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BACKGROUND: Evaluate the association between serum urea at admission and during hospital stay with return of spontaneous circulation (ROSC) and in-hospital mortality in patients with in-hospital cardiac arrest (IHCA). METHODS: This retrospective study included patients over 18 years with IHCA attended from May 2018 to December 2022. The exclusion criteria were the absence of exams to calculate delta urea and the express order of "do-not-resuscitate". Data were collected from the electronic medical records. Serum admission urea and urea 24 hours before IHCA were also collected and used to calculate delta urea. RESULTS: A total of 504 patients were evaluated; 125 patients were excluded due to the absence of variables to calculate delta urea and 5 due to "do-not-resuscitate" order. Thus, we included 374 patients in the analysis. The mean age was 65.0 ± 14.5 years, 48.9% were male, 45.5% had ROSC, and in-hospital mortality was 91.7%. In logistic regression models, ROSC was associated with lower urea levels 24 hours before IHCA (OR: 0.996; CI95%: 0.992-1.000; p: 0.032). In addition, increased levels of urea 24 hours before IHCA (OR: 1.020; CI95%: 1.008-1.033; p: 0.002) and of delta urea (OR: 1.001; CI95%: 1.001-1.019; p: 0.023) were associated with in-hospital mortality. ROC curve analysis showed that the area under the ROC curve for mortality prediction was higher for urea 24 hours before IHCA (Cutoff > 120.1 mg/dL) than for delta urea (Cutoff > 34.83 mg/dL). CONCLUSIONS: In conclusion, increased serum urea levels during hospital stay were associated with worse prognosis in IHCA.
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Paro Cardíaco , Mortalidad Hospitalaria , Urea , Humanos , Masculino , Femenino , Urea/sangre , Anciano , Estudios Retrospectivos , Persona de Mediana Edad , Paro Cardíaco/sangre , Paro Cardíaco/mortalidad , Tiempo de Internación/estadística & datos numéricos , Retorno de la Circulación Espontánea , Pronóstico , HospitalizaciónAsunto(s)
Paro Cardíaco , Humanos , Temperatura , Humedad , Pronóstico , Hospitales , Estudios RetrospectivosRESUMEN
Cardiovascular diseases (CVD) are the major cause of global mortality, accounting for 31% of deaths worldwide. Healthy eating habits based on the consumption of bioactive molecules present in plant-based diets can contribute to the prevention of CVD. In this context, the consumption of common beans (Phaseolus vulgaris L.) is relevant. There are several species of beans, all of which provide proteins, carbohydrates, dietary fiber, vitamins, minerals, and phenolic compounds. More recently, the complexity of phytochemical components has expanded, including the role of antinutritional factors in nutrient bioavailability and immune responses. Experimental and clinical studies have shown that the consumption of beans results in less food consumption, control of body weight, and improvement of metabolic biochemical parameters. Thus, the consumption of beans is associated with a decrease in CVD risk factors. To date, there have been no interventional studies assessing CVD outcomes, such as hospitalization, infarction, and mortality, in the context of bean consumption. Furthermore, studies on the effect of bean consumption on metabolomics and intestinal microbiota are lacking. The purpose of this review is to explore the nutritional properties of beans and discuss the main effects of the consumption of beans on cardiovascular health. In conclusion, eating habits based on the consumption of bioactive molecules present in beans can contribute to the prevention of cardiovascular disease. Furthermore, there is a large gap in the literature regarding the consumption of beans associated with clinical outcomes, such as hospitalization and mortality.
