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Documento de consenso sobre la anemia y déficit de hierro en insuficiencia cardiaca: Consejo Interamericano de Falla Cardiaca e Hipertensión Pulmonar (CIFACAH) de la Sociedad Interamericana de Cardiología (SIAC)
(Instituto Nacional de Cardiología Ignacio Chávez, 2023)
Descripción Anatómica de la Arteria Polar Renal Accesoria y su Relación con la Hipertensión Arterial
(Sociedad Chilena de Anatomía, 2020)
336
Int. J. Morphol.,
38(2):336-339, 2020.
Descripción Anatómica de la Arteria Polar Renal Accesoria
y su Relación con la Hipertensión Arterial
Anatomical Description of Accessory Renal Polar Artery...
de la arteria polar renal accesoria y su relación con la hipertensión arterial. Int. J. Morphol., 38(2):336-339, 2020. RESUMEN: La irrigación renal incluye la arteria renal y las arterias renales accesorias. Uno de estos vasos accesorios es la...
de la arteria polar renal accesoria y su relación con la hipertensión arterial. Int. J. Morphol., 38(2):336-339, 2020. RESUMEN: La irrigación renal incluye la arteria renal y las arterias renales accesorias. Uno de estos vasos accesorios es la...
Efecto de la dieta nórdica en el control de los factores de riesgo de enfermedad cardiovascular: Revisión sistemática
(Soc Chilena Nutrición, Bromatología & Toxicología, 2021)
Introduction: The Nordic Diet has been proposed and implemented as another healthy alternative to the classic
Mediterranean diet, both for daily living and also for the control and treatment of cardiovascular diseases. Objective:
To review the scientific evidence currently published on the association between the uptake of the Nordic Diet
(ND) and its protective effect for cardiovascular risk. Methods: An electronic search of the scientific literature was
performed, using keywords, based on randomized controlled clinical trials and case-control studies, published in
PubMed and Cochrane from 2010 to date. We included: adult subjects of both sexes, with cardiovascular risk factors
such as overweight, dyslipidemia, high blood pressure and/or insulin resistance. Results: Of the five randomized
controlled clinical trials included in this review, the ND significantly reduces levels of LDL-C, LDL/HDL ratio, and
apoB/apoA ratio, in addition to significantly reducing body weight and waist circumference. Regarding triglyceride
levels, VLDL, insulin sensitivity and blood pressure, only one study demonstrated significantly favorable effects of
these variables and the Sysdiet study was able to demonstrate an anti-inflammatory effect of the ND. Conclusion:
The ND has considerably beneficial effects on different cardiovascular risk factors such as obesity, dyslipidemia and
inflammation, making it an additional healthy alternative to the Mediterranean diet or the DASH diet in the control
and prevention of cardiovascular diseases....
de riesgo cardiovascular como sobrepeso, dislipidemia, hipertensión arterial y/o resistencia a la insulina. Resultados: De los 5 ECA incluidos en esta revisión, se demostró que la DN reduce significativamente los niveles de LDL-C, el radio LDL/HDL y...
de riesgo cardiovascular como sobrepeso, dislipidemia, hipertensión arterial y/o resistencia a la insulina. Resultados: De los 5 ECA incluidos en esta revisión, se demostró que la DN reduce significativamente los niveles de LDL-C, el radio LDL/HDL y...
Estradiol en la patogénesis de la hipertensión pulmonar arterial (HPA) : rol de la actividad estrogénica y del metabolismo hormonal sobre células de la musculatura arterial lisa
(Universidad de Chile, 2023)
Antecedentes: La hipertensión pulmonar (HP) es una enfermedad crónica, progresiva y actualmente incurable. Esta puede ser clasificada según su etiología y área pulmonar afectada. Para nuestro interés consideramos la HP arterial idiopática (HPAi...
