The Prognostic Impact of Pericardial Fluid Cytology in Malignant Pericardial Effusion.

OBJECTIVE: Malignant pericardial effusion may affect almost 15 of the patients with underlying malignancies which deteriorates the prognosis. The prognostic significance of pericardial fluid cytology is under-represented in previous studies. METHODS: A total of 73 patients with symptomatic pericardial effusion treated with pericardiocentesis were included in this retrospective analysis. Macroscopic appearance, biochemical features, and cytological findings were obtained. Patients were divided into 3 groups: (i) without malignancy, (ii) with malignancy and negative cytology, and (iii) with malignancy and positive cytology. Survival data were searched via governmental death notification system. RESULTS: Mean age of the study group was 62 ± 15, and 54% (40) of the patients were female. On the cytological evaluation, 17 patients (23.3%) revealed positive cancer cytology, whereas 56 patients (76.7%) revealed negative cancer cytology. The median follow-up period was 840 days, and 34 patients (46.5%) died during follow-up. The survival rate of Group 3 was found to be significantly worse compared to Groups 1 and 2, no statistical difference was found between Groups 1 and 2 in terms of survival (Group 1 vs. Group 2 P =.078; Group 1 vs. Group 3 P <.001; Group 2 vs. Group 3 P =.041). CONCLUSION: Cytological evaluation is an important step in patients with malignant pericardial effusion. Positive pericardial fluid cytology indicates a poorer prognosis.

Effects of Smoking on Very-Long Term Mortality after First ST Elevation Myocardial Infarction. / Efeitos do Ato de Fumar na Mortalidade de Longo Prazo após Infarto do Miocárdio por Elevação de ST.

BACKGROUND: The smoking paradox has been a matter of debate for acute myocardial infarction patients for more than two decades. Although there is huge evidence claiming that is no real paradox, publications supporting better outcomes in post-MI smokers are still being released. OBJECTIVE: To explore the effect of smoking on very long-term mortality after ST Elevation myocardial infarction (STEMI). METHODS: This study included STEMI patients who were diagnosed between the years of 2004-2006 at three tertiary centers. Patients were categorized according to tobacco exposure (Group 1: non-smokers; Group 2: <20 package*years users, Group 3: 20-40 package*years users, Group 4: >40 package*years users). A Cox regression model was used to estimate the relative risks for very long-term mortality. P value <0.05 was considered as statistically significant. RESULTS: There were 313 patients (201 smokers, 112 non-smokers) who were followed-up for a median period of 174 months. Smokers were younger (54±9 vs. 62±11, p: <0.001), and the presence of cardiometabolic risk factors were more prevalent in non-smokers. A univariate analysis of the impact of the smoking habit on mortality revealed a better survival curve in Group 2 than in Group 1. However, after adjustment for confounders, it was observed that smokers had a significantly increased risk of death. The relative risk became higher with increased exposure (Group 2 vs. Group 1; HR: 1.141; 95% CI: 0.599 to 2.171, Group 3 vs Group 1; HR: 2.130; 95% CI: 1.236 to 3.670, Group 4 vs Group 1; HR: 2.602; 95% CI: 1.461 to 4.634). CONCLUSION: Smoking gradually increases the risk of all-cause mortality after STEMI.

FUNDAMENTO: O paradoxo do fumante tem sido motivo de debate para pacientes com infarto agudo do miocárdio (IM) há mais de duas décadas. Embora haja muitas evidências demonstrando que não existe tal paradoxo, publicações defendendo desfechos melhores em fumantes pós-IM ainda são lançadas. OBJETIVO: Explorar o efeito do fumo na mortalidade de longo prazo após infarto do miocárdio por elevação de ST (STEMI). MÉTODOS: Este estudo incluiu pacientes com STEMI que foram diagnosticados entre 2004 e 2006 em três centros terciários. Os pacientes foram categorizados de acordo com a exposição ao tabaco (Grupo 1: não-fumantes; Grupo 2: <20 pacotes*anos; Grupo 3: 2-040 pacotes*anos; Grupo 4: >40 pacotes*anos). Um modelo de regressão de Cox foi utilizado para estimar os riscos relativos para mortalidade de longo prazo. O valor de p <0,05 foi considerado como estatisticamente significativo. RESULTADOS: Trezentos e treze pacientes (201 fumantes e 112 não-fumantes) foram acompanhados por um período médio de 174 meses. Os fumantes eram mais novos (54±9 vs. 62±11, p: <0,001), e a presença de fatores de risco cardiometabólicos foi mais prevalente entre os não-fumantes. Uma análise univariada do impacto do hábito de fumar na mortalidade revelou uma curva de sobrevivência melhor no Grupo 2 do que no Grupo 1. Porém, após ajustes para fatores de confusão, observou-se que os fumantes tinham um risco de morte significativamente maior. O risco relativo tornou-se maior de acordo com a maior exposição (Grupo 2 vs. Grupo 1: RR: 1,141; IC95%: 0,599 a 2.171; Grupo 3 vs. Grupo 1: RR: 2,130; IC95%: 1,236 a 3,670; Grupo 4 vs. Grupo 1: RR: 2,602; IC95%: 1,461 a 4,634). CONCLUSÃO: O hábito de fumar gradualmente aumenta o risco de mortalidade por todas as causas após STEMI.

