Alterações eletrocardiográficas em pacientes com Leishmaniose Tegumentar Americana tratados com antimoniato de meglumina: revisão integrativa / Electrocardiographic changes in patients with American tegumentary leishmaniasis treated with meglumine antimoniate: integrative review

Introdução: a Leishmaniose Tegumentar Americana (LTA) é uma infecção zoonótica cujo tratamento é realizado com a droga antimoniato de meglumina (AM). Objetivo: Relatar as alterações eletrocardiográficas decorrentes do uso de AM em pacientes com LTA. Metodologia: foi realizada uma revisão integrativa da literatura por meio das bases de dados BIREME, PUBMED, COCHRANE, SCIELO e literatura cinzenta, usando como estratégia de busca o cruzamento dos seguintes descritores, nos idiomas português e inglês: leishmaniose cutânea, eletrocardiografia, meglumina e toxicidade. Não foi estipulado um intervalo temporal para que um maior número de publicações fosse obtido. Resultados: foram encontrados 134 artigos, desses apenas 09 atenderam aos critérios de inclusão. As principais alterações eletrocardiográficas encontradas durante a terapêutica foram as alterações de repolarização ventricular, com destaque para o prolongamento do intervalo QT corrigido pela frequência cardíaca. Já entre as alterações mais graves em termos de morbimortalidade, destacam-se as arritmias ventriculares complexas, principalmente a Torsade de pointes. Discussão: em todos os artigos selecionados foram encontradas alterações ao eletrocardiograma (ECG) durante o tratamento com AM, sendo recomendado em todos os pacientes, o acompanhamento eletrocardiográfico. Apenas um estudo excluiu as alterações do ECG basal, presença de comorbidades e uso de drogas cardiotóxicas sendo esses possíveis vieses para avaliação da toxicidade cardíaca diretamente provocada pelo antimonial. Conclusão: considerando as alterações na repolarização ventricular e as possíveis arritmias ventriculares em pacientes em tratamento para LTA em uso de AM, o acompanhamento eletrocardiográfico é recomendado durante a terapêutica de todos esses pacientes, sendo útil para prevenção de complicações cardiovasculares importantes.

Introduction: American Tegumentary Leishmaniasis (ATL) is a zoonotic infection whose treatment is carried out with the meglumine antimoniate drug (AM). Objective: To report the electrocardiographic changes resulting from the use of AM in patients with ATL. Methodology: an integrative literature review was carried out using the BIREME, PUBMED, COCHRANE, SCIELO and gray literature databases, using as a search strategy the crossing of the following descriptors, in Portuguese and English: cutaneous leishmaniasis, electrocardiography, meglumine and toxicity. A time interval was not stipulated in order to obtain a greater number of publications. Results: we found 134 articles, of which only 9 met the inclusion criteria. The main electrocardiographic changes found during therapy were changes in ventricular repolarization, with emphasis on the prolongation of the QT interval corrected by heart rate. Already the most serious changes in terms of morbidity and mortality, complex ventricular arrhythmias, especially Torsade de pointes, stand out. Discussion: changes in the electrocardiogram (ECG) were found in all selected articles during treatment with AM, with electrocardiographic monitoring being recommended in all patients. Only one study excluded: changes in the baseline ECG, the presence of comorbidities and / or use of cardiotoxic drugs, these being possible biases to assess cardiac toxicity directly caused by the antimonial. Conclusion: considering the changes in ventricular repolarization and possible ventricular arrhythmias in patients undergoing treatment for ATL using AM, electrocardiographic monitoring is recommended during the therapy of all these patients, being useful for the prevention of important cardiovascular complications.

Microcirculation improvement after short-term infusion of vasopressin in septic shock is dependent on noradrenaline

OBJECTIVES: To assess the impact of vasopressin on the microcirculation and to develop a predictive model to estimate the probability of microcirculatory recruitment in patients with septic shock. METHODS: This prospective interventional study included patients with septic shock receiving noradrenaline for less than 48 hours. We infused vasopressin at 0.04 U/min for one hour. Hemodynamic measurements, including sidestream dark-field imaging, were obtained immediately before vasopressin infusion, 1 hour after vasopressin infusion and 1 hour after vasopressin withdrawal. We defined patients with more than a 10% increase in total vascular density and perfused vascular density as responders. ClinicalTrials.gov: NCT02053675. RESULTS: Eighteen patients were included, and nine (50%) showed improved microcirculation after infusion of vasopressin. The noradrenaline dose was significantly reduced after vasopressin (p=0.001) and was higher both at baseline and during vasopressin infusion in the responders than in the non-responders. The strongest predictor for a favorable microcirculatory response was the dose of noradrenaline at baseline (OR=4.5; 95% CI: 1.2-17.0; p=0.027). For patients using a noradrenaline dose higher than 0.38 mcg/kg/min, the probability that microcirculatory perfusion would be improved with vasopressin was 53% (sensitivity 78%, specificity 77%). CONCLUSIONS: In patients with septic shock for no longer than 48 h, administration of vasopressin is likely to result in an improvement in microcirculation when the baseline noradrenaline dose is higher than 0.38 mcg/kg/min.

