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BACKGROUND: Enoxaparin was superior to unfractionated heparin (UFH), regardless of fibrinolytic agent in ST-elevation myocardial infarction (STEMI) patients receiving fibrinolytic therapy in ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment - Thrombolysis in Myocardial Infarction 25) trial. OBJECTIVE: This post hoc analysis compared outcomes with streptokinase plus enoxaparin to the standard regimen of fibrin-specific lytic (FSL) plus UFH and to the newer combination of FSL plus enoxaparin. METHODS: In ExTRACT-TIMI 25, STEMI patients received either streptokinase or a FSL (alteplase, reteplase or tenecteplase) at the physician's discretion and were randomized to enoxaparin or UFH, stratified by fibrinolytic type. Thirty-day outcomes were adjusted for baseline characteristics, region, in-hospital percutaneous coronary intervention (PCI) and a propensity score for the choice of lytic. RESULTS: The primary trial endpoint of 30-day death/myocardial infarction (MI) occurred in fewer patients in the streptokinase-enoxaparin cohort (n = 2083) compared with FSL-UFH (n = 8141) [10.2% vs 12.0%, adjusted odds ratio [OR(adj)] 0.76; 95% CI 0.62, 0.93; p = 0.008]. Major bleeding was significantly increased with streptokinase-enoxaparin compared with FSL-UFH (OR(adj) 2.74; 95% CI 1.81; 4.14; p < 0.001) but intracranial haemorrhage (ICH) was similar (OR(adj) 0.90; 95% CI 0.40, 2.01; p = 0.79). Net clinical outcomes, defined as either death/MI/major bleeding or as death/MI/ICH tended to favour streptokinase-enoxaparin compared with FSL-UFH (OR(adj) 0.88; 95% CI 0.73, 1.06; p = 0.17; and OR(adj) 0.77; 95% CI 0.63, 0.93; p = 0.008, respectively). Patients receiving FSL-enoxaparin (n = 8142) and streptokinase-enoxaparin therapies experienced similar adjusted rates of the primary endpoint (OR(adj) 1.08; 95% CI 0.87, 1.32; p = 0.49) and net clinical outcomes. CONCLUSIONS: Our results suggest that fibrinolytic therapy with the combination of streptokinase and the potent anticoagulant agent enoxaparin resulted in similar adjusted outcomes compared with more costly regimens utilizing a FSL. [ABSTRACT FROM AUTHOR]

Objective: To assess the impact of hyperglycemia in different age-groups of patients with acute myocardial infarction (AMI).Research Design and Methods: A total of 2,027 patients with AMI were categorized into one of five age-groups: <50 years (n = 301), ≥50 and <60 (n = 477), ≥60 and <70 (n = 545), ≥70 and <80 (n = 495), and ≥80 years (n = 209). Hyperglycemia was defined as initial glucose ≥115 mg/dL.Results: The adjusted odds ratios for hyperglycemia predicting hospital mortality in groups 1-5 were, respectively, 7.57 (P = 0.004), 3.21 (P = 0.046), 3.50 (P = 0.003), 3.20 (P < 0.001), and 2.16 (P = 0.021). The adjusted P values for correlation between glucose level (as a continuous variable) and mortality were 0.007, <0.001, 0.043, <0.001, and 0.064. The areas under the ROC curves (AUCs) were 0.785, 0.709, 0.657, 0.648, and 0.613. The AUC in group 1 was significantly higher than those in groups 3-5.Conclusions: The impact of hyperglycemia as a risk factor for hospital mortality in AMI is more pronounced in younger patients. [ABSTRACT FROM AUTHOR]

High-density lipoprotein (HDL) is associated with decreased incidence of cardiovascular events, and its functionality also influences prognosis. Exercise is an important tool to improve prognosis in the post-infarction (MI) population, but the role of exercise on HDL functionality is poorly understood. Sixty-two patients with acute MI were randomized in a supervised exercise program for 12-14 weeks (exercise group-EG) or a control group (CG). The main objective of the study was to analyze the role of exercise on esterified cholesterol (EC) and unesterified cholesterol (UC) transfer to HDL. For the total population, the baseline mean rate of EC transfer to HDL was 2.53 ± 0.83 and at the end of follow-up, it was 2.74 ± 0.64 ( p = 0.03). The figures for UC were, respectively, 4.08 ± 1.2 and 4.4 ± 1.06 ( p = 0.02). The difference (follow-up minus baseline) for EC was 0.15 ± 0.84 for the control group and 0.27 ± 0.69 for the exercise group ( p = 0.53); for UC, the figures were 0.28 ± 1.14 and 0.35 ± 0.96 ( p = 0.80), respectively, for the control and exercise groups. In post-MI patients, 12-14 weeks of supervised exercise did not improve HDL functionality.