Efeitos do Ato de Fumar na Mortalidade de Longo Prazo após Infarto do Miocárdio por Elevação de ST / Effects of Smoking on Very-Long Term Mortality after First ST Elevation Myocardial Infarction

Resumo Fundamento O paradoxo do fumante tem sido motivo de debate para pacientes com infarto agudo do miocárdio (IM) há mais de duas décadas. Embora haja muitas evidências demonstrando que não existe tal paradoxo, publicações defendendo desfechos melhores em fumantes pós-IM ainda são lançadas. Objetivo Explorar o efeito do fumo na mortalidade de longo prazo após infarto do miocárdio por elevação de ST (STEMI). Métodos Este estudo incluiu pacientes com STEMI que foram diagnosticados entre 2004 e 2006 em três centros terciários. Os pacientes foram categorizados de acordo com a exposição ao tabaco (Grupo 1: não-fumantes; Grupo 2: <20 pacotes*anos; Grupo 3: 2-040 pacotes*anos; Grupo 4: >40 pacotes*anos). Um modelo de regressão de Cox foi utilizado para estimar os riscos relativos para mortalidade de longo prazo. O valor de p <0,05 foi considerado como estatisticamente significativo. Resultados Trezentos e treze pacientes (201 fumantes e 112 não-fumantes) foram acompanhados por um período médio de 174 meses. Os fumantes eram mais novos (54±9 vs. 62±11, p: <0,001), e a presença de fatores de risco cardiometabólicos foi mais prevalente entre os não-fumantes. Uma análise univariada do impacto do hábito de fumar na mortalidade revelou uma curva de sobrevivência melhor no Grupo 2 do que no Grupo 1. Porém, após ajustes para fatores de confusão, observou-se que os fumantes tinham um risco de morte significativamente maior. O risco relativo tornou-se maior de acordo com a maior exposição (Grupo 2 vs. Grupo 1: RR: 1,141; IC95%: 0,599 a 2.171; Grupo 3 vs. Grupo 1: RR: 2,130; IC95%: 1,236 a 3,670; Grupo 4 vs. Grupo 1: RR: 2,602; IC95%: 1,461 a 4,634). Conclusão O hábito de fumar gradualmente aumenta o risco de mortalidade por todas as causas após STEMI.

Abstract Background The smoking paradox has been a matter of debate for acute myocardial infarction patients for more than two decades. Although there is huge evidence claiming that is no real paradox, publications supporting better outcomes in post-MI smokers are still being released. Objective To explore the effect of smoking on very long-term mortality after ST Elevation myocardial infarction (STEMI). Methods This study included STEMI patients who were diagnosed between the years of 2004-2006 at three tertiary centers. Patients were categorized according to tobacco exposure (Group 1: non-smokers; Group 2: <20 package*years users, Group 3: 20-40 package*years users, Group 4: >40 package*years users). A Cox regression model was used to estimate the relative risks for very long-term mortality. P value <0.05 was considered as statistically significant. Results There were 313 patients (201 smokers, 112 non-smokers) who were followed-up for a median period of 174 months. Smokers were younger (54±9 vs. 62±11, p: <0.001), and the presence of cardiometabolic risk factors were more prevalent in non-smokers. A univariate analysis of the impact of the smoking habit on mortality revealed a better survival curve in Group 2 than in Group 1. However, after adjustment for confounders, it was observed that smokers had a significantly increased risk of death. The relative risk became higher with increased exposure (Group 2 vs. Group 1; HR: 1.141; 95% CI: 0.599 to 2.171, Group 3 vs Group 1; HR: 2.130; 95% CI: 1.236 to 3.670, Group 4 vs Group 1; HR: 2.602; 95% CI: 1.461 to 4.634). Conclusion Smoking gradually increases the risk of all-cause mortality after STEMI.

Neutrophil gelatinase-associated lipocalin levels in isolated coronary artery ectasia.

BACKGROUND: The pathophysiology of coronary artery ectasia (CAE) is still unknown. Inflammation and degradation of connective tissue may have a role in the development of coronary ectasia. In the present study, the authors examined neutrophil gelatinase-associated lipocalin (NGAL) levels in isolated CAE patients. METHODS: Thirty-five patients with isolated CAE (25 males; mean age, 59±10 years) and 35 age- and sex-matched healty volunteers (22 males; mean age, 57±11 years) who had been shown to have normal coronary arteries were included in the study. Basal characteristics were recorded. Serum NGAL levels were determined with an enzyme-linked immunosorbent assay kit. RESULTS: NGAL levels were significantly higher in the isolated CAE group than in the control group (65.1±13 vs 53.7±19 ng/mL; P=0.006). There were also significant difference in NGAL levels according to the number of ectatic coronary arteries (58.1±13, 70.9±9, and 71.1±11 ng/mL for 1, 2, and 3 arteries, respectively; P=0.015). Level of NGAL was lowest in patients who have only 1 ectatic coronary artery. CONCLUSION: Serum NGAL levels increased in patients with isolated CAE, and NGAL may play a crucial role in the development and/or progression of coronary artery ectasia.