Microcirculation improvement after short-term infusion of vasopressin in septic shock is dependent on noradrenaline.

OBJECTIVES: To assess the impact of vasopressin on the microcirculation and to develop a predictive model to estimate the probability of microcirculatory recruitment in patients with septic shock. METHODS: This prospective interventional study included patients with septic shock receiving noradrenaline for less than 48 hours. We infused vasopressin at 0.04 U/min for one hour. Hemodynamic measurements, including sidestream dark-field imaging, were obtained immediately before vasopressin infusion, 1 hour after vasopressin infusion and 1 hour after vasopressin withdrawal. We defined patients with more than a 10% increase in total vascular density and perfused vascular density as responders. ClinicalTrials.gov: NCT02053675. RESULTS: Eighteen patients were included, and nine (50%) showed improved microcirculation after infusion of vasopressin. The noradrenaline dose was significantly reduced after vasopressin (p=0.001) and was higher both at baseline and during vasopressin infusion in the responders than in the non-responders. The strongest predictor for a favorable microcirculatory response was the dose of noradrenaline at baseline (OR=4.5; 95% CI: 1.2-17.0; p=0.027). For patients using a noradrenaline dose higher than 0.38 mcg/kg/min, the probability that microcirculatory perfusion would be improved with vasopressin was 53% (sensitivity 78%, specificity 77%). CONCLUSIONS: In patients with septic shock for no longer than 48 h, administration of vasopressin is likely to result in an improvement in microcirculation when the baseline noradrenaline dose is higher than 0.38 mcg/kg/min.

Comparison between respiratory changes in the inferior vena cava diameter and pulse pressure variation to predict fluid responsiveness in postoperative patients.

PURPOSE: The objective of our study was to assess the reliability of the distensibility index of the inferior vena cava (dIVC) as a predictor of fluid responsiveness in postoperative, mechanically ventilated patients and compare its accuracy with that of the pulse pressure variation (PPV) measurement. MATERIALS AND METHODS: We included postoperative mechanically ventilated and sedated patients who underwent volume expansion with 500mL of crystalloids over 15minutes. A response to fluid infusion was defined as a 15% increase in the left ventricular outflow tract velocity time integral according to transthoracic echocardiography. The inferior vena cava diameters were recorded by a subcostal view using the M-mode and the PPV by automatic calculation. The receiver operating characteristic (ROC) curves were generated for the baseline dIVC and PPV. RESULTS: Twenty patients were included. The area under the ROC curve for dIVC was 0.84 (95% confidence interval, 0.63-1.0), and the best cutoff value was 16% (sensitivity, 67%; specificity, 100%). The area under the ROC curve for PPV was 0.92 (95% confidence interval, 0.76-1.0), and the best cutoff was 12.4% (sensitivity, 89%; specificity, 100%). A noninferiority test showed that dIVC cannot replace PPV to predict fluid responsiveness (P=.28). CONCLUSION: The individual PPV discriminative properties for predicting fluid responsiveness in postoperative patients seemed superior to those of dIVC.

Duration of hemodynamic effects of crystalloids in patients with circulatory shock after initial resuscitation.