Aims: Cardiogenic shock (CS) and cardiac arrest (CA) are serious complications in ST-elevation myocardial infarction (STEMI) patients, with lack of long-term data according to their timing of occurrence. This study sought to determine the incidence and relationship between the timing of occurrence and prognostic impact of CS and CA complicating STEMI in the long-term follow-up., Methods and Results: We conducted a retrospective analysis of consecutive STEMI patients treated between 2004 and 2017. Patients were divided into four groups based on the occurrence of neither CA nor CS, CA only, CS only, and both CA and CS (CA-CS-, CA+, CS+, and CA+CS+, respectively). Adjusted Cox regression analysis was used to assess the independent association between the CS and CA categories and mortality. A total of 1603 STEMI patients were followed for a median of 3.6 years. CA and CS occurred in the 12.2% and 15.9% of patients, and both impacted long-term mortality [adjusted hazard ratio (HR) = 2.59, 95% confidence interval (CI): 1.53-4.41, P < 0.001; HR = 3.16, 95% CI: 2.21-4.53, P < 0.001, respectively). CA+CS+ occurred in 7.3%, with the strongest association with higher mortality (adjusted HR = 5.36; 95% CI: 3.80-7.55, P < 0.001). Using flexible parametric models with B-splines, the increased mortality was restricted to the first ∼10 months. In addition, overall mortality rates were higher at all timings (all with P < 0.001), except for CA during initial cardiac catheterization ( P < 0.183)., Conclusion: CS and CA complicating patients presenting with STEMI were associated with higher long-term mortality rate, especially in the first 10 months. Both CS+ and CA+ at any timeframe impacted outcomes, except for CA+ during the initial cardiac catheterization, although this will have to be confirmed in larger future studies, given the relatively small number of patients., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Introdution: COVID-19 is associated with an increased risk of thrombotic events. However, the contribution of platelet reactivity (PR) to the aetiology of the increased thrombotic risk associated with COVID-19 remains unclear. Our aim was to evaluate PR in stable patients diagnosed with COVID-19 and hospitalized with respiratory symptoms (mainly dyspnoea and dry cough), in comparison with a control group comprised of non-hospitalized healthy controls., Methods: Observational, case control study that included patients with confirmed COVID-19 (COVID-19 group, n = 60) and healthy individuals matched by age and sex (control group, n = 60). Multiplate electrode aggregometry (MEA) tests were used to assess PR with adenosine diphosphate (MEA-ADP, low PR defined as < 53 AUC), arachidonic acid (MEA-ASPI, low PR < 86 AUC) and thrombin receptor-activating peptide 6 (MEA-TRAP, low PR < 97 AUC) in both groups., Results: The rates of low PR with MEA-ADP were 27.5% in the COVID-19 group and 21.7% in the control group (OR = 1.60, p = 0.20); with MEA-ASPI, the rates were, respectively, 37.5% and 22.5% (OR = 3.67, p < 0.001); and with MEA-TRAP, the incidences were 48.5% and 18.8%, respectively (OR = 9.58, p < 0.001). Levels of D-dimer, fibrinogen, and plasminogen activator inhibitor 1 (PAI-1) were higher in the COVID-19 group in comparison with the control group (all p < 0.05). Thromboelastometry was utilized in a subgroup of patients and showed a hypercoagulable state in the COVID-19 group., Conclusion: Patients hospitalized with non-severe COVID-19 had lower PR compared to healthy controls, despite having higher levels of D-dimer, fibrinogen, and PAI-1, and hypercoagulability by thromboelastometry., Trial Registration: ClinicalTrials.gov identifier, NCT04447131., (© 2021. The Author(s), under exclusive licence to Springer Healthcare Ltd., part of Springer Nature.)

Objectives: Returning to work after an episode of acute coronary syndrome (ACS) is challenging for many patients, and has both personal and social impacts. There are limited data regarding the working status in the very long-term after ACS., Methods: We retrospectively analyzed 1,632 patients who were working prior to hospitalization for ACS in a quaternary hospital and were followed-up for up to 17 years. Adjusted models were developed to analyze the variables independently associated with actively working at the last contact, and a prognostic predictive index for not working at follow-up was developed., Results: The following variables were significantly and independently associated with actively working at the last contact: age>median (hazard-ratio [HR], 0.76, p<0.001); male sex (HR, 1.52, p<0.001); government health insurance (HR, 1.36, p<0.001); history of angina (HR, 0.69, p<0.001) or myocardial infarction (MI) (HR, 0.76, p=0.005); smoking (HR, 0.81, p=0.015); ST-elevation MI (HR, 0.81, p=0.021); anterior-wall MI (HR, 0.75, p=0.001); non-primary percutaneous coronary intervention (PCI) (HR, 0.77, p=0.002); fibrinolysis (HR, 0.61, p<0.001); cardiogenic shock (HR, 0.60, p=0.023); statin (HR, 3.01, p<0.001), beta-blocker (HR, 1.26, p=0.020), angiotensin-converting enzyme (ACE) inhibitor/angiotensin II receptor blocker (ARB) (HR, 1.37, p=0.001) at hospital discharge; and MI at follow-up (HR, 0.72, p=0.001). The probability of not working at the last contact ranged from 24.2% for patients with no variables, up to 80% for patients with six or more variables., Conclusions: In patients discharged after ACS, prior and in-hospital clinical variables, as well as the quality of care at discharge, have a great impact on the long-term probability of actively working.