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Enfermedades Cardiovasculares , Phaseolus , Humanos , Enfermedades Cardiovasculares/prevención & control , Phaseolus/metabolismo , Minerales , Valor Nutritivo , Fibras de la DietaRESUMEN
BACKGROUND: To assess the prevalence of frailty by the Clinical Frailty Scale (CFS) and the 5-item FRAIL scale and their association with hospitalization in hemodialysis (HD) patients. METHODS: This was a prospective observational study. We included patients of both genders ≥ 18 years old in HD treatment for at least 3 months. Demographic, clinical, and routine laboratory data were retrieved from the medical charts. Two different frailty assessment tools were used, the CFS and the FRAIL scale. Participants were followed up for 9 months and hospitalizations for all causes were evaluated. A Venn diagram was constructed to show the overlap of possible frailty and pre-frailty. Cox regression was used to identify the association between frailty and hospitalization. The significance level was 5%. RESULTS: A total of 137 subjects were included in the analysis. The median age was 61 (52-67) years and 60% were male. The hospitalization rate and mortality in 9 months were 22.6% and 7.29%, respectively. Regarding frailty, the overall prevalence was 13.8% assessed by CFS and 36.5% according to the FRAIL scale. In the Cox regression, frailty by FRAIL scale was associated with a 2.8-fold increase in the risk of hospitalization (OR = 2.880; 95% CI = 1.361-6.096; p = 0.006), but frailty assessed by the CFS was not associated with the need for hospitalization. CONCLUSION: In HD patients, the FRAIL scale proved to be an easy-to-apply tool, identifying a high prevalence of frailty and being a predictor of hospital admission.
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Fragilidad , Humanos , Masculino , Femenino , Anciano , Persona de Mediana Edad , Adolescente , Fragilidad/epidemiología , Anciano Frágil , Hospitalización , Estudios Prospectivos , Diálisis RenalRESUMEN
Cardiac remodeling is defined as a group of molecular, cellular, and interstitial changes that clinically manifest as changes in the heart's size, mass, geometry, and function after different stimuli. It is important to emphasize that remodeling plays a pathophysiological role in the onset and progression of ventricular dysfunction and subsequent heart failure. Therefore, strategies to mitigate this process are critical. Different factors, including neurohormonal activation, can regulate the remodeling process and increase cell death, alterations in contractile and regulatory proteins, alterations in energy metabolism, changes in genomics, inflammation, changes in calcium transit, metalloproteases activation, fibrosis, alterations in matricellular proteins, and changes in left ventricular geometry, among other mechanisms. More recently, the role of reactive oxygen species and oxidative stress as modulators of remodeling has been gaining attention. Therefore, this review assesses the role of oxidative stress as a therapeutic target of cardiac remodeling.
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AIM: Evaluate the influence of doxycycline, an anti-inflammatory and matrix metalloproteinase (MMP) inhibitor, on the attenuation of chronic doxorubicin-induced cardiotoxicity in rats. METHODS: We allocated male Wistar rats into four groups: control (C), doxorubicin (D), doxycycline (inhibitor of MMP, IM), and Dox + doxycycline (DIM). Groups IM and DIM received doxycycline (5 mg/kg, IP) once a week for 4 weeks. In addition, 48 h after every doxycycline injection, groups D and DIM received Dox (5 mg/kg, IP). We performed echocardiogram and evaluated TIMP-4 and collagen I protein expression, MMP-2 activity, and oxidative stress and myocardial metabolism. RESULTS: Doxorubicin promotes left atrium (LA) and left ventricle (LV) dilatation and decreases in LV fractional shortening, which was improved by doxycycline. Moreover, doxycycline attenuated the LV cardiomyocyte hypertrophy and collagen type I expression. Doxorubicin increased phosphofructokinase and decreased beta-hydroxyacyl Co-A dehydrogenase, pyruvate dehydrogenase, citrate synthase, and ATP synthase activity, which was partially attenuated by doxycycline. Lastly, doxycycline improved antioxidant enzyme activity in the DIM group. CONCLUSION: Doxorubicin increases oxidative stress and promotes changes in myocardial energy metabolism, accompanied by structural and functional changes. Doxycycline attenuated the doxorubicin-induced cardiotoxicity, at least in part, through changes in myocardial energy metabolism.
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The cardiac remodeling after myocardial infarction is characterized by inflammation and oxidative stress. Thus, this study aimed to test the hypothesis that jaboticaba, due to its anti-inflammatory and antioxidants properties, attenuates cardiac remodeling after myocardial infarction. Wistar rats were submitted to myocardial infarction due to coronary artery occlusion, and divided into four experimental groups: C, sham control animals; I, animals submitted to myocardial infarction, received a standard diet; IJ2, animals submitted to myocardial infarction, received a standard diet plus 2% jaboticaba; and IJ4, animals submitted to myocardial infarction, received a standard diet plus 4% jaboticaba. After a three-month follow-up, echocardiography, histology, oxidative stress, and cardiac energy metabolism were analyzed. There was no difference in infarct size or mortality among the infarcted groups. The IJ4 group displayed improved diastolic function, as assessed by isovolumetric relaxation time normalized to the heart rate. As expected, the percentage of collagen was higher in all infarcted groups than in the C group. However, the IJ2 group had less collagen than groups I and IJ4. The IJ4 group presented lower PFK activity than I and IJ2, and lower pyruvate dehydrogenase activity than controls, whereas the IJ2 group showed no differences compared to the control group in both LDH and ATP synthase activity. The 2% and 4% doses attenuated lipid peroxidation and increased the activity of glutathione peroxidase compared with the I group. In conclusion, jaboticaba attenuated the remodeling process after myocardial infarction, which was associated with decreased oxidative stress and improved energy metabolism.
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Calcium is the most abundant extracellular cation in the body, and it is responsible for structural and enzymatic functions. Calcium homeostasis is regulated by 3 factors: calcitonin, vitamin D, and parathyroid hormone (PTH). Hypercalcemia is defined by a serum calcium concentration >10.5 mg/dL, and it is classified into mild, moderate, and severe, depending on calcium values. Most cases are caused by primary hyperparathyroidism and malignancies. Various mechanisms are involved in the pathophysiology of hypercalcemia, such as excessive PTH production, production of parathyroid hormone-related protein (PTHrp), bone metastasis, extrarenal activation of vitamin D, and ectopic PTH secretion. The initial approach is similar in most cases, but a definitive treatment depends on etiology, that is why etiological investigation is mandatory in all cases. The majority of patients are asymptomatic and diagnosed during routine exams; only a small percentage of patients present with severe manifestations which can affect neurological, muscular, gastrointestinal, renal, and cardiovascular systems. Clinical manifestations are related to calcium levels, with higher values leading to more pronounced symptoms. Critically ill patients should receive treatment as soon as diagnosis is made. Initial treatment involves vigorous intravenous hydration and drugs to reduce bone resorption such as bisphosphonates and, more recently, denosumab, in refractory cases; also, corticosteroids and calcitonin can be used in specific cases. This review aims to provide a clinical update on current concepts of the pathophysiology of calcium homeostasis, epidemiology, screening, clinical presentation, diagnosis, and management of hypercalcemia.
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Calcio/metabolismo , Técnicas de Diagnóstico del Sistema Digestivo , Manejo de la Enfermedad , Diagnóstico Precoz , Hipercalcemia/diagnóstico , Humanos , Hipercalcemia/sangre , Hipercalcemia/terapiaRESUMEN
OBJECTIVE: To evaluate whether there is a relationship between diet quality and bone health in a group of elderly Brazilian women. METHODS: A cross-sectional study was performed with 105 elderly women. Participants were evaluated regarding diet quality (good, needing improvement, and poor) and its relationship with bone mineral density (BMD), bone-specific alkaline phosphatase (BSAP), and C-telopeptide (CTX). RESULTS: Fifty eight participants (55.2%) presented a poor-quality diet and 47 (44.8%) required dietary improvements, while no subjects presented a good quality diet. The group requiring dietary improvements had lower CTX [0.35 (0.05;1.09) vs. 0.52 (0.10;1.45); p = 0.03)] and BSAP (38.7 ± 12.9 U/L vs. 46.10 ± 15.2 U/L; p < 0.01) levels than the poor-quality diet group. Groups did not differ in terms of BMD. CONCLUSION: In this group of elderly Brazilian women, there was a relationship between diet quality and bone health, where worse diet quality was associated with higher levels of bone remodelling markers.