BACKGROUND: In the later stages of circulatory shock, monitoring should help to avoid fluid overload. In this setting, volume expansion is ideally indicated only for patients in whom the cardiac index (CI) is expected to increase. Crystalloids are usually the choice for fluid replacement. As previous studies evaluating the hemodynamic effect of crystalloids have not distinguished responders from non-responders, the present study was designed to evaluate the duration of the hemodynamic effects of crystalloids according to the fluid responsiveness status. METHODS: This is a prospective observational study conducted after the initial resuscitation phase of circulatory shock (>6 h vasopressor use). Critically ill, sedated adult patients monitored with a pulmonary artery catheter who received a fluid challenge with crystalloids (500 mL infused over 30 min) were included. Hemodynamic variables were measured at baseline (T0) and at 30 min (T1), 60 min (T2), and 90 min (T3) after a fluid bolus, totaling 90 min of observation. The patients were analyzed according to their fluid responsiveness status (responders with CI increase >15% and non-responders ≤15% at T1). The data were analyzed by repeated measures of analysis of variance. RESULTS: Twenty patients were included, 14 of whom had septic shock. Overall, volume expansion significantly increased the CI: 3.03 ± 0.64 L/min/m(2) to 3.58 ± 0.66 L/min/m(2) (p < 0.05). From this period, there was a progressive decrease: 3.23 ± 0.65 L/min/m(2) (p < 0.05, T2 versus T1) and 3.12 ± 0.64 L/min/m(2) (p < 0.05, period T3 versus T1). Similar behavior was observed in responders (13 patients), 2.84 ± 0.61 L/min/m(2) to 3.57 ± 0.65 L/min/m(2) (p < 0.05) with volume expansion, followed by a decrease, 3.19 ± 0.69 L/min/m(2) (p < 0.05, T2 versus T1) and 3.06 ± 0.70 L/min/m(2) (p < 0.05, T3 versus T1). Blood pressure and cardiac filling pressures also decreased significantly after T1 with similar findings in both responders and non-responders. CONCLUSIONS: The results suggest that volume expansion with crystalloids in patients with circulatory shock after the initial resuscitation has limited success, even in responders.

Diabetes subdiagnosticado e necrose miocárdica: preditores de hiperglicemia no infarto do miocárdio / Unrecognized diabetes and myocardial necrosis: predictors of hyperglycemia in myocardial infarction

FUNDAMENTO: Hiperglicemia na fase aguda do infarto do miocárdio é importante fator prognóstico. Entretanto, sua fisiopatologia não está completamente elucidada. OBJETIVO: Analisar simultaneamente correlação entre hiperglicemia e marcadores bioquímicos relacionados ao estresse,metabolismo glicídico e lipídico, coagulação, inflamação e necrose miocárdica. MÉTODOS: Oitenta pacientes com infarto agudo do miocárdio foram incluídos prospectivamente. Os parâmetros analisados foram: glicose, hormônios do estresse (cortisol e norepinefrina), fatores do metabolismo glicídico [hemoglobina glicada (HbA1c), insulina], lipoproteínas (colesterol total, LDL, HDL, LDL eletronegativa minimamente modificada e adiponectina), glicerídeos (triglicérides, VLDL e ácido graxo), fatores da coagulação (fator VII, fibrinogênio,inibidor do ativador do plasminogênio-1), inflamação (proteína C reativa ultrassensível) e necrose miocárdica (CK-MB e troponina). Variáveis contínuas foram convertidas em graus de pertinência por intermédio de lógica fuzzy. RESULTADOS: Houve correlação significativa entre hiperglicemia e metabolismo glicídico (p < 0,001), lipoproteínas (p = 0,03) e fatores de necrose (p = 0,03). Na análise multivariada, somente metabolismo glicídico (OR = 4,3; IC = 2,1-68,9 e p < 0,001) e necrose miocárdica (OR = 22,5; IC = 2-253 e p = 0,012) mantiveram correlação independente e significativa.Para análise da influência da história de diabetes mellitus , modelo de regressão, incluindo somente pacientes sem diabetes mellitus foi desenvolvido, e os resultados não alteraram. Finalmente, no modelo ajustado para idade, sexo e variáveis clínicas(história de diabetes mellitus, hipertensão arterial e dislipidemia), três variáveis mantiveram associação significativa e independente com hiperglicemia: metabolismo glicídico (OR = 24,1; IC = 4,8-122,1 e p < 0,001) necrose miocárdica (OR = 21,9; IC = 1,3-360,9 e p = 0,03) e história de DM (OR = 27, IC = 3,7-195,7 e p = 0,001). CONCLUSÃO: Marcadores do metabolismo glicídico e necrose miocárdica foram os melhores preditores de hiperglicemia em pacientes com infarto agudo do miocárdio.

