Browsing by Author "Verdejo, Hugo E."

Now showing 1 - 9 of 9
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    Comparison of a radiofrequency-based wireless pressure sensor to Swan-Ganz catheter and echocardiography for ambulatory assessment of pulmonary artery pressure in heart failure
    (ELSEVIER SCIENCE INC, 2007) Verdejo, Hugo E.; Castro, Pablo F.; Concepcion, Roberto; Ferrada, Marcela A.; Alfaro, Mario A.; Alcaino, Milton E.; Deck, Carlos C.; Bourge, Robert C.
    Objectives The goal of this work was to evaluate the accuracy of a new heart failure (HF) sensor (HFS) (Heart Failure Sensor, CardioMEMS Inc., Atlanta, Georgia) pulmonary artery pressure (PAP) monitoring compared with Swan-Ganz (SG) (Hospira, Inc., Lake Forest, Illinois) catheterization and echocardiography (ECHO) in ambulatory HIF patients.
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    Galectin-3 Promotes Pro-Hypertrophic Communication Between Fibroblasts and Cardiomyocytes
    (LIPPINCOTT WILLIAMS & WILKINS, 2017) Bustamante, Mario; Oyarzun, Ingrid; Mancilla, Georthan; Quiroga, Clara; Verdejo, Hugo E.; Castro, Pablo
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    Impaired cardiac autophagy in patients developing postoperative atrial fibrillation
    (MOSBY-ELSEVIER, 2012) Garcia, Lorena; Verdejo, Hugo E.; Kuzmicic, Jovan; Zalaquett, Ricardo; Gonzalez, Sergio; Lavandero, Sergio; Corbalan, Ramon
    Objectives: Postoperative atrial fibrillation (POAF) is a common complication after on-pump heart surgery. Several histologic abnormalities, such as interstitial fibrosis and vacuolization, have been described in atrial samples from patients developing POAF. This ultrastructural remodeling has been associated with the establishment of a proarrhythmic substrate. We studied whether atrial autophagy is activated in patients who develop POAF.
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    Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress
    (COMPANY BIOLOGISTS LTD, 2011) Bravo, Roberto; Miguel Vicencio, Jose; Parra, Valentina; Troncoso, Rodrigo; Pablo Munoz, Juan; Bui, Michael; Quiroga, Clara; Rodriguez, Andrea E.; Verdejo, Hugo E.; Ferreira, Jorge; Iglewski, Myriam; Chiong, Mario; Simmen, Thomas; Zorzano, Antonio; Hill, Joseph A.; Rothermel, Beverly A.; Szabadkai, Gyorgy; Lavandero, Sergio
    Increasing evidence indicates that endoplasmic reticulum (ER) stress activates the adaptive unfolded protein response (UPR), but that beyond a certain degree of ER damage, this response triggers apoptotic pathways. The general mechanisms of the UPR and its apoptotic pathways are well characterized. However, the metabolic events that occur during the adaptive phase of ER stress, before the cell death response, remain unknown. Here, we show that, during the onset of ER stress, the reticular and mitochondrial networks are redistributed towards the perinuclear area and their points of connection are increased in a microtubule-dependent fashion. A localized increase in mitochondrial transmembrane potential is observed only in redistributed mitochondria, whereas mitochondria that remain in other subcellular zones display no significant changes. Spatial re-organization of these organelles correlates with an increase in ATP levels, oxygen consumption, reductive power and increased mitochondrial Ca2+ uptake. Accordingly, uncoupling of the organelles or blocking Ca2+ transfer impaired the metabolic response, rendering cells more vulnerable to ER stress. Overall, these data indicate that ER stress induces an early increase in mitochondrial metabolism that depends crucially upon organelle coupling and Ca2+ transfer, which, by enhancing cellular bioenergetics, establishes the metabolic basis for the adaptation to this response.
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    Insulin Stimulates Mitochondrial Fusion and Function in Cardiomyocytes via the Akt-mTOR-NF kappa B-Opa-1 Signaling Pathway
    (AMER DIABETES ASSOC, 2014) Parra, Valentina; Verdejo, Hugo E.; Iglewski, Myriam; del Campo, Andrea; Troncoso, Rodrigo; Jones, Deborah; Zhu, Yi; Kuzmicic, Jovan; Pennanen, Christian; Lopez Crisosto, Camila; Jana, Fabian; Ferreira, Jorge; Noguera, Eduard; Chiong, Mario; Bernlohr, David A.; Klip, Amira; Hill, Joseph A.; Rothermel, Beverly A.; Abel, Evan Dale; Zorzano, Antonio; Lavandero, Sergio
    Insulin regulates heart metabolism through the regulation of insulin-stimulated glucose uptake. Studies have indicated that insulin can also regulate mitochondrial function. Relevant to this idea, mitochondrial function is impaired in diabetic individuals. Furthermore, the expression of Opa-1 and mitofusins, proteins of the mitochondrial fusion machinery, is dramatically altered in obese and insulin-resistant patients. Given the role of insulin in the control of cardiac energetics, the goal of this study was to investigate whether insulin affects mitochondrial dynamics in cardiomyocytes. Confocal microscopy and the mitochondrial dye MitoTracker Green were used to obtain three-dimensional images of the mitochondrial network in cardiomyocytes and L6 skeletal muscle cells in culture. Three hours of insulin treatment increased Opa-1 protein levels, promoted mitochondrial fusion, increased mitochondrial membrane potential, and elevated both intracellular ATP levels and oxygen consumption in cardiomyocytes in vitro and in vivo. Consequently, the silencing of Opa-1 or Mfn2 prevented all the metabolic effects triggered by insulin. We also provide evidence indicating that insulin increases mitochondrial function in cardiomyocytes through the Akt-mTOR-NFB signaling pathway. These data demonstrate for the first time in our knowledge that insulin acutely regulates mitochondrial metabolism in cardiomyocytes through a mechanism that depends on increased mitochondrial fusion, Opa-1, and the Akt-mTOR-NFB pathway.