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Densidad Ósea , Huesos , Anciano , Fosfatasa Alcalina , Biomarcadores , Estudios Transversales , Dieta , Femenino , HumanosRESUMEN
Septic shock is associated with unacceptably high mortality rates, mainly in developing countries. New adjunctive therapies have been explored to reduce global mortality related to sepsis. Considering that metabolic changes, mitochondrial dysfunction and increased oxidative stress are specific disorders within the path of septic shock, several micronutrients that could act in cellular homeostasis have been studied in recent decades. Thiamine, also known as vitamin B1, plays critical roles in several biological processes, including the metabolism of glucose, synthesis of nucleic acids and reduction of oxidative stress. Thiamine deficiency could affect up to 70% of critically ill patients, and thiamine supplementation appears to increase lactate clearance and decrease the vasopressor dose. However, there is no evident improvement in the survival of septic patients. Other micronutrients such as vitamin C and D, selenium and zinc have been tested in the same context but have not been shown to improve the outcomes of these patients. Some problems related to the neutrality of these clinical trials are the study design, doses, route, timing, length of intervention and the choice of endpoints. Recently, the concept that multi-micronutrient administration may be better than single-micronutrient administration has gained strength. In general, clinical trials consider the administration of a single micronutrient as a drug. However, the antioxidant defense is a complex system of endogenous agents in which micronutrients act as cofactors, and the physiological interactions between micronutrients are little discussed. In this context, the association of thiamine, vitamin C and corticoids was tested as an adjunctive therapy in septic shock resulting in a significant decrease in mortality. However, after these initial results, no other study conducted with this combination could reproduce those benefits. In addition, the use of low-dose corticosteroids is recommended in patients with septic shock who do not respond to vasopressors, which can affect the action of thiamine. Therefore, given the excellent safety profile, good biologic rationale and promising clinical studies, this review aims to discuss the mechanisms behind and the evidence for single or combined thiamine supplementation improving the prognosis of patients with septic shock.
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Background: Chronic obstructive pulmonary disease (COPD) has a functional definition. However, differences in clinical characteristics and systemic manifestations make COPD a heterogeneous disease and some manifestations have been associated with different risks of acute exacerbations, hospitalizations, and death. Objective: Therefore, the objective of the study was to evaluate possible clinical clusters in COPD at two study centers in Brazil and identify the associated exacerbation and mortality rate during 1 year of follow-up. Methods: We included patients with COPD and all underwent an evaluation composed of the Charlson Index, body mass index (BMI), current pharmacological treatment, smoking history (packs-year), history of exacerbations/hospitalizations in the last year, spirometry, six-minute walking test (6MWT), quality of life questionnaires, dyspnea, and hospital anxiety and depression scale. Blood samples were also collected for measurements of C-reactive protein (CRP), blood gases, laboratory analysis, and blood count. For the construction of the clusters, 13 continuous variables of clinical importance were considered: hematocrit, CRP, triglycerides, low density lipoprotein, absolute number of peripheral eosinophils, age, pulse oximetry, BMI, forced expiratory volume in the first second, dyspnea, 6MWD, total score of the Saint George Respiratory Questionnaire and packs-year of smoking. We used the Ward and K-means methods and determined the best silhouette value to identify similarities of individuals within the cluster (cohesion) in relation to the other clusters (separation). The number of clusters was determined by the heterogeneity values of the cluster, which in this case was determined as four clusters. Results: We evaluated 301 COPD patients and identified four different groups of COPD patients. The first cluster (203 patients) was characterized by fewer symptoms and lower functional severity of the disease, the second cluster by higher values of peripheral eosinophils, the third cluster by more systemic inflammation and the fourth cluster by greater obstructive severity and worse gas exchange. Cluster 2 had an average of 959±3 peripheral eosinophils, cluster 3 had a higher prevalence of nutritional depletion (46.1%), and cluster 4 had a higher BODE index. Regarding the associated comorbidities, we found that only obstructive sleep apnea syndrome and pulmonary thromboembolism were more prevalent in cluster 4. Almost 50% of all patients presented an exacerbation during 1 year of follow-up. However, it was higher in cluster 4, with 65% of all patients having at least one exacerbation. The mortality rate was statistically higher in cluster 4, with 26.9%, vs 9.6% in cluster 1. Conclusion: We could identify four clinical different clusters in these COPD populations, that were related to different clinical manifestations, comorbidities, exacerbation, and mortality rate. We also identified a specific cluster with higher values of peripheral eosinophils.