BACKGROUND: Hyperglycemia in the acute phase of myocardial infarction is an important prognostic factor. However, its pathophysiology is not fully understood. OBJECTIVE: To analyze simultaneously the correlation between hyperglycemia and biochemical markers related to stress, glucose and lipid metabolism, coagulation, inflammation, and myocardial necrosis. METHODS Eighty patients with acute myocardial infarction were prospectively included. The following parameters were analyzed: blood glucose; stress hormones (cortisol and norepinephrine); glucose metabolism factors [glycated hemoglobin (HbA1c); insulin]; lipoproteins (total cholesterol, LDL, HDL, minimally modified electronegative LDL, and adiponectin); glycerides (triglycerides, VLDL and fatty acids); coagulation factors (factor VII, fibrinogen, plasminogen activator inhibitor-1); inflammation (high-sensitivity C reactive protein); and myocardial necrosis (CK-MB and troponin). Continuous variables were converted into degrees of relevance using fuzzy logic. RESULTS: Significant correlation was observed between hyperglycemia and glucose metabolism (p < 0.001), lipoproteins (p = 0.03), and necrosis factors (p = 0.03). In the multivariate analysis, only glucose metabolism (OR = 4.3; CI = 2.1-68.9; and p < 0.001) and myocardial necrosis (OR = 22.5; CI = 2-253; and p = 0.012) showed independent and significant correlation. For the analysis of the influence of history of diabetes mellitus, a regression model including only patients without diabetes mellitus was developed, and the results did not change. Finally, in the model adjusted for age, gender, and clinical variables (history of diabetes mellitus, hypertension and dyslipidemia), three variables maintained a significant and independent association with hyperglycemia: glucose metabolism (OR = 24.1; CI = 4.8-122.1; and p < 0.001), myocardial necrosis (OR = 21.9; CI = 1.3-360.9; and p = 0.03), and history of DM (OR = 27; CI = 3.7-195.7; and p = 0.001). CONCLUSION: Glucose metabolism and myocardial necrosis markers were the best predictors of hyperglycemia in patients with acute myocardial infarction.

Unrecognized diabetes and myocardial necrosis: predictors of hyperglycemia in myocardial infarction.

BACKGROUND: Hyperglycemia in the acute phase of myocardial infarction is an important prognostic factor. However, its pathophysiology is not fully understood. OBJECTIVE: To analyze simultaneously the correlation between hyperglycemia and biochemical markers related to stress, glucose and lipid metabolism, coagulation, inflammation, and myocardial necrosis. METHODS Eighty patients with acute myocardial infarction were prospectively included. The following parameters were analyzed: blood glucose; stress hormones (cortisol and norepinephrine); glucose metabolism factors [glycated hemoglobin (HbA1c); insulin]; lipoproteins (total cholesterol, LDL, HDL, minimally modified electronegative LDL, and adiponectin); glycerides (triglycerides, VLDL and fatty acids); coagulation factors (factor VII, fibrinogen, plasminogen activator inhibitor-1); inflammation (high-sensitivity C reactive protein); and myocardial necrosis (CK-MB and troponin). Continuous variables were converted into degrees of relevance using fuzzy logic. RESULTS: Significant correlation was observed between hyperglycemia and glucose metabolism (p < 0.001), lipoproteins (p = 0.03), and necrosis factors (p = 0.03). In the multivariate analysis, only glucose metabolism (OR = 4.3; CI = 2.1-68.9; and p < 0.001) and myocardial necrosis (OR = 22.5; CI = 2-253; and p = 0.012) showed independent and significant correlation. For the analysis of the influence of history of diabetes mellitus, a regression model including only patients without diabetes mellitus was developed, and the results did not change. Finally, in the model adjusted for age, gender, and clinical variables (history of diabetes mellitus, hypertension and dyslipidemia), three variables maintained a significant and independent association with hyperglycemia: glucose metabolism (OR = 24.1; CI = 4.8-122.1; and p < 0.001), myocardial necrosis (OR = 21.9; CI = 1.3-360.9; and p = 0.03), and history of DM (OR = 27; CI = 3.7-195.7; and p = 0.001). CONCLUSION: Glucose metabolism and myocardial necrosis markers were the best predictors of hyperglycemia in patients with acute myocardial infarction.