Background: Previous evidence suggests that acute treatment with statins reduce atherosclerotic complications, including periprocedural myocardial infarction, but currently, there are no large, adequately powered studies to define the effects of early, high-dose statins in patients with acute coronary syndrome (ACS) and planned invasive management., Objectives: The main goal of Statins Evaluation in Coronary procedUres and REvascularization (SECURE-PCI) Trial is to determine whether the early use of a loading dose of 80 mg of atorvastatin before an intended percutaneous coronary intervention followed by an additional dose of 80 mg 24 hours after the procedure will be able to reduce the rates of major cardiovascular events at 30 days in patients with an ACS., Design: The SECURE-PCI study is a pragmatic, multicenter, double-blind, placebo-controlled randomized trial planned to enroll around 4,200 patients in 58 different sites in Brazil. The primary outcome is the rate of major cardiovascular events at 30 days defined as a composite of all-cause mortality, nonfatal acute myocardial infarction, nonfatal stroke, and coronary revascularization., Summary: The SECURE PCI is a large randomized trial testing a strategy of early, high-dose statin in patients with ACS and will provide important information about the acute treatment of this patient population., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Data from over 4 decades have reported a higher incidence of silent infarction among patients with diabetes mellitus (DM), but recent publications have shown conflicting results regarding the correlation between DM and presence of pain in patients with acute coronary syndromes (ACS)., Objective: Our primary objective was to analyze the association between DM and precordial pain at hospital arrival. Secondary analyses evaluated the association between hyperglycemia and precordial pain at presentation, and the subgroup of patients presenting within 6 hours of symptom onset., Methods: We analyzed a prospectively designed registry of 3,544 patients with ACS admitted to a Coronary Care Unit of a tertiary hospital. We developed multivariable models to adjust for potential confounders., Results: Patients with precordial pain were less likely to have DM (30.3%) than those without pain (34.0%; unadjusted p = 0.029), but this difference was not significant after multivariable adjustment, for the global population (p = 0.84), and for subset of patients that presented within 6 hours from symptom onset (p = 0.51). In contrast, precordial pain was more likely among patients with hyperglycemia (41.2% vs 37.0% without hyperglycemia, p = 0.035) in the overall population and also among those who presented within 6 hours (41.6% vs. 32.3%, p = 0.001). Adjusted models showed an independent association between hyperglycemia and pain at presentation, especially among patients who presented within 6 hours (OR = 1.41, p = 0.008)., Conclusion: In this non-selected ACS population, there was no correlation between DM and hospital presentation without precordial pain. Moreover, hyperglycemia correlated significantly with pain at presentation, especially in the population that arrived within 6 hours from symptom onset.

Background: It is well known that the occurrence of bleeding increases in-hospital mortality in patients with acute coronary syndromes (ACS), and there is a good correlation between bleeding risk scores and bleeding incidence. However, the role of bleeding risk score as mortality predictor is poorly studied., Objective: The main purpose of this paper was to analyze the role of bleeding risk score as in-hospital mortality predictor in a cohort of patients with ACS treated in a single cardiology tertiary center., Methods: Out of 1655 patients with ACS (547 with ST-elevation ACS and 1118 with non-ST-elevation ACS), we calculated the ACUITY/HORIZONS bleeding score prospectively in 249 patients and retrospectively in the remaining 1416. Mortality information and hemorrhagic complications were also obtained., Results: Among the mean age of 64.3 ± 12.6 years, the mean bleeding score was 18 ± 7.7. The correlation between bleeding and mortality was highly significant (p < 0.001, OR = 5.296), as well as the correlation between bleeding score and in-hospital bleeding (p < 0.001, OR = 1.058), and between bleeding score and in-hospital mortality (adjusted OR = 1.121, p < 0.001, area under the ROC curve 0.753, p < 0.001). The adjusted OR and area under the ROC curve for the population with ST-elevation ACS were, respectively, 1.046 (p = 0.046) and 0.686 ± 0.040 (p < 0.001); for non-ST-elevation ACS the figures were, respectively, 1.150 (p < 0.001) and 0.769 ± 0.036 (p < 0.001)., Conclusions: Bleeding risk score is a very useful and highly reliable predictor of in-hospital mortality in a wide range of patients with acute coronary syndromes, especially in those with unstable angina or non-ST-elevation acute myocardial infarction.