Background: Pulmonary hypertension (PH) is a chronic, progressive, and currently incurable disease. It can be classified according to its etiology and affected lung area. Idiopathic arterial PH (iPAH) is our interest, since it is a disease that currently only has palliative treatments, and an unknown origin. HPAi is characterized by an increase in pulmonary artery blood pressure. Said pressure is regulated mainly by the pulmonary artery smooth muscle layer cells (PASMCs). When the pathology occurs, the PASMCs undergo a "cancerous type" phenotypic change that leads to a sustained proliferation that causes a decrease in the lumen of the artery, increasing the pressure. When this process is sustained over time, right ventricular failure occurs, which can be fatal. Additionally, these cells present mitochondrial dysfunction. This dysfunction is manifested by a metabolic change from obtaining energy by oxidative phosphorylation towards a preferentially glycolytic metabolism, associated with an increase in DRP1-mediated mitochondrial fission. This phenotype is correlated with lower oxygen consumption and lower mitochondrial potential. Among the major risk factors for HPAi are increased levels of plasma estradiol (E2) and being female. When men and women are compared, the latter have a longer survival time thanks to the cardiovascular protective factor of estrogen. This phenomenon is called "the estrogen paradox". There is evidence of mitogenic action of E2 in PASMCs. Likewise, in recent years it has been described that E2 can be metabolized, and its metabolites also exert biological responses. Of our attention are methoxyestrogens, considered among the main metabolites of E2. In this classification we highlight 2-methoxyestradiol (2-ME) and 4-methoxyestradiol (4-ME). 2-ME has been shown to reduce HP in in vivo models. However, the effect on PASMCs of 4-ME is unknown. Additionally, the effects of estrogens are exerted through the so-called estrogen receptors (ERα and ERβ and GPER), indicating that the probable "cancer" or "hypertensive" phenotype that is triggered in PASMCs, which is induced by estrogens, it may be associated with cell signaling processes and gene transcription triggered by the activation of these receptors. Hypothesis: 17β-estradiol and its metabolite 4-methoxyestradiol induce proliferation of hPASMCs through a mechanism dependent on the inhibition of mitochondrial function and the classical and non-classical estrogen receptor pathways, reflecting the pathological phenotype found in Idiopathic pulmonary arterial hypertensives patients. Specific objectives:1) To evaluate the effect of 17β-estradiol and its metabolite 4-methoxyestradiol on the generation of hPASMCs. 2) Determine the effect of 17β-estradiol and its metabolite 4-methoxyestradiol on mitochondrial function. 3) To evaluate the participation of the ERα, ERβ and GPER receptors in the effects on hPASMC induced by 17β-estradiol and 4-methoxyestradiol. 4) Analyze transcriptional regulation networks associated with energy and hormonal metabolism that are controlled by estrogen nodes in transcriptional databases of lung tissue from HPAi patients. Experimental Design: In vitro model: hPASMCs treated with E2 (0-100 nM) for 24 and 48 hours were used. Cell proliferation was evaluated by MTS assay, cell cycle analysis by propidium iodide (IP), proliferation and viability by trypan blue exclusion, cell viability using IP and annexin V, and cell proliferation by Ki67 immunodetection. Likewise, the production of mitochondrial reactive oxygen species (mtROS) was analyzed using MitoSOX, mitochondrial potential using safranin and oxygen consumption using high-resolution respirometry. Estrogen receptor analysis: hPASMCs were pretreated with the inhibitors Fulvestrant or G36 for 3 hours and then stimulated with 100 nM E2 or 10 nM 4-ME for 48 hours. Relative cell proliferation was assessed by MTS and cell count by trypan blue exclusion. In silico model: Gene expression databases from indexed publications reporting HPAi patients were filtered by sex and age, matched, and analyzed using the Cytoscape program. Results: I) E2 (10 nM and 100 nM) and 4-ME (5 nM and 10 nM) significantly increased cell proliferation of hPASMCs. II) E2 (10 nM) and 4-ME (5 and 10 nM) significantly increased mtROS in hPASMCs. III) Treatment with E2 (10 nM and 100 nM) and 4-ME (5 nM and 10 nM) decreased mitochondrial potential in hPASMCs. IV) Estrogen treatments altered mitochondrial respiration significantly in hPASMCs. V) hPASMCs proliferation induced by 100 nM E2 is mediated by ERα and/or ERβ (classical pathway). VI) hPASMCs proliferation induced by 4-ME 10 nM is mediated by GPER (non-classical pathway). VII) In HPAi, the transcriptional networks are mainly governed by pathways associated with estrogen receptors and their metabolism, generating a disruption in the metabolic balance. Conclusions: Estrogenic pathways are master regulators in HPAi transcriptional reprogramming. E2 and 4-ME induce the proliferation of hPASMCs, increasing the production of mtROS and decreasing the mitochondrial potential. Estrogens significantly affect the rate of mitochondrial oxygen consumption. Estrogen-induced proliferation differs in the receptors used, being the effect of E2 mediated through the classical pathway and 4-ME through the non-classical pathway....