Diabetes mellitus e intolerância à glicose são subdiagnosticados nas unidades de terapia intensiva / Diabetes mellitus and impaired glucose tolerance are underdiagnosed in intensive care units

OBJETIVO: Avaliar a presença de diabetes mellitus e a intolerância à glicose em pacientes internados em unidades de terapia intensiva. MÉTODOS: Foram incluídos pacientes clínicos, em pós-operatório de cirurgias eletivas e de urgência, e excluídos aqueles com história de diabetes mellitus. Para o diagnóstico de alterações prévias da glicemia, utilizou-se a dosagem da hemoglobina glicada (HbA1c) na admissão do paciente, sendo classificado em normal (<5,7%), intolerante à glicose (5,7-6,4%) ou diabético (>6,4%). Durante os 3 primeiros dias da internação, foram avaliados o controle glicêmico e as complicações clínicas. A evolução para óbito foi acompanhada por 28 dias. Para as análises estatísticas, utilizaram-se testes do qui-quadrado, ANOVA, teste t de Student, Kruskall-Wallis ou Mann Whitney. RESULTADOS: Foram incluídos 30 pacientes, 53% do gênero feminino, idade de 53,4±19,7 anos e APACHE II de 13,6±6,6. A maioria dos pacientes foi admitida por sepse grave ou choque séptico, seguido por pós-operatório de cirurgias eletivas, oncológicas, politraumatismo e cirurgia de urgência. Ao classificar esses pacientes segundo a HbA1c, apesar da ausência prévia de história de diabetes mellitus, apenas 13,3% tinham HbA1c normal, 23,3% tinham níveis compatíveis com o diagnóstico de diabetes mellitus e 63,3% eram compatíveis com intolerância à glicose. Houve associação significativa entre o diagnóstico de diabetes mellitus ou intolerância a glicose e o uso de droga vasoativa (p=0,04). CONCLUSÃO: Foi encontrada alta prevalência de diabetes mellitus e intolerância à glicose, sem diagnóstico prévio, em pacientes internados em uma unidade de terapia intensiva geral.

OBJECTIVE: To evaluate the presence of diabetes mellitus and impaired glucose tolerance in intensive care unit inpatients. METHODS: The study included patients in post-surgical care for elective and emergency surgery and excluded those patients with known diabetes mellitus. To diagnose prior serum glucose level disorders, we considered the value of glycated hemoglobin (HbA1c) at the time of admission, classifying the patients as normal (<5.7%), glucose intolerant (5.7-6.4%) or diabetic (>6.4%). During the first 3 days of the patient's hospital stay, glycemic control and clinical complications were assessed. Mortality was monitored for 28 days. For the statistical analyses, chi-square, ANOVA, student's t, Kruskal-Wallis or Mann Whitney tests were used. RESULTS: Thirty patients were included in the present study, 53% of whom were women; the patients had a mean age of 53.4±19.7 years and an APACHE II score of 13.6±6.6. The majority of patients were admitted for severe sepsis or septic shock followed by post-operative care for elective surgery, oncological surgery, multiple traumas and emergency surgery. When classifying these patients according to HbA1c, despite the absence of a prior history of diabetes mellitus, only 13.3% had a normal HbA1c level, 23.3% had levels compatible with the diagnosis of diabetes mellitus and 63.3% had levels compatible with impaired glucose tolerance. We found a significant association between the diagnosis of diabetes mellitus or impaired glucose tolerance and the use of vasoactive drugs (p=0.04). CONCLUSION: A high prevalence of undiagnosed diabetes mellitus and impaired glucose tolerance was observed in inpatients at a general intensive care unit.

Diabetes mellitus and impaired glucose tolerance are underdiagnosed in intensive care units.

OBJECTIVE: To evaluate the presence of diabetes mellitus and impaired glucose tolerance in intensive care unit inpatients. METHODS: The study included patients in post-surgical care for elective and emergency surgery and excluded those patients with known diabetes mellitus. To diagnose prior serum glucose level disorders, we considered the value of glycated hemoglobin (HbA1c) at the time of admission, classifying the patients as normal (<5.7%), glucose intolerant (5.7-6.4%) or diabetic (>6.4%). During the first 3 days of the patient's hospital stay, glycemic control and clinical complications were assessed. Mortality was monitored for 28 days. For the statistical analyses, chi-square, ANOVA, student's t, Kruskal-Wallis or Mann Whitney tests were used. RESULTS: Thirty patients were included in the present study, 53% of whom were women; the patients had a mean age of 53.4±19.7 years and an APACHE II score of 13.6±6.6. The majority of patients were admitted for severe sepsis or septic shock followed by post-operative care for elective surgery, oncological surgery, multiple traumas and emergency surgery. When classifying these patients according to HbA1c, despite the absence of a prior history of diabetes mellitus, only 13.3% had a normal HbA1c level, 23.3% had levels compatible with the diagnosis of diabetes mellitus and 63.3% had levels compatible with impaired glucose tolerance. We found a significant association between the diagnosis of diabetes mellitus or impaired glucose tolerance and the use of vasoactive drugs (p=0.04). CONCLUSION: A high prevalence of undiagnosed diabetes mellitus and impaired glucose tolerance was observed in inpatients at a general intensive care unit.

