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1.
Med. crít. (Col. Mex. Med. Crít.) ; 34(5): 273-278, Sep.-Oct. 2020. tab, graf
Article in Spanish | LILACS-Express | LILACS | ID: biblio-1405535

ABSTRACT

Resumen: La ventilación mecánica es común en pacientes críticos. La asincronía paciente-ventilador existe cuando las fases de la respiración administradas por el ventilador no coinciden con las del paciente. Las asincronías son frecuentes e infradiagnosticadas, éstas se han asociado con desenlaces desfavorables como son: mayor duración de ventilación mecánica, estancia en la unidad de terapia intensiva, mortalidad, incomodidad del paciente, alteraciones del sueño y disfunción diafragmática. Esta revisión describe los desenlaces adversos reportados que se han asociado a la presencia de asincronías en pacientes adultos bajo ventilación mecánica invasiva. La evidencia actual sugiere que el mejor enfoque para manejar las asincronías es ajustar la configuración del ventilador y mejorar su detección. Si bien la mayoría de la evidencia proviene de estudios observacionales y ensayos clínicos aleatorizados realizados en poblaciones heterogéneas y con un número limitado de pacientes, los resultados sugieren desenlaces desfavorables clínicamente significativos en los pacientes que experimentan un índice de asincronía elevado. Por lo anterior, es necesario generar mayor evidencia en este tópico.


Abstract: Mechanical ventilation is common in critically ill patients. Patient-ventilator asynchrony exists when the breathing phases administered by the ventilator do not match those of the patient. They are frequent but underdiagnosed, and have been associated with worse outcomes because they negatively affect patient comfort, length of mechanical ventilation, length of stay in the intensive care unit and mortality. This review describes the negative outcomes associated with the presence of asynchronies in adult patients with invasive mechanical ventilation. Current evidence suggests that the best approach to handle asynchronies is to adjust the fan settings and improve the quality of detection. While most of this evidence comes from observational studies and randomized clinical trials which were done with heterogeneous populations and a limited number of patients, the results suggest less favorable clinically significant outcomes in patients with asynchronies. So it is necessary to generate more evidence in this topic.


Resumo: A ventilação mecânica é comum em pacientes críticos. A assincronia paciente-ventilador existe quando as fases da respiração fornecida pelo ventilador não coincidem com as do paciente. As assincronas são frequentes e subdiagnosticadas, tendo sido associadas a desfechos desfavoráveis como: maior tempo de ventilação mecânica, permanência em unidade de terapia intensiva, mortalidade, desconforto do paciente, distúrbios do sono e disfunção diafragmática. Esta revisão descreve os resultados adversos relatados que foram associados à presença de assincronia em pacientes adultos sob ventilação mecânica invasiva. A evidência atual sugere que a melhor abordagem para gerenciar assincronias é ajustar as configurações do ventilador e melhorar a detecção do ventilador. Embora a maioria das evidências provenha de estudos observacionais e ensaios clínicos randomizados conduzidos em populações heterogêneas e com um número limitado de pacientes, os resultados sugerem resultados clinicamente desfavoráveis significativos em pacientes que apresentam uma alta taxa de assincronia. Portanto, é necessário gerar mais evidências sobre este tema.