To discuss and share knowledge about advances in the care of patients with thrombotic disorders, the Fifth International Symposium of Thrombosis and Anticoagulation was held in Belo Horizonte, Minas Gerais, Brazil, on October 18-19, 2012. This scientific program was developed by clinicians for clinicians and was promoted by three major clinical research institutes: the Brazilian Clinical Research Institute, the Duke Clinical Research Institute of the Duke University School of Medicine, and Hospital do Coração Research Institute. Comprising 2 days of academic presentations and open discussion, the symposium had as its primary goal to educate, motivate, and inspire internists, cardiologists, hematologists, and other physicians by convening national and international visionaries, thought-leaders, and dedicated clinician-scientists. This paper summarizes the symposium proceedings.

Background: We examined the prevalence of undiagnosed diabetes or prediabetes and associations with ischemic outcomes among non-ST-segment elevation acute coronary syndrome (ACS) patients., Methods: We categorized 8795 EARLY ACS trial patients into one of the following groups: "known diabetes" (n = 2860 [32.5%]; reported on the case report form), "undiagnosed diabetes" (n = 1069 [12.2%]; no diabetes history and fasting glucose ≥126 mg/dL or hemoglobin A1c ≥6.5%), "prediabetes" (n = 947 [10.8%]; fasting glucose ≥110 to <126 mg/dL, or "normal" (n = 3919 [44.5%]). Adjusted associations of known diabetes, undiagnosed diabetes, and prediabetes (versus normal) with 30-day and 1-year outcomes were determined., Results: Undiagnosed diabetes was associated with greater 30-day death or myocardial infarction (MI) (ORadj 1.28, 95% CI 1.05-1.57), driven primarily by greater 30-day mortality (ORadj 1.65, 95% CI 1.09-2.48). Known diabetic patients had 30-day death or MI outcomes similar to those of normal patients, but 30-day mortality was higher (ORadj 1.40, 95% CI 1.01-1.93). Prediabetic patients had 30-day death or MI outcomes similar to those of normal patients. One-year mortality was greater among known diabetic patients (HRadj 1.38, 95% CI 1.13-1.67) but not among those with undiagnosed diabetes or prediabetes., Conclusions: Undiagnosed diabetes and prediabetes were common among high-risk non-ST-segment elevation ACS patients. Routine screening for undiagnosed diabetes may be useful since these patients seem to have worse short-term outcomes and deserve consideration of alternative management strategies., (Copyright © 2013 Mosby, Inc. All rights reserved.)

Introduction: Monitoring of disease activity and the best therapeutic approach are a challenge in Takayasu arteritis (TA). When associated with acute coronary syndromes (ACS), the best interventional treatment has not been established. The objective of this study was to describe the baseline characteristics, clinical manifestations, treatment and long-term outcome of patients with TA and ACS., Methods: We retrospectively analyzed eight patients between 2004 and 2010. The following data were obtained: age, gender, clinical and electrocardiographic manifestations, Killip class, risk factors for ACS, markers of myocardial necrosis (CK-MB and troponin), creatinine clearance, left ventricular ejection fraction, inflammatory markers (C-reactive protein and erythrocyte sedimentation rate [ESR]), medication during hospital stay, angiographic findings, treatment (medical, percutaneous or surgical) and long-term outcome. Statistical data were expressed as percentages and absolute values., Results: All eight patients were women, median age 49 years. Typical chest pain was present in 37.5%. Elevated ESR was observed in 85.7%. Three patients underwent coronary artery bypass grafting, three underwent percutaneous coronary angioplasty (two with bare-metal stents and one with a drug-eluting stent) and two were treated medically. In-hospital mortality was 25%. There were no deaths during a mean follow-up of 30 months., Conclusions: In our study, patients who were discharged home had good outcomes in long-term follow-up with medical, percutaneous or surgical treatment. ESR appears to be associated with ACS in TA., (Copyright © 2012 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.)

To discuss and share knowledge about advances in the care of patients with thrombotic disorders, the Fourth International Symposium of Thrombosis and Anticoagulation was held in Salvador, Bahia, Brazil, from October 20-21, 2011. This scientific program was developed by clinicians for clinicians and was promoted by three major clinical research institutes: the Brazilian Clinical Research Institute, the Duke Clinical Research Institute of the Duke University School of Medicine, and Hospital do Coração Research Institute. Comprising 2 days of academic presentations and open discussion, the symposium had as its primary goal to educate, motivate, and inspire internists, cardiologists, hematologists, and other physicians by convening national and international visionaries, thought-leaders, and dedicated clinician-scientists. This paper summarizes the symposium proceedings.