Effect of beta-blockers on the risk of atrial fibrillation in patients with acute myocardial infarction.

INTRODUCTION: Oral beta-blockers improve the prognosis of patients with acute myocardial infarction, while atrial fibrillation worsens the prognosis of this population. The reduction of atrial fibrillation incidence in patients treated with beta-blockers could at least in part explain the benefits of this drug. OBJECTIVE: To investigate the effect of beta-blockers on the incidence of atrial fibrillation in patients with acute myocardial infarction. METHODS: We analyzed 1401 patients with acute myocardial infarction and evaluated the occurrence or absence of atrial fibrillation, the use of oral beta-blockers and mortality during the first 24 hours. RESULTS: a) The use of beta-blockers was inversely correlated with the presence of atrial fibrillation (rho = 0.004; OR = 0.54). b) Correlations with mortality were as follows: 31.5% in patients with atrial fibrillation, 9.2% in those without atrial fibrillation (rho < 0.001; Odds Ratio = 4.52), and 17.5% in patients not treated with beta-blockers and 6.7% in those who received the drug (rho < 0.001; OR = 0.34). c) Adjusted Models: The presence of atrial fibrillation was independently correlated with mortality (OR = 2.48, rho = 0.002). The use of beta-blockers was inversely and independently correlated with mortality (OR = 0.53; rho = 0.002). The patients who used beta-blockers showed a lower risk of atrial fibrillation (OR = 0.59; rho = 0.029) in the adjusted model. CONCLUSION: The presence of atrial fibrillation and the absence of oral beta-blockers increased in-hospital mortality in patients with acute myocardial infarction. Oral beta-blockers reduced the incidence of atrial fibrillation, which might be at least partially responsible for the drug's benefit.

Effect of â-blockers on the risk of atrial fibrillation in patients with acute myocardial infarction

INTRODUCTION: Oral â-blockers improve the prognosis of patients with acute myocardial infarction, while atrial fibrillation worsens the prognosis of this population. The reduction of atrial fibrillation incidence in patients treated with â-blockers could at least in part explain the benefits of this drug. OBJECTIVE: To investigate the effect of â-blockers on the incidence of atrial fibrillation in patients with acute myocardial infarction. METHODS: We analyzed 1401 patients with acute myocardial infarction and evaluated the occurrence or absence of atrial fibrillation, the use of oral â-blockers and mortality during the first 24 hours. RESULTS: a) The use of â-blockers was inversely correlated with the presence of atrial fibrillation (ñ = 0.004; OR = 0.54). b) Correlations with mortality were as follows: 31.5 percent in patients with atrial fibrillation, 9.2 percent in those without atrial fibrillation (ñ < 0.001; Odds Ratio = 4.52), and 17.5 percent in patients not treated with â-blockers and 6.7 percent in those who received the drug (ñ < 0.001; OR = 0.34). c) Adjusted Models: The presence of atrial fibrillation was independently correlated with mortality (OR = 2.48, ñ = 0.002). The use of â-blockers was inversely and independently correlated with mortality (OR = 0.53; ñ = 0.002). The patients who used â-blockers showed a lower risk of atrial fibrillation (OR = 0.59; ñ = 0.029) in the adjusted model. CONCLUSION: The presence of atrial fibrillation and the absence of oral â-blockers increased in-hospital mortality in patients with acute myocardial infarction. Oral â-blockers reduced the incidence of atrial fibrillation, which might be at least partially responsible for the drug's benefit.

Hiperglicemia no infarto agudo do miocárdio: correlações fisiopatológicas / Hyperglycemia during acute myocardial infarction: pathophysiology correlations