Relation between serum monocyte chemoattractant protein-1 and coronary collateral development.

BACKGROUND: The degree of coronary collateral development is not same in every patient with similar degree of coronary stenosis. In animal studies monocyte chemoattractant protein-1 (MCP-1) has been found to be related to collateral vessel development. In this study we investigated whether a higher serum MCP-1 level is related to better coronary collateral vessel development in patients with stable coronary artery disease. METHOD: Eighty-three patients with stable angina pectoris, who have at least one coronary stenosis equal to or greater than 70% at coronary angiography, were prospectively enrolled. Serum MCP-1 and vascular endothelial growth factor (VEGF) levels were studied. Coronary collateral development was graded according to the Rentrop method. Patients with grade 2-3 collateral developments were included in good collateral group and formed group I. The patients with grade 0-1 collateral developments were included in poor collateral group and formed group II. RESULTS: The serum MCP-1 level was significantly higher in good collateral group (288 ± 277 pg/ml vs. 132 ± 64 pg/ml; P<0.001). There was also a positive correlation between serum MCP-1 level and Rentrop score (r=0.39, P<0.001). The patients in the good collateral group also had a significantly higher number of coronary arteries with significant stenosis (1.7 ± 0.7 vs. 1.4 ± 0.6, P=0.049), and higher VEGF levels (322 ± 147 pg/ml vs. 225 ± 161 pg/ml, P=0.007). In multivariate analysis, only serum MCP-1 level (P=0.014, odds ratio: 1.01, 95% confidence interval: 1.002-1.019) was independently related to good coronary collateral development. CONCLUSION: Higher serum MCP-1 level is related to better coronary collateral development.

Gemcitabine-induced acute coronary syndrome: a case report.

OBJECTIVES: To report a case of metastatic leiomyosarcoma, in which a patient developed chest pain accompanied by acute left bundle-branch block (LBBB) after gemcitabine infusion. CLINICAL PRESENTATION AND INTERVENTION: A 59-year-old woman admitted with bilateral pulmonary nodules had classic risk factors for coronary heart disease and coronary stenosis as demonstrated by previous coronary angiography. She was treated with gemcitabine infusion, and 30 min later she experienced severe chest pain accompanied by acute LBBB confirmed by ECG. We suspected gemcitabine-induced coronary vasospasm exacerbated by the preexisting coronary artery disease as the cause of the acute coronary syndrome. The patient was subsequently treated with antianginal therapy and percutaneous coronary intervention. Her chest pain resolved and LBBB disappeared. She was discharged 2 days later without any further cardiac events. No additional cancer therapy was given and she died 5 months later, due to disease progression. CONCLUSION: This case showed that chemotherapeutic agents must be administered with intensive cardiac monitoring especially in patients with cardiac disease and well-known risk factors to prevent the development of cardiac complications, despite an agent not being known to be 'cardiotoxic'.

Relationship between elevated levels of serum uric acid and saphenous vein graft disease.

OBJECTIVES: Several studies have shown an association between elevated serum uric acid (SUA) levels and coronary heart disease and cardiovascular mortality. We investigated the relationship between SUA levels and the patency of saphenous vein grafts (SVG) after coronary artery bypass graft (CABG) surgery. STUDY DESIGN: The study included 192 patients (152 men, 40 women) who underwent elective coronary angiography after a mean of 5.6 years following CABG surgery, which involved the use of at least one SVG. The patients were divided into two groups depending on the extent of SVG patency. Stenosis of 50% or greater within the SVG was accepted as hemodynamically significant. Serum uric acid levels were determined with the enzymatic colorimetric method. RESULTS: Ninety patients (71 men, 19 women; mean age 62+/-8 years) were found to have patent SVG. Stenotic SVGs were detected in 102 patients (81 men, 21 women; mean age 62+/-10 years). The time interval between surgery and angiography was significantly longer in the stenotic group (p<0.001). Compared to patients without SVG disease, the mean SUA level was significantly higher in patients with SVG disease (4.9+/-1.2 mg/dl vs 5.8+/-1.4 mg/dl; p=0.02). Serum uric acid levels were similar in patients having stenosis in a single vein graft or multiple vein grafts (p=0.224). In multiple regression analysis, SVG disease was independently associated with SUA (p<0.001), diabetes mellitus (p=0.028), and smoking (p=0.039). CONCLUSION: Our results show that there is a significant association between increased SUA levels and SVG disease in patients undergoing CABG, which may justify the need for early screening for hyperuricemia and antiuricemic treatment.