To discuss and share knowledge around advances in the care of patients with thrombotic disorders, the Third International Symposium of Thrombosis and Anticoagulation was held in São Paulo, Brazil, from October 14-16, 2010. This scientific program was developed by clinicians for clinicians, and was promoted by four major clinical research institutes: the Brazilian Clinical Research Institute, the Duke Clinical Research Institute of the Duke University School of Medicine, the Canadian VIGOUR Centre, and the Uppsala Clinical Research Center. Comprising 3 days of academic presentations and open discussion, the symposium had as its primary goal to educate, motivate, and inspire internists, cardiologists, hematologists, and other physicians by convening national and international visionaries, thought-leaders, and dedicated clinician-scientists. This paper summarizes the symposium proceedings.

Aims: To evaluate the association of bleeding with mortality in ST-elevation myocardial infarction (STEMI)., Methods and Results: We studied 20 323 patients with STEMI receiving fibrinolytic therapy and an antithrombin in ExTRACT-TIMI 25. Relationships between in-hospital bleeding, patient characteristics, treatments, and in-hospital cardiovascular complications with mortality were evaluated using Cox models. Likelihood ratios estimated each variable's model contribution. High 30-day mortality after major bleeding (n = 309, 37.6% mortality) was driven by the poor prognosis of intracranial haemorrhage (ICH; n = 143, 65.4% mortality, model contribution 7.8%). The adjusted hazard ratios (HRs) for 30-day death for any major bleeding and for ICH were 2.9 [2.4-3.6] and 10.3 [8.2-12.8], respectively. Neither non-ICH major nor minor bleeding was associated with 30-day death after adjustment. Cardiogenic shock (HR 13.5, 61% contribution) and age (HR 1.6/decade, 17% contribution) were most strongly correlated with 30-day death. Among 30-day survivors, age (HR 1.6/decade, contribution 43%) and heart rate (HR 1.2 per 10 b.p.m., contribution 18%) were most strongly associated with mortality between Days 31 and 365., Conclusion: Cardiogenic shock, age, and ICH were important independent correlates of 30-day and 1-year mortality in STEMI patients receiving fibrinolytic therapy. In-hospital non-ICH major and minor bleeding were not independently associated with increased mortality at 30 days or 1 year.

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.

Background: Hemoglobin (Hgb) and creatinine clearance (CrCl) are readily-available, routinely-obtained laboratory parameters that predict acute coronary syndrome outcomes. We sought to develop a laboratory index (LI) to predict early mortality in ST-elevation myocardial infarction (STEMI) and determine the additional risk stratification offered by adding the LI to the TIMI Risk Score (TRS) for STEMI., Methods and Results: The association between Hgb and CrCl values obtained at hospitalization and 30-day mortality was evaluated in 14,373 STEMI patients undergoing fibrinolysis in Intravenous NPA for the Treatment of Infarcting Myocardium Early II-Thrombolysis In Myocardial Infarction-17 (InTIME II-TIMI 17). Logistic regression models determined the optimal combination of laboratory variables into a LI. Prognostic utility of the LI was validated in 18,427 STEMI patients from Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment (ExTRACT)-TIMI 25. In InTIME II, Hgb levels <15.0 g/dL and CrCl <100 mL/min were significantly and independently associated with increased risk of death (OR(adj) 1.22, 95% CI 1.15-1.29 for each 1 g/dL decrease in Hgb, P < .001, and OR(adj) 1.23, 95% CI 1.17-1.29 for each 10 mL/min decrease in CrCl, P < .001, respectively). In multivariable analysis, the optimal weighting of Hgb and CrCl to form an LI to predict mortality was (15-Hgb) + (100-CrCl)/8. The LI revealed a 10-fold increase in death across prespecified groups (P < .001). The LI offered additional risk stratification across all TRS groups and improved the discriminatory ability of the TRS (c-statistic from 0.755 to 0.789, P < .001). External validation in ExTRACT showed similar enhancement of the prognostic capacity of the TRS (c-statistic from 0.747 to 0.777, P < .001)., Conclusions: The LI is a simple, powerful tool to predict death in STEMI, either separately or with the TRS.