Introdução- A hiperglicemia (HG), durante o infarto agudo do miocárdio (IAM), está associada com aumento de mortalidade hospitalar em pacientes diabéticos e não diabéticos. Entretanto, não é conhecido o mecanismo responsável por esta associação. Assim estudou-se, simultaneamente, a correlação entre a glicemia e marcadores bioquímicos relacionados ao sistema neuro-humoral de estresse, metabolismo glicídico e lipídico, sistema de coagulação e inflamatório. Métodos- 80 pacientes foram incluídos consecutiva e prospectivamente. Foram realizadas duas coletas de sangue, a primeira com 24h a 48h do início dos sintomas do IAM (fase aguda) e a segunda após 3 meses do IAM (fase crônica), sempre com 12h de jejum. Foram analisados os seguintes parâmetros: glicose, cortisol, noradrenalina, hemoglobina glicada (HbA1c), insulina, LDL minimamente modificada eletronegativa, ácidos graxos livres (AGL), adiponectina, factor VII da coagulação, fibrinogênio, inibidor do ativação do plasminogênio tipo 1, proteína C reativa ultra-sensível (PCRus), colesterol total (c) e frações e triglicérides. Nas correlações univariadas entre glicemia e as variáveis contínuas empregou-se o teste de correlação de Pearson. As análises multivariadas foram feitas através de regressão logística (variáveis qualitativas) e modelo linear generalizado (quando as variáveis independentes incluídas foram quantitativas e nominais). Resultados- Na fase aguda, a glicemia correlacionou-se significativamente com HbA1c (r=0,75, p<0,001), insulina (r=0,25, p<0,001), AGL (r=0,3, p=0,01), adiponectina (r=-0,22, p=0,05), LDL-c (r=-0,25, p=0,03), VLDL-c (r=0,24, p=0,03) e triglicérides (r=0,27, p=0,01). No modelo multivariado, as variáveis correlacionadas de forma independente com a glicemia, na fase aguda, foram: HbA1c (p<0,001), insulina (p<0,001), e AGL (p=0,013). Para analisar uma variável de confusão, a história de diabetes mellitus (DM), incluiu-se esta variável num modelo, juntamente com as variáveis acima...

Introduction- Hyperglycemia (HG) is an important prognostic factor in acute myocardial infarction (AMI). However, the pathophysiology is poorly understood. So we proposed a simultaneous correlation between glycemia and biochemical markers of stress, glucose and lipid metabolism, coagulation and inflammation system. Methods- Eighty AMI patients were included prospectively. Blood were collected between 24h and 48h from the pain (acute phase), and 3 months post AMI (chronic phase), with 12-h fasting. These parameters were analyzed: glucose, cortisol, norepinephrine, hemoglobin glycated (HbA1c), insulin, minimally modified electronegative LDL, free fatty acids (FFA), adiponectin, factor VII coagulant, fibrinogen, plasminogen activator inhibitor-1, high sensitive C reaction protein (hsCRP), total cholesterol (c) and fractions and triglyceride. The relationships between glucose and continuous variables were assessed by Pearsons correlation coefficient (r) and multivariate analysis with linear regression. Results- At acute phase, glucose correlated significantly with HbA1c (r=0.75, p<0.001), insulin (r=0.25, p<0.001), FFA (r=0.3, p=0.01), adiponectin (r=-0.22, p=0.05), LDL-c (r=-0.25, p=0.03), VLDL-c (r=0.24, p=0.03) and triglyceride (r=0.27, p=0.01). In a multivariate model, variables correlated were: HbA1c (p<0.001), insulin (p<0.001), and FFA (p=0.013). At the chronic phase, glucose correlated significantly with cortisol (r=0.31, p=0.01), norepinephrine (r=0.54, p<0.001), HbA1c (r=0.78, p<0.001) and hsCRP (r=0.46, p<0,001). By multivariable analysis, only HbA1c (p<0.001) and norepinephrine (p<0.001) remained correlated. Conclusion- HbA1c was the main variable that correlated significantly and independently with glycemia at acute and chronic phases, suggesting that HG during AMI can represent an exacerbation of abnormal glucose metabolism previously not diagnosed.

Coronary artery bypass grafting in acute myocardial infarction. Analysis of preoperative predictors of mortality.

OBJECTIVE: To assess preoperative predictors of mortality in patients undergoing coronary artery bypass grafting (CABG) within the first 30 days of acute myocardial infarction (AMI). METHODS: Between March 1998 and July 2002, 753 AMI patients were consecutively and prospectively entered into a database, 135 (17.9%) of whom underwent isolated CABG and were enrolled in this study. The following prognostic factors were assessed by multivariate analysis: age, gender, diabetes, history of previous AMI, CABG or coronary angioplasty (PTCA), anterior infarct location, Q-wave AMI, the use of fibrinolytics, elapsed time from AMI to the procedure, and presence of complications in the preoperative period. RESULTS: Overall in-hospital mortality was 6.7%, ranging from 12.5% in patients with preoperative complications to 1.4% in those with no complications. Only history of previous angioplasty (p = 0.037) and cardiogenic shock (p = 0.002) showed a statistically significant correlation with postoperative mortality. The use of thrombolytics, on the other hand, in the initial management of AMI showed a negative correlation with mortality (p = 0.035). CONCLUSION: CABG in the acute phase of MI is associated with distinct operative mortality, depending on the patients preoperative clinical condition. Among those factors analyzed, preoperative cardiogenic shock and history of previous angioplasty were predictive of worse prognosis in this group of patients.

