Papel de la inflamación y la adhesión leucocitaria en la fisiopatología del daño orgánico en la hipertensión arterial.

La hipertensión arterial aumenta el estrés oxidativo, el cual a su vez impide una adecuada función endotelial. La disfunción endotelial es común en los pacientes hipertensos; se asocia con inflamación, incremento de algunos mediadores de la inflamación y daño a órgano blanco. En presencia de disfunción endotelial, se expresan en el endotelio vascular moléculas de adhesión, las cuales facilitan el rodamiento de los leucocitos (especialmente monocitos) sobre la pared arterial, así como su paso al espacio subendotelial. Estas moléculas se han asociado con algunas complicaciones de la hipertensión arterial. Se ha identificado un posible nexo entre inflamación e hipertensión arterial, y recientemente se ha destacado el papel de la inflamación en el desarrollo de las complicaciones cardiovasculares de la enfermedad, en este escrito revisaremos los mecanismos que contribuyen a ese nexo, así como el papel de la inflamación en el desarrollo de complicaciones en el paciente hipertenso

High triglyceride to HDL-cholesterol ratio as a biochemical marker of severe outcomes in COVID-19 patients

Background & aims Coronavirus disease 2019 (COVID-19) patients with severe complications have shown comorbidities with cardiovascular-disease, hypertension and type 2 diabetes mellitus; clinical disorders that share the common metabolic alterations of insulin resistance and dyslipidaemia. A high triglyceride to high density lipoprotein cholesterol (Tg/HDL c) ratio has been associated with reduced insulin sensitivity, metabolic syndrome and adverse cardiovascular events. Our aim in this study was to determine the association between different components of the lipid profile and particularly the Tg/HDL c ratio with severe complications like the requirement of invasive mechanical ventilation in COVID-19 patients. Methods We collected demographic, clinical and biochemical data to conduct a cohort study in 43 adult patients with confirmed COVID-19 diagnosis by quantitative polymerase chain reaction (qPCR) at baseline and in the subsequent 15 days. Patients were subjected to a very similar treatment scheme with the JAK1/2 inhibitor ruxolitinib. Descriptive statistics, variable association and logistic regression were applied to identify predictors of disease severity among elements and calculations from the lipid profile. Results Patients were aged 57 ± 14 years; 55.8% were male from which 75% required hospitalization and 44.2% were female who 58% were hospitalized. The most common comorbidities were type 2 diabetes mellitus (58%) and hypertension (40%). Hospitalized and critical care patients showed lower HDL c blood levels and increased Tg/HDL c ratio than those with outpatient management and mild/asymptomatic COVID-19. Tg/HDL c ratio correlated with variables of disease severity such as lactate dehydrogenase (LDH) levels (r = 0.356; p < 0.05); National Early Warning Score 2 (NEWS 2) (r = 0.495; p < 0.01); quick sequential organ failure assessment (qSOFA) (r = 0.538; p < 0.001); increased need of oxygen support (r = 0.447; p < 0.01) and requirement of mechanical ventilation (r = 0.378; p < 0.05). Tg/HDL c ratio had a negative correlation with partial oxygen saturation/fraction of inspired oxygen (SaO 2/FiO2) ratio (r = −0.332;p < 0.05). Linear regression analysis showed that Tg/HDL c ratio can predict increases in inflammatory factors like LDH (p < 0.01); ferritin (p < 0.01) and D-dimer (p < 0.001). Logistic regression model indicated that ≥7.45 Tg/HDL c ratio predicts requirement of invasive mechanical ventilation (OR 11.815, CI 1.832–76.186, p < 0.01). Conclusions The Tg/HDLc ratio can be used as an early biochemical marker of COVID-19 severe prognosis with requirement of invasive mechanical ventilation

Wohnungsgemeinnuetzigkeit morgen: Dokumentation d. Symposiums zur Novellierung d. WGG vom 19. - 20. Maerz 1987 in Bonn

Includes 6 articlesAvailable from Bibliothek des Instituts fuer Weltwirtschaft, ZBW, Duesternbrook Weg 120, D-24105 Kiel C 151543 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman