that the adhesion of activated PMNs in reperfused myocardium is mediated by the PMN adhesion molecule CD-18. In the present study, we performed experiments to determine if the specific anti-CD-18 monoclonal antibody (MAb) R15.7 can prevent PMN adhesion and PMN-mediated reperfusion injury in the heart. METHODS AND RESULTS Studies were performed with isolated, Langendorff-perfused rat hearts (nine per group) in which the hearts were subjected to 20 minutes of global ischemia followed by 45 minutes of reperfusion. Human PMNs (50 million) and rat plasma (HNRP) were infused directly into the coronary circulation of nonischemic and postischemic hearts. When HNRP was administered to nonischemic hearts, no significant alterations in coronary flow, left ventricular developed pressure, or left ventricular end-diastolic pressure were observed. When hearts were reperfused in the presence of HNRP, however, marked impairment of contractile function was observed with more than 90% reduction in coronary flow throughout the reperfusion period (P < .001 versus baseline). In addition, left ventricular developed pressure was significantly depressed (P < .001 versus baseline) throughout the reperfusion period in the HNRP group and recovered to only 13.0 +/- 3.0% at 45 minutes of reperfusion. Moreover, left ventricular end-diastolic pressure was significantly elevated (P < .001) in the HNRP group throughout the reperfusion period. Treatment with the anti-CD-18 monoclonal antibody MAb R15.7 (20 micrograms/mL) at the time of reperfusion resulted in a 92.9 +/- 4.9% recovery of coronary flow (P < .001 versus HNRP) as well as a 71.0 +/- 10.1% recovery of left ventricular developed pressure (P < .001 versus HNRP). Administration of MAb R15.7 also very significantly attenuated the elevation in left ventricular end-diastolic pressure that was observed in the untreated HNRP (30.2 +/- 7.8 versus 110.3 +/- 10.3 mm Hg, P < .001) at 45 minutes of reperfusion. Cardiac myeloperoxidase activity, an index of PMN accumulation, was markedly reduced in the MAb R15.7 group at 45 minutes of reperfusion compared with the HNRP group (0.03 +/- 0.01 versus 0.3 +/- 0.05, P < .001). To determine that the protective effect of MAb R15.7 was based on functional blocking of CD-18, additional experiments were performed with identical concentrations of MAb 3.1, which binds to the alpha-subunit of LFA-1. This PMN-binding but non-CD-18-blocking antibody had little effect on the recovery of postischemic function or coronary flow and did not reduce tissue myeloperoxidase activity. CONCLUSIONS The administration of a specific anti-CD-18 monoclonal antibody, MAb R15.7, attenuates much of the PMN-mediated contractile dysfunction associated with this in vitro model of myocardial ischemia-reperfusion injury by limiting PMN accumulation. We conclude that CD-18-mediated adhesion may play a critical role in the pathogenesis of PMN-induced myocardial injury.

1. Introducao Em 2013, a Sociedade Brasileira de Cardiologia publicou as “Diretrizes Brasileiras de Antiagregantes Plaquetarios e Anticoagulantes em Cardiologia”. Ao longo dos ultimos anos, novos estudos foram realizados, fornecendo informacoes importantes sobre o uso desses medicamentos, tanto de maneira isolada quanto em associacoes. E hora, portanto, de revermos as nossas diretrizes e atualiza-las com o novo conhecimento produzido. Realizamos uma extensa revisao da literatura e optamos por enfatizar, nesta atualizacao, 6 grandes assuntos da pratica clinica que sofreram inovacoes [...]