Cirurgia de revascularização na fase aguda do infarto do miocárdio: análise dos fatores pré-operatórios preditores de mortalidade / Coronary artery bypass grafting in acute myocardial infarction: analysis of preoperative predictors of mortality / Coronary artery bypass grafting in acute myocardial infarction: analysis of preoperative predictors of mortality

OBJETIVO: Analisar os fatores pré-operatórios preditores de mortalidade, em pacientes submetidos à RM nos primeiros 30 dias após infarto agudo do miocárdio (IAM). MÉTODOS: Entre 3/1998 e 7/2002, foram incluídos, consecutiva e prospectivamente, em um banco de dados, 753 pacientes com IAM, sendo que 135 (17,9 por cento) foram submetidos à revascularização miocárdica (RM) isolada e incluídos neste estudo. Estudaram-se os seguintes fatores prognósticos, através de análise multivariada: idade, sexo, diabete, história de IAM, RM ou angioplastia (ATC), localização do IAM, IAM Q, uso de fibrinolítico, intervalo entre o IAM e a cirurgia, presença de complicações no pré-operatório. RESULTADOS: A mortalidade hospitalar global foi de 6,7 por cento, variando de 12,5 por cento nos pacientes portadores de complicações pré-operatórias a 1,4 por cento naqueles sem complicações. Tiveram correlação estatisticamente significante com a mortalidade pós-operatória apenas história prévia de angioplastia (p=0,037) e choque cardiogênico (p=0,002). Em contrapartida, o uso de trombolítico na abordagem inicial do IAM apresentou correlação negativa com a mortalidade (p=0,035). CONCLUSÃO: A RM na fase aguda do IAM é um procedimento que apresenta mortalidade cirúrgica distinta, na dependência da condição clínica pré-operatória do paciente. Dentre os fatores analisados, a presença de choque cardiogênico pré-operatório e história de angioplastia prévia determinaram pior prognóstico neste grupo de pacientes.

OBJECTIVE: To assess preoperative predictors of mortality in patients undergoing coronary artery bypass grafting (CABG) within the first 30 days of acute myocardial infarction (AMI). METHODS: Between March 1998 and July 2002, 753 AMI patients were consecutively and prospectively entered into a database, 135 (17.9 percent) of whom underwent isolated CABG and were enrolled in this study. The following prognostic factors were assessed by multivariate analysis: age, gender, diabetes, history of previous AMI, CABG or coronary angioplasty (PTCA), anterior infarct location, Q-wave AMI, the use of fibrinolytics, elapsed time from AMI to the procedure, and presence of complications in the preoperative period. RESULTS: Overall in-hospital mortality was 6.7 percent, ranging from 12.5 percent in patients with preoperative complications to 1.4 percent in those with no complications. Only history of previous angioplasty (p = 0.037) and cardiogenic shock (p = 0.002) showed a statistically significant correlation with postoperative mortality. The use of thrombolytics, on the other hand, in the initial management of AMI showed a negative correlation with mortality (p = 0.035). CONCLUSION: CABG in the acute phase of MI is associated with distinct operative mortality, depending on the patientÆs preoperative clinical condition. Among those factors analyzed, preoperative cardiogenic shock and history of previous angioplasty were predictive of worse prognosis in this group of patients.

Aneurisma de artéria pulmonar como manifestação da doença de Behçet / Pulmonary artery aneurysm as a manifestation of Behçet disease: case report and review

A doença de Behçet pode ser acompanhada de manifestações pulmonares, às vezes letais se não tratadas adequadamente. Descreve-se o caso de um homem de 53 anos com história de episódios de aftas orais e febre havia vários anos, dois quadros febris prolongados nos últimos dois anos, uveíte tratada com corticóide havia 21 meses, hemoptise havia um mês e emagrecimento de 7kg. Ao exame físico apresentava aftas orais, pseudofoliculite e turvação visual. Os estudos radiológicos evidenciaram dilatação aneurismática de artéria pulmonar. Tratado com corticóide, foi feita lobectomia inferior esquerda e o exame anatomopatológico foi compatível com arterite de artéria pulmonar. O paciente foi tratado com clorambucil por oito meses e mantém-se bem, decorridos 18 meses da cirurgia