Background: Previous studies have demonstrated that leukocytosis and hyperglycemia verified at the admission of patients with acute myocardial infarction (AMI) are associated with intrahospital mortality. However, little is known on the long-term impact of these markers., Objective: To evaluate the short-and long-term influence of the levels of glucose and leukocytes on the prognosis of patients with AMI., Methods: A total of 809 patients with AMI were retrospectively assessed (mean age: 63.2 +/- 12.87 yrs) and prospectively and consecutively included in a specific database., Results: a) At the intrahospital phase, the mean values were compared between patients that died and those who survived: Leukocytosis: 12156+/-5977 vs 10337+/-3528 (p=0.004, 95%CI = 976-2663); Glucose 176+/-105 mg/dl vs 140+/-72 mg/dl (p<0.001, 95%CI = 19.4 - 52.6), respectively. b) With the adjusted mode, the same pattern was observed [p values: 0.002 (t-ratio 3.05), 0.04 (t-ratio 2.06), respectively]. c) Long-term follow-up: the univariate analysis showed P values of 0.001 (t-ratio 3.3), <0.001 (t-ratio 4.16), respectively. The multivariate analysis showed P=0.001 (t-ratio 3.35), 0.08 (t-ratio 1.75), respectively. (d) After the exclusion of the intrahospital deaths, the leukocyte (P=0.989) and glucose levels (P=0.144) did not remain significantly correlated with mortality. The same result was observed at the multivariate analysis., Conclusion: The levels of glucose and leukocytes at the hospital admission of patients with AMI are excellent predictors of intrahospital mortality and poor predictors of long-term death.

Introduction: In elderly patients with acute myocardial infarction, very little is known about the role of surgical myocardial revascularization and percutaneous coronary intervention (invasive therapies--IT), especially in the context of long-term outcomes after hospital discharge., Methods: We analyzed 1588 patients with MI who had been included prospectively in a databank and followed for up to 7.5 years. In this population, 548 patients were >70 years old (elderly group--EG), and 1040 were <70 years of age (younger group--YG); 1088 underwent IT during hospitalization, and the remaining 500 were treated medically (conservative therapy--CT). Patients were monitored either by visit or by phone at least once a year. A standard questionnaire was administered to all patients. The impact of IT was analyzed with both non-adjusted and adjusted models., Results: By the end of the follow-up period, the survival rates for the IT and CT groups were, respectively, 71.9% versus 47.2% in the global population (hazard ratio=0.55, P<0.001), 81.5% versus 66.6% in the YG (hazard ratio=0.68, P=0.018) and 48.8% versus 20.3% in the EG (hazard ratio=0.58, P<0.001). In the adjusted models, the hazard ratios were 0.62 (P<0.001) in the global population, 0.74 in the YG (P=0.073) and 0.64 (P=0.001) in the EG., Conclusion: Long-term follow-up of patients with myocardial infarction revealed that IT during the in-hospital phase was at least as effective in elderly patients as in younger patients.

Background: Little is known, especially in our country, about the influence of health insurance plans on the long term outcome of patients after acute myocardial infarction (AMI)., Objective: To assess the outcome of patients with AMI who are covered by the National Health System (SUS) or other health insurance plans., Methods: We analyzed 1,588 patients with AMI (mean age of 63.3 + 12.9 years, 71.7% male) who were included prospectively into a specific database and followed up for up to 7.55 years. Of this total, 1,003 were placed in the "SUS" group and 585 in the "other insurance plans" group. We applied chi-square, log-rank and Cox (stepwise) to the different statistical analyses. The long term multivariate model with mortality as a dependent variable included 18 independent variables., Results: In-hospital mortality rates in the "other insurance plans" and "SUS" groups were 11.4% and 10.3%, respectively (p = 0.5); in the long term, survival chances in the groups were respectively, 70.4% + 2.9 and 56.4% + 4.0 (p = 0.001, hazard-ratio = 1.43, or a 43% higher chance of death in the "SUS" group). In the adjusted model, the 'SUS' group had a significantly higher chance of death (a 36% higher chance, p = 0.005). Surgical revascularization and angioplasty improved the prognosis of these patients, whereas age and previous history of infarction, diabetes or heart failure worsened the prognosis., Conclusions: Relative to patients with other insurance plans, SUS users present similar mortality rates during hospital stay, but their prognosis is worse in the long term, thus reinforcing the need for additional efforts to improve the care provided to these patients after hospital discharge.