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Enfermedad Pulmonar Obstructiva Crónica , Calidad de Vida , Brasil/epidemiología , Volumen Espiratorio Forzado , Humanos , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Pruebas de Función Respiratoria , Índice de Severidad de la EnfermedadRESUMEN
The objective of this study was to analyze the impact of different modalities and intensities of exercise training on cardiac remodeling started early after experimental myocardial infarction (MI). Male Wistar rats, weighing 200-250 g, were subjected to experimental MI. After 5 days, the animals were allocated into three experimental groups and observed for three months: S (sedentary control animals), C (animals subjected to continuous low-intensity training), and HIT (animals subjected to high-intensity interval training). Low-intensity exercise training was performed at a treadmill speed corresponding to 40% VO2 max, which was kept unchanged throughout the entire session (i.e., continuous low-intensity training). High-intensity interval training was performed in such a way that rats run during 3 min at 60% VO2 max, followed by 4-minute intervals at 85% VO2 max (i.e., high-intensity interval training). After the follow-up period, we studied hypertrophy and ventricular geometry, functional alterations in vivo and in vitro, oxidative stress, apoptosis, and cardiac energetic metabolism. Our data showed that both high-intensity interval and continuous low-intensity modalities improved cardiac energetic metabolism variables in comparison with sedentary infarcted animals. In addition, high-intensity interval training decreased cardiac oxidative stress, associated with improved diastolic function. On the other hand, the continuous low-intensity group showed impairment of cardiac function. Therefore, altogether, our data suggest that high-intensity interval training could be the best modality for early physical exercise after MI and should be better studied in this clinical scenario.
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Infarto del Miocardio/terapia , Condicionamiento Físico Animal/métodos , Remodelación Ventricular/inmunología , Animales , Masculino , Infarto del Miocardio/fisiopatología , Ratas , Ratas WistarRESUMEN
The objective of this study was to evaluate Spondias mombin L. (SM) pulp and its influence on cardiac remodelling after myocardial infarction (MI). Male Wistar rats were assigned to four groups: a sham group (animals underwent simulated surgery) that received standard chow (S; n = 20), an infarcted group that received standard chow (MI; n = 24), an infarcted group supplemented with 100 mg of SM/kg bodyweight/d, (MIS100; n = 23) and an infarcted group supplemented with 250 mg of SM/kg bodyweight/d (MIS250; n = 22). After 3 months of treatment, morphological, functional and biochemical analyses were performed. MI induced structural and functional changes in the left ventricle with worsening systolic and diastolic function, and SM supplementation at different doses did not influence these variables as analysed by echocardiography and an isolated heart study (P > .05). However, SM supplementation attenuated cardiac remodelling after MI, reducing fibrosis (P = .047) and hypertrophy (P = .006). Biomarkers of oxidative stress, inflammatory processes and energy metabolism were further investigated in the myocardial tissue. SM supplementation improved the efficiency of energy metabolism and decreased lipid hydroperoxide in the myocardium [group S (n = 8): 267.26 ± 20.7; group MI (n = 8): 330.14 ± 47.3; group MIS100 (n = 8): 313.8 ± 46.2; group MIS250: 294.3 ± 38.0 nmol/mg tissue; P = .032], as well as decreased the activation of the inflammatory pathway after MI. In conclusion, SM supplementation attenuated cardiac remodelling processes after MI. We also found that energy metabolism, oxidative stress and inflammation are associated with this effect. In addition, SM supplementation at the highest dose is more effective.