Background: Pulmonary hypertension (PH) is a chronic, progressive, and currently incurable disease. It can be classified according to its etiology and affected lung area. Idiopathic arterial PH (iPAH) is our interest, since it is a disease that currently only has palliative treatments, and an unknown origin. HPAi is characterized by an increase in pulmonary artery blood pressure. Said pressure is regulated mainly by the pulmonary artery smooth muscle layer cells (PASMCs). When the pathology occurs, the PASMCs undergo a "cancerous type" phenotypic change that leads to a sustained proliferation that causes a decrease in the lumen of the artery, increasing the pressure. When this process is sustained over time, right ventricular failure occurs, which can be fatal. Additionally, these cells present mitochondrial dysfunction. This dysfunction is manifested by a metabolic change from obtaining energy by oxidative phosphorylation towards a preferentially glycolytic metabolism, associated with an increase in DRP1-mediated mitochondrial fission. This phenotype is correlated with lower oxygen consumption and lower mitochondrial potential. Among the major risk factors for HPAi are increased levels of plasma estradiol (E2) and being female. When men and women are compared, the latter have a longer survival time thanks to the cardiovascular protective factor of estrogen. This phenomenon is called "the estrogen paradox". There is evidence of mitogenic action of E2 in PASMCs. Likewise, in recent years it has been described that E2 can be metabolized, and its metabolites also exert biological responses. Of our attention are methoxyestrogens, considered among the main metabolites of E2. In this classification we highlight 2-methoxyestradiol (2-ME) and 4-methoxyestradiol (4-ME). 2-ME has been shown to reduce HP in in vivo models. However, the effect on PASMCs of 4-ME is unknown. Additionally, the effects of estrogens are exerted through the so-called estrogen receptors (ERα and ERβ and GPER), indicating that the probable "cancer" or "hypertensive" phenotype that is triggered in PASMCs, which is induced by estrogens, it may be associated with cell signaling processes and gene transcription triggered by the activation of these receptors. Hypothesis: 17β-estradiol and its metabolite 4-methoxyestradiol induce proliferation of hPASMCs through a mechanism dependent on the inhibition of mitochondrial function and the classical and non-classical estrogen receptor pathways, reflecting the pathological phenotype found in Idiopathic pulmonary arterial hypertensives patients. Specific objectives:1) To evaluate the effect of 17β-estradiol and its metabolite 4-methoxyestradiol on the generation of hPASMCs. 2) Determine the effect of 17β-estradiol and its metabolite 4-methoxyestradiol on mitochondrial function. 3) To evaluate the participation of the ERα, ERβ and GPER receptors in the effects on hPASMC induced by 17β-estradiol and 4-methoxyestradiol. 4) Analyze transcriptional regulation networks associated with energy and hormonal metabolism that are controlled by estrogen nodes in transcriptional databases of lung tissue from HPAi patients. Experimental Design: In vitro model: hPASMCs treated with E2 (0-100 nM) for 24 and 48 hours were used. Cell proliferation was evaluated by MTS assay, cell cycle analysis by propidium iodide (IP), proliferation and viability by trypan blue exclusion, cell viability using IP and annexin V, and cell proliferation by Ki67 immunodetection. Likewise, the production of mitochondrial reactive oxygen species (mtROS) was analyzed using MitoSOX, mitochondrial potential using safranin and oxygen consumption using high-resolution respirometry. Estrogen receptor analysis: hPASMCs were pretreated with the inhibitors Fulvestrant or G36 for 3 hours and then stimulated with 100 nM E2 or 10 nM 4-ME for 48 hours. Relative cell proliferation was assessed by MTS and cell count by trypan blue exclusion. In silico model: Gene expression databases from indexed publications reporting HPAi patients were filtered by sex and age, matched, and analyzed using the Cytoscape program. Results: I) E2 (10 nM and 100 nM) and 