Aims: We compared outcomes of ST-elevation myocardial infarction (STEMI) patients randomized to a strategy of either enoxaparin or unfractionated heparin (UFH) to support fibrinolysis., Methods and Results: In the Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment-Thrombolysis in Myocardial Infarction Study 25 (ExTRACT-TIMI 25) trial, 20,479 patients undergoing fibrinolysis for STEMI with a fibrin-specific agent (N = 16,283) or streptokinase (SK) (N = 4139) were randomized to enoxaparin throughout their hospitalization or UFH for at least 48 h. The primary end point of death or nonfatal recurrent MI through 30 days occurred in 12.0% of patients in the UFH and 9.8% in the enoxaparin groups when treated with fibrin-specific lytics [odds ratio(adjusted) (OR(adj)) 0.78; 95% CI 0.70-0.87; P < 0.001] and 11.8 vs. 10.2%, respectively, when treated with SK (OR(adj) 0.83; 95% CI 0.66-1.04; P = 0.10; P(interaction) = 0.58). Major bleeding rates including intracranial hemorrhage within the fibrin-specific cohort were 1.2 and 2.0% in the UFH and enoxaparin groups, respectively (P < 0.001) and 2.0% in UFH and 2.4% in enoxaparin patients in the SK cohort (P = 0.16). Interaction tests between antithrombin- and lytic-type were non-significant (P = 0.20). Death, nonfatal MI, or major bleeding was significantly reduced with enoxaparin in the fibrin-specific cohort (OR(adj) 0.82; 95% CI 0.74-0.91; P < 0.001) and favoured enoxaparin in the SK cohort (OR(adj) 0.89; 95% CI 0.72-1.10; P = 0.29; P(interaction) = 0.53)., Conclusion: The benefits of an enoxaparin strategy over UFH were observed in both SK and fibrin-specific-treated STEMI patients. Therefore, an enoxaparin strategy is preferred over UFH to support fibrinolysis for STEMI regardless of lytic agent.

Background: A substantial proportion of patients treated with fibrinolytics for acute myocardial infarction (AMI) is subsequently submitted to surgical or percutaneous revascularization procedures during the same hospitalization. However, data comparing these procedures are scarce in the literature. The purpose of this study was to analyze the outcomes of a population with AMI who, during the in-hospital phase, received fibrinolytic therapy followed by coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI)., Methods: The study population included 3532 patients submitted to CABG (N=574) or PCI (N=2958), out of 15,114 patients studied in the InTIME-2 trial. Among patients treated with PCI there were no differences between those who received stents or isolated balloon angioplasty, so that their data were pooled for analysis., Results: CABG and PCI groups were compared regarding all-cause mortality (at 30 days and one year post-AMI) and non-fatal events (reinfarction, need of additional post-discharge revascularization and re-hospitalization for an ischemic event) within 30 days after MI. There was no significant difference in mortality rates between the groups--both unadjusted and adjusted--at 30 days and one year post-MI. The unadjusted 30-day rates of combined fatal and non-fatal events were 10.3% for the CABG group, and 15.3% for the PCI group (odds-ratio 0.64, P=0.0017), but the adjusted odds-ratio for the combined endpoint only achieved borderline significance (P=0.048)., Conclusion: Mortality rates for CABG and PCI were similar up to one year after AMI, but CABG tends to carry a better event-free survival in the first 30 days.

It is reported the case of a 71 year old male patient admitted to the emergency service pale and with systemic arterial hypertension and thoracic pain. In the diagnostic investigation, there was no evidence of compatible with acute myocardial ischemia. The thorax x-ray showed important enlargement of the mediastinum. In the echocardiogram the ascending aorta measured 47 mm, at the level of the pulmonary artery. One day after the echo, submitted to exam of magnetic resonance (RNM), the ascending aorta had a diameter of 62 mm, without false lumen flow or intimal "flap", but showing intramural hematoma envolving the ascending aorta and the proximal portion of the aorta. It was submitted to the surgical correction, being accomplished by resection of the ascending aorta and part of the aortic arch (hemiarch), with preservation of the aortic valve with suspension of the comissures. The patient had uneventful recovery, being discharged in the 9th postoperative day. We emphasized the similarity of the clinical presentation of the intramural hematoma of the aorta with that of aortic dissection, the importance of establishing correct diagnosis and the best treatment.

We described a case of left ventricular pseudoaneurysm associated to a severe mitral regurgitation, complicating a inferolaterodorsal acute myocardial infarction. The lesion was found in a routine echocardiogram during the in-hospital follow-up. The well-succeeded surgical strategy and the good clinical evolution of the patient were distinguished.

Whereas altered nitric oxide (NO.) formation from endothelial nitric oxide synthase (NOS) causes impaired vascular reactivity in a number of cardiovascular diseases, questions remain regarding how endothelial injury results in impaired NO. formation. It is unknown if loss of NOS expression or activity is required or if other factors are involved. Detergent treatment has been used to induce endothelial dysfunction. Therefore, NOS and NO. synthesis were characterized in a rat heart model of endothelial injury and dysfunction induced by the detergent Triton X-100. Cardiac NO. formation was directly measured by electron paramagnetic resonance spectroscopy. NOS activity was determined by the L-[(14)C]arginine conversion assay. Western blots and immunohistology were applied to define the amounts of NOS present in heart tissue before and after Triton treatment. Immunoelectron microscopy was performed to assess intracellular NOS distribution. A short bolus of Triton X-100, 0.25%, abolished responses to histamine and calcium ionophore while preserving response to nitroprusside. Complete blockade of NO. generation occurred after Triton treatment, but NOS activity assayed with addition of exogenous substrate and cofactors was unchanged, and identical 135-kDa NOS bands were seen on Western blots, indicating that NOS was not removed from the heart or structurally damaged by Triton. Immunohistochemistry showed no change in NOS localization after Triton treatment, and immunoelectron microscopy revealed similar NOS distribution in the plasma membrane and intracellular membranes. These results demonstrate that the endothelial dysfunction was due to decreased NO. synthesis but was not caused by loss or denaturation of NOS. Thus endothelial dysfunction due to mild endothelial membrane injury may occur in the presence of active NOS and is triggered by loss of NOS substrates or cofactors.