2.
Semin Arthritis Rheum ; 49(2): 273-278, 2019 10.
Article in English | MEDLINE | ID: mdl-30853116

ABSTRACT

INTRODUCTION: In previous studies we showed that prevalence of myocardial fibrosis as assessed by late enhancement on cardiac MRI in SSc patients is 45% and is associated to diffuse disease (dcSSc) and lower left ventricle ejection fraction; microvascular damage defined as decreased perfusion on cardiac MRI after adenosine infusion, was also very frequent (79%). Our aim was to identify baseline characteristics associated to the development of cardiovascular outcomes (heart failure, coronary artery disease, arrhythmias, vasculopathy, elevated systolic pulmonary artery pressure and death) in SSc patients with previously documented myocardial fibrosis and microvascular damage. PATIENTS AND METHODS: We included 62 SSc patients who participated in the study of prevalence of myocardial fibrosis (2008-2010) and in our local SSc cohort. We performed baseline clinical evaluation, cardiac MRI, coronary CT angiography, transthoracic echocardiogram, and yearly clinical and cardiovascular evaluation that included Medsger's severity scale items, electrocardiogram, echocardiogram, chest X-ray or HRCT and spirometry; we registered presence and severity of internal organ involvement and cardiovascular outcomes. Ordinal variables were analyzed using Chi square test and Fisher test when appropriate, numeric variables were compared using Student's t-test or Mann Whitney U when appropriate, logistic regression and Cox proportional hazard ratio were used to perform multivariable analysis. RESULTS: We obtained follow-up information from 62 patients (29 dcSSc, 33 lcSSc), mean follow-up was 43.5 months. Multivariable analysis showed that elevated basal ultrasensitive CRP was associated to mortality (p = 0.004, OR: 11.9, 95% CI 2.1-65.7) and recurrent digital tip ischemic ulcers (p = 0.001, OR 26.8, 95% CI 3,9-181.3) on follow-up. Myocardial fibrosis, particularly in the middle segments (p = 0.01, OR: 11.49, 95% CI 1.6-83), and older age (p = 0.02, OR: 1.11, 95% CI 1.01-1.22) were associated to heart failure on follow-up. Higher maximum mRSS was associated to coronary artery disease (p = 0.02, OR: 1.2, 95% CI 1.02-1.38), while insertion point fibrosis (p = 0.001, OR: 12.5 95% CI 2.7-56.6) was associated to recurrent digital tip ischemic ulcers. CONCLUSIONS: This study shows that myocardial fibrosis, elevated ultrasensitive CRP, and higher maximum mRSS are independent predictors of cardiovascular outcomes in SSc patients. Future studies should focus on early preventive and therapeutic strategies for this group of patients.


Subject(s)
C-Reactive Protein/metabolism , Cardiovascular Diseases/etiology , Fibrosis/etiology , Heart/diagnostic imaging , Myocardium/pathology , Scleroderma, Systemic/complications , Adult , Cardiovascular Diseases/blood , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/pathology , Computed Tomography Angiography , Echocardiography , Female , Fibrosis/blood , Fibrosis/diagnostic imaging , Fibrosis/pathology , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Scleroderma, Systemic/blood , Scleroderma, Systemic/diagnostic imaging , Scleroderma, Systemic/pathology
3.
PLoS One ; 10(5): e0126727, 2015.
Article in English | MEDLINE | ID: mdl-25993664

ABSTRACT

INTRODUCTION: Human leukocyte antigen (HLA) polymorphism studies in Systemic Sclerosis (SSc) have yielded variable results. These studies need to consider the genetic admixture of the studied population. Here we used our previously reported definition of genetic admixture of Mexicans using HLA class I and II DNA blocks to map genetic susceptibility to develop SSc and its complications. METHODS: We included 159 patients from a cohort of Mexican Mestizo SSc patients. We performed clinical evaluation, obtained SSc-associated antibodies, and determined HLA class I and class II alleles using sequence-based, high-resolution techniques to evaluate the contribution of these genes to SSc susceptibility, their correlation with the clinical and autoantibody profile and the prevalence of Amerindian, Caucasian and African alleles, blocks and haplotypes in this population. RESULTS: Our study revealed that class I block HLA-C*12:03-B*18:01 was important to map susceptibility to diffuse cutaneous (dc) SSc, HLA-C*07:01-B*08:01 block to map the susceptibility role of HLA-B*08:01 to develop SSc, and the C*07:02-B*39:05 and C*07:02-B*39:06 blocks to map the protective role of C*07:02 in SSc. We also confirmed previous associations of HLA-DRB1*11:04 and -DRB1*01 to susceptibility to develop SSc. Importantly, we mapped the protective role of DQB1*03:01 using three Amerindian blocks. We also found a significant association for the presence of anti-Topoisomerase I antibody with HLA-DQB1*04:02, present in an Amerindian block (DRB1*08:02-DQB1*04:02), and we found several alleles associated to internal organ damage. The admixture estimations revealed a lower proportion of the Amerindian genetic component among SSc patients. CONCLUSION: This is the first report of the diversity of HLA class I and II alleles and haplotypes Mexican patients with SSc. Our findings suggest that HLA class I and class II genes contribute to the protection and susceptibility to develop SSc and its different clinical presentations as well as different autoantibody profiles in Mexicans.


Subject(s)
Autoantibodies/immunology , Histocompatibility Antigens Class II/immunology , Histocompatibility Antigens Class I/immunology , Scleroderma, Systemic/classification , Scleroderma, Systemic/immunology , Alleles , Black People/genetics , Case-Control Studies , DNA Topoisomerases/metabolism , Demography , Disease Susceptibility/immunology , Female , HLA-DQ beta-Chains/immunology , Humans , Male , Mexico , Middle Aged , Principal Component Analysis , White People/genetics
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