4-ME (5 nM and 10 nM) significantly increased cell proliferation of hPASMCs. II) E2 (10 nM) and 4-ME (5 and 10 nM) significantly increased mtROS in hPASMCs. III) Treatment with E2 (10 nM and 100 nM) and 4-ME (5 nM and 10 nM) decreased mitochondrial potential in hPASMCs. IV) Estrogen treatments altered mitochondrial respiration significantly in hPASMCs. V) hPASMCs proliferation induced by 100 nM E2 is mediated by ERα and/or ERβ (classical pathway). VI) hPASMCs proliferation induced by 4-ME 10 nM is mediated by GPER (non-classical pathway). VII) In HPAi, the transcriptional networks are mainly governed by pathways associated with estrogen receptors and their metabolism, generating a disruption in the metabolic balance. Conclusions: Estrogenic pathways are master regulators in HPAi transcriptional reprogramming. E2 and 4-ME induce the proliferation of hPASMCs, increasing the production of mtROS and decreasing the mitochondrial potential. Estrogens significantly affect the rate of mitochondrial oxygen consumption. Estrogen-induced proliferation differs in the receptors used, being the effect of E2 mediated through the classical pathway and 4-ME through the non-classical pathway....
Prevalence of hypertension in students of 4th grade to 9th grade in a school in santiago (Chile) Prevalencia de hipertensión arterial en alumnos de 4o básico a 1o medio en un colegio de Santiago (Chile)
(Universidad del Norte, 2013)
Prevalence of hypertension in students of 4th grade to 9th grade in a school in
santiago (Chile) Prevalencia de hipertensión arterial en alumnos de 4o básico a
1o medio en un colegio de Santiago (Chile)
Uribe Blanco...
Efectos del tratamiento con péptido natriurético auricular (ANP) en las variables fisiológicas cardiopulmonares de corderos recién nacidos en altura con hipertensión pulmonar
(Universidad de Chile, 2017)
La hipertensión pulmonar en los recién nacidos es una patología causada por múltiples factores. Uno de ellos es la hipoxia aguda y/o crónica que altera los mecanismos que ocurren normalmente en la transición cardiovascular y respiratoria de feto a...
Pulmonary hypertension in newborns is a pathology caused by multiple factors. One of which is acute and / or chronic hypoxia that alters the mechanisms that normally occur in the cardiovascular and respiratory transition from fetus to newborn, phenomenon that occurs in gestations at great geographical altitudes or in lowland gestations with placental insufficiency. This generates an important vasoconstriction and arterial hypertension in the pulmonary circulation, remodeling of the pulmonary vessels, reduction of the vascular lumen and increasing the pulmonary vascular resistance, which can lead to right ventricular hypertrophy, and eventually heart failure and death. In addition, the efficacy and availability of current treatments is markedly limited. Atrial natriuretic peptide (ANP) is a cGMP-dependent vasodilator, so the aim of this study was to propose a therapy based on this peptide to reduce pulmonary arterial pulmonary pressure (mPAP) and pulmonary vascular resistance (PVR). For that, 14 lambs gestated and born in the highlands (3,600 m) of 3 or 4 days of age were catheterized under anesthesia, presenting high mPAP due to height. 2 lambs were used for dose testing. 6 patients were given 0.9% NaCl (controls) and another 6 were given ANP for 7 days, during which time the cardiopulmonary variables were evaluated daily. At the end of this period, the neonates underwent an episode of overhyped acute hypoxia assessing the drug's response to a hypoxic crisis. Animals treated daily with ANP showed an acute decrease in mPAP that remained after the infusion during the first 2 days of treatment. From the third day onwards the decrease was only significant during infusion period. In addition, chronic treatment with the drug produced an absence of pulmonary vasoconstriction during the episode of superimposed acute hypoxia. It is concluded that the ANP could be considered as a drug to be used in pulmonary hypertensive crises that occur in the pathology studied. However, a treatment option that will last as days go by should be looked for....