While the L-arginine conversion assay has been utilized to measure nitric oxide synthase (NOS) activity in isolated enzyme and pure cell preparations, this method often fails to provide accurate measurements in whole tissues. Biological tissues contain variable amounts of unlabeled substrate and enzymes are present which can compete for substrate or independently form the product L-citrulline. NOS-independent conversion of radiolabeled L-arginine to L-citrulline occurs due to arginase- and ornithine transcarbamylase-mediated reactions and this limits the accuracy of this assay for measurement of NOS activity. In heart tissue, NOS-independent L-citrulline formation was observed which could not be blocked by the NOS inhibitor L-NAME but was blocked by the arginase inhibitor L-ornithine. To eliminate the effect of arginase-mediated L-citrulline formation, KCl-washed membrane particulate fractions were obtained by high-speed centrifugation. While arginase-mediated nonspecific activity was 85% concentrated in the cytosol, 93% of NOS activity was localized within the particulate fraction of the heart. The remaining arginase activity found in the crude pellet was mostly removed by a one-step KCl wash purification and when incubation periods of 8 min were utilized specific and accurate measurements of NOS activity were obtained. NOS enzymatic properties were defined for rat heart preparations with a Km of 2.9 microM for L-arginine. All NOS activity detected was calcium-dependent suggesting it originated from the constitutive endothelial isoform. Thus, NOS-independent activity can be largely eliminated from the heart tissue by assaying KCl-washed membrane particulate fractions and this enables accurate quantitation of NOS activity., (Copyright 1998 Academic Press.)

Endothelial nitric-oxide synthase (eNOS) is an important regulator of endothelial function and vascular tone in biological tissues. While endothelial dysfunction occurs following ischemia and has been attributed to altered NO. formation, the biochemical basis for this dysfunction is unknown. Therefore, studies were performed to determine the effects of myocardial ischemia and reperfusion on eNOS in isolated rat hearts subjected to periods of global ischemia or ischemia followed by reperfusion. eNOS activity was assayed by L-[14C]arginine to L-[14C]citrulline conversion and alterations in the amount and distribution of eNOS determined by Western blotting and immunohistochemistry. While activity was preserved after 30 min of ischemia with a value of 1.1 +/- 0.1 pmol x min-1 x mg of protein-1, it decreased by 77% after 60 min and became nearly undetectable after 120 min. Reperfusion resulted in only a partial restoration of activity. The decline in activity with ischemia was due, in part, to a loss of eNOS protein. Hemodynamic studies showed that the onset of impaired vascular reactivity paralleled the loss of functional eNOS. Subjecting isolated eNOS to conditions of acidosis, which occur during ischemia, followed by restoration of pH as occurs on reperfusion, caused a combination of reversible and irreversible loss of activity similar to that seen in ischemic and reperfused hearts. Thus, loss of endothelial function following ischemia is paralleled by a loss of eNOS activity due to a combination of pH-dependent denaturation and proteolysis.

Purpose: To evaluate the effects of gemfibrozil and pravastatin in coronary artery disease patients with HDL-cholesterol (HDL-C) < 35 mg/dl)., Methods: Twenty-nine patients (20 males, 60 +/- 9) were divided in a gemfibrozil group (G) (1200 mg/day n = 15) and a pravastatin group (P) (10 or 20 mg n = 10 and 4, respectively). The plasma lipid profile (LP) e.g. total cholesterol (TC), fractions and triglycerides (TG) was determined at 4 and 12 weeks of treatment., Results: HDL-C was not affected in P, TC and LDL-cholesterol (LDL-C) reductions were superior to those in G (31.3% vs 13.4% and 38.7 and 11.5%, p < 0.05 and < 0.01 respectively). In G HDL-C raised by 50% (12th week p < 0.01). Gemfibrozil reduced TG levels in 44.7% while in P it varied -32.2% (12th week p < 0.01 and < 0.05 respectively)., Conclusion: Gemfibrozil is more effective in reducing TG and raising HDL-C than pravastatin. On the other hand, pravastatin was more potent in reducing LDL-C levels.