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Anacardiaceae/química , Suplementos Dietéticos , Infarto del Miocardio/metabolismo , Infarto del Miocardio/patología , Estrés Oxidativo , Extractos Vegetales/farmacología , Remodelación Ventricular , Animales , Antioxidantes/química , Antioxidantes/farmacología , Biomarcadores , Peso Corporal , Cromatografía Líquida de Alta Presión , Citocinas/metabolismo , Modelos Animales de Enfermedad , Ecocardiografía , Metabolismo Energético/efectos de los fármacos , Pruebas de Función Cardíaca , Inmunohistoquímica , Mediadores de Inflamación/metabolismo , Infarto del Miocardio/tratamiento farmacológico , Infarto del Miocardio/etiología , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/química , Ratas , Remodelación Ventricular/efectos de los fármacosRESUMEN
BACKGROUND: Inflammatory bowel disease (IBD) patients present a higher risk of developing cardiovascular diseases due to the presence of chronic inflammation, which plays an essential role in atherogenesis. Therefore, the aim of the study was to evaluate the cardiovascular risk between patients with IBD and healthy control individuals. MATERIALS AND METHODS: A total of 52 consecutive IBD outpatients from a tertiary hospital and 37 healthy controls were enrolled. Data collected included age, sex, smoking status, presence of comorbidities, disease activity, ongoing medical treatment, body mass index, arterial blood pressure, and cardiovascular risk. The cardiovascular risk was based on the Framingham risk score and ultrasonography variables, such as the carotid intima-media thickness and the presence of atherosclerotic plaque in the carotid. Multivariate logistic regression or multiple linear regression analysis was performed at a significance level of 5%. RESULTS: No differences were observed between groups with regard to age, sex, smoking status, comorbidities, blood pressure, body mass index, lipid profile, and Framingham risk score. In the IBD group, fasting glucose [95 (86.2-107.3) mg/dL vs 86 (79-100) mg/dL, p=0.041], carotid intima-media thickness (0.69±0.12 mm vs 0.63±0.12 mm, p=0.031), and atherosclerotic carotid plaque (25% vs 5.4%, p=0.032) were higher compared with those in the control group. Multivariate logistic regression analysis showed that patients with IBD presented a 6.45-fold higher risk of carotid atherosclerotic plaque (odds ratio: 6.45; 95% confidence interval: 1.035-40.216; p<0.046). CONCLUSION: Patients with IBD are at an increased risk of atherosclerosis and, consequently, an increased risk for cardiovascular diseases.
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BACKGROUND: Tobacco smoke is one of the most significant risk factors for cardiovascular diseases and damages in the myocardial tissue directly. Cardiac magnetic resonance (CMR) has been used and is a promising tool to evaluate morphometry and cardiac function in humans. The objective of this study was to evaluate associations of smoking with morphometry and cardiac function by CMR technique in young adult smokers. METHODS: Altogether, 49 volunteers (22 smokers and 27 non-smokers) were included in the study. The comparisons between groups were performed by multiple linear regression adjusting for body mass index and gender. RESULTS: In the morphometric and functional evaluation of the left ventricle, we observed statistical significant lower values of end-diastolic volume (EDV) (p = 0.02), ejection volume (EV) (p = 0.001) and indexed ejection volume (IEV) (p = 0.007) in smokers when compared to no-smoker group. Right ventricle showed statistical significant lower values of EDV (p = < 0.001), end-systolic volume (p = 0.01), EV (p = < 0.001), IEV (p = 0.001), indexed end-diastolic volume (p = 0.001) and major axis (p = 0.01) in smokers when compared to non-smokers group. CONCLUSIONS: There is a strongly association of smoking in young adult and cardiac function decline, even adjusted by cofounders, which compromises the proper functioning of the heart. Evidence confirms that smoking can directly influence the cardiac function, even without atherosclerosis or other chronic comorbidities, associated with increased risk of cardiovascular diseases.
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Ventrículos Cardíacos/diagnóstico por imagen , Imagen por Resonancia Magnética , No Fumadores , Fumadores , Fumar/efectos adversos , Volumen Sistólico , Función Ventricular Izquierda , Función Ventricular Derecha , Adulto , Estudios Transversales , Femenino , Voluntarios Sanos , Ventrículos Cardíacos/fisiopatología , Humanos , Masculino , Valor Predictivo de las Pruebas , Fumar/fisiopatologíaRESUMEN
BACKGROUND & AIMS: Stroke is the leading cause of disability in adult life. Oropharyngeal dysphagia occurs in 65-90% of patients, and its identification in the acute phase of stroke can prevent complications. The aim of this study was to verify whether oropharyngeal dysphagia during stroke hospitalization is associated with functional capacity, as assessed by the modified Rankin Scale (mRs), and mortality 90 days after stroke. MATERIALS AND METHODS: A prospective cohort study evaluating 201 patients hospitalized in the Stroke Unit was carried out. Dysphagia was evaluated during hospitalization using both a specific protocol to evaluate swallowing biomechanics and the Functional Oral Intake Scale (FOIS), in which FOIS 1-3 reflects tube feeding, 4-5 reflects oral feeding requiring food consistency changes, and 6-7 reflects oral feeding with no changes in food consistency. An mRs≥3 at 90 days after discharge was considered disability. The data were adjusted for the National Institute of Health Stroke Scale score, sex, age, stroke-associated pneumonia, type of stroke, and presence of thrombolysis. The significance level was set at 5%. RESULTS: Of the 201 patients evaluated, 42.8% (86) who had dysphagia were older, had a higher severity of stroke, and pneumonia rate. A FOIS score of 6-7 was a protective factor against disability (mRs≥3) (OR: 0.17; CI: 0.005-0.56; p = 0.004), and tube feeding use at hospital discharge increased the risk of mRs≥3 (OR: 14.97; CI: 2.68-83.65; p = 0.002) and mortality (OR: 9.79; CI: 2.21-43.4; p = 0.003) within 90 days after stroke. Pneumonia was the leading cause of death, however dysphagia and tube feeding at discharge were associated with death from any cause. CONCLUSION: Dysphagia or tube feeding use at discharge are markers of poor prognosis after the first stroke. Our data suggest the importance of early evaluation of dysphagia and closely monitoring the tube fed patients following stroke.
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Trastornos de Deglución/epidemiología , Nutrición Enteral/estadística & datos numéricos , Accidente Cerebrovascular/mortalidad , Accidente Cerebrovascular/fisiopatología , Anciano , Anciano de 80 o más Años , Trastornos de Deglución/mortalidad , Trastornos de Deglución/fisiopatología , Femenino , Hospitalización , Humanos , Masculino , Persona de Mediana Edad , Alta del Paciente , Pronóstico , Estudios Prospectivos , Factores de Riesgo , Accidente Cerebrovascular/complicaciones , Tasa de SupervivenciaRESUMEN
BACKGROUND: The objective of our study was to evaluate the association of serum malondialdehyde (MDA) and protein carbonyl concentration with intensive care unit (ICU) mortality in patients with septic shock. METHODS: We prospectively evaluated 175 patients aged over 18 years with septic shock upon ICU admission. However, 16 patients were excluded. Thus, 159 patients were enrolled in the study. In addition, we evaluated 16 control patients. At the time of the patients' enrollment, demographic information was recorded. Blood samples were taken within the first 24 hours of the patient's admission to determine serum MDA and protein carbonyl concentrations. RESULTS: The mean age was 67.3 ± 15.9 years, 44% were males, and the ICU mortality rate was 67.9%. Median MDA concentration was 1.53 (0.83-2.22) µmol/L, and median protein carbonyl concentration was 24.0 (12.7-32.8) nmol/mL. Patients who died during ICU stay had higher protein carbonyl concentration. However, there was no difference in MDA levels between these patients. Receiver operating characteristic curve analysis showed that higher levels of protein carbonyl were associated with ICU mortality (area under the curve: 0.955; 95% confidence interval [CI]: 0.918-0.992; P < .001) at the cutoff of >22.83 nmol/mL (sensibility: 80.4% and specificity: 98.1%). In the logistic regression models, protein carbonyl concentrations (odds ratio [OR]: 1.424; 95% CI: 1.268-1.600; P < .001), but not MDA concentrations (OR: 1.087; 95% CI: 0.805-1.467; P = .59), were associated with ICU mortality when adjusted for age, gender, and Acute Physiology and Chronic Health Evaluation (APACHE) II score; and when adjusted by APACHE II score, lactate, and urea; protein carbonyl concentrations (OR: 1.394; 95% CI: 1.242-1.564; P < .001); and MDA (OR: 1.054; 95% CI: 0.776-1.432; P = .73). CONCLUSION: In conclusion, protein carbonyl, but not MDA, concentration is associated with ICU mortality in patients with septic shock.