Pulmonary hypertension in newborns is a pathology caused by multiple factors. One of which is acute and / or chronic hypoxia that alters the mechanisms that normally occur in the cardiovascular and respiratory transition from fetus to newborn, phenomenon that occurs in gestations at great geographical altitudes or in lowland gestations with placental insufficiency. This generates an important vasoconstriction and arterial hypertension in the pulmonary circulation, remodeling of the pulmonary vessels, reduction of the vascular lumen and increasing the pulmonary vascular resistance, which can lead to right ventricular hypertrophy, and eventually heart failure and death. In addition, the efficacy and availability of current treatments is markedly limited. Atrial natriuretic peptide (ANP) is a cGMP-dependent vasodilator, so the aim of this study was to propose a therapy based on this peptide to reduce pulmonary arterial pulmonary pressure (mPAP) and pulmonary vascular resistance (PVR). For that, 14 lambs gestated and born in the highlands (3,600 m) of 3 or 4 days of age were catheterized under anesthesia, presenting high mPAP due to height. 2 lambs were used for dose testing. 6 patients were given 0.9% NaCl (controls) and another 6 were given ANP for 7 days, during which time the cardiopulmonary variables were evaluated daily. At the end of this period, the neonates underwent an episode of overhyped acute hypoxia assessing the drug's response to a hypoxic crisis. Animals treated daily with ANP showed an acute decrease in mPAP that remained after the infusion during the first 2 days of treatment. From the third day onwards the decrease was only significant during infusion period. In addition, chronic treatment with the drug produced an absence of pulmonary vasoconstriction during the episode of superimposed acute hypoxia. It is concluded that the ANP could be considered as a drug to be used in pulmonary hypertensive crises that occur in the pathology studied. However, a treatment option that will last as days go by should be looked for....
Rol de la hormona mineralorticoide aldosterona como modulador de la respuesta inmune adquirida
(Universisdad de Chile, 2008)
primario (PA)
ha sido atribuido tradicionalmente al desarrollo de hipertensión en respuesta a elevados
niveles de aldosterona plasmática. Sin embargo, estudios recientes han demostrado que
aldosterona promueve el daño vascular de manera independiente al...
La vía de señalización Rho/Rho-cinasa en la enfermedad y el remodelado cardiovascular
(Sociedad Española de Cardiología, 2005)
hipertensión arterial, la hipertensión pulmonar, el espasmo cerebral y coronario, la reestenosis postangioplastía y la disfunción eréctil....
El empleo como determinante social del acceso a tratamiento médico de adultos diagnosticados con hipertensión en Chile : un análisis longitudinal
(Universidad de Chile, 2016)
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El!empleo!como!determinante!social!del!acceso!a!
tratamiento!médico!de!adultos!diagnosticados!con!
hipertensión!en!Chile:!un!análisis!longitudinal!
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Tesis...
!determinante!de!carga!de!enfermedad!R!siendo!responsables!del!84%!de! la!pérdida!de!años!de!vida!(AVISA)!(5).!! ! Dentro!de!las!ENT!en!Chile!y!el!mundo,!la!hipertensión!arterial!se!define!como!una! de!las!principales!causas!de!morbimortalidad!y!como!uno!de!los!factores!de!riesgo! con...
!determinante!de!carga!de!enfermedad!R!siendo!responsables!del!84%!de! la!pérdida!de!años!de!vida!(AVISA)!(5).!! ! Dentro!de!las!ENT!en!Chile!y!el!mundo,!la!hipertensión!arterial!se!define!como!una! de!las!principales!causas!de!morbimortalidad!y!como!uno!de!los!factores!de!riesgo! con...