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    Left Atrial Dysfunction Is a Predictor of Postcoronary Artery Bypass Atrial Fibrillation: Association of Left Atrial Strain and Strain Rate Assessed by Speckle Tracking
    (WILEY, 2011) Gabrielli, Luigi; Corbalan, Ramon; Cordova, Samuel; Enriquez, Andres; Mc Nab, Paul; Verdejo, Hugo E.; Godoy, Ivan; Zalaquett, Ricardo; Lavandero, Sergio
    Background: Even though atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass grafting (CABG), its etiology remains poorly understood. Several factors are linked to postoperative AF (POAF), including advanced age and systemic inflammation. However, left atrial (LA) contractile dysfunction has not been evaluated in the perioperative scenario. Aim: To evaluate LA function through strain and strain rate in patients with coronary artery disease undergoing CABG and its correlation with POAF. Methods: We studied 70 patients undergoing CABG in sinus rhythm at the time of surgery. Preoperative echocardiography with evaluation of LA strain and strain rate by speckle tracking was performed. The occurrence of POAF was evaluated by continuous monitoring. Baseline and postoperative C-reactive protein (CRP) levels were measured to evaluate systemic inflammation. Results: After 1-week follow-up 26% of subjects developed AF. LA strain s wave (LASs) and LA strain rate s (LASRs) and a wave (LASRa) were significantly decreased in patients who developed POAF: LASs (10 +/- 1% vs. 24 +/- 1%, P < 0.001), LASRs (0.6 +/- 0.1 sec1 vs. 1.2 +/- 0.1 sec-1, P < 0.001), LASRa (-0.6 +/- 0.1 sec1 vs. 1.8 +/- 0.1 sec-1, P < 0.001). LASRs, LASRa, age, and LA volume were independent predictors of POAF. CRP at baseline was similar irrespective of POAF development. Conclusions: LA dysfunction, evaluated by strain and strain rate is an independent predictor of POAF and contributes to classic risk factors like age and atrial volume. (Echocardiography 2011;28:1104-1108)
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    Mitochondrial Dynamics: a Potential New Therapeutic Target for Heart Failure
    (EDICIONES DOYMA S A, 2011) Kuzmicic, Jovan; del Campo, Andrea; Lopez Crisosto, Camila; Morales, Pablo E.; Pennanen, Christian; Bravo Sagua, Roberto; Hechenleitner, Jonathan; Zepeda, Ramiro; Castro, Pablo F.; Verdejo, Hugo E.; Parra, Valentina; Chiong, Mario; Lavandero, Sergio
    Mitochondria are dynamic organelles able to vary their morphology between elongated interconnected mitochondrial networks and fragmented disconnected arrays, through events of mitochondrial fusion and fission, respectively. These events allow the transmission of signaling messengers and exchange of metabolites within the cell. They have also been implicated in a variety of biological processes including embryonic development, metabolism, apoptosis, and autophagy. Although the majority of these studies have been confined to noncardiac cells, emerging evidence suggests that changes in mitochondrial morphology could participate in cardiac development, the response to ischemia-reperfusion injury, heart failure, and diabetes mellitus. In this article, we review how the mitochondrial dynamics are altered in different cardiac pathologies, with special emphasis on heart failure, and how this knowledge may provide new therapeutic targets for treating cardiovascular diseases. Full English text available from: www.revespcardiol.org (C) 2011 Sociedad Espanola de Cardiologia. Published by Elsevier Espana, SI. All rights reserved.
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    Predictors of acute coronary syndrome without ST segment elevation and risk stratification in the chest pain unit
    (SOC MEDICA SANTIAGO, 2008) Gabrielli, Luigi A.; Castro, Pablo F.; Verdejo, Hugo E.; McNab, Paul A.; Llevaneras, Silvana A.; Mardonez, Jose M.; Corbalan, Ramon L.
    Background: Nearly 10016 of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis. Aim: To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit. Material and methods: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression. Results: In a four years period, 1,168 patients aged 62 +/- 23 years (69% males), were studied. After initial evaluation, 62% of the patients were admitted to the hospital for further testing and in 71% of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated With a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95% confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95% CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95% CI 1.25-2.69), age over 65 years (OR 1. 73, 95% CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95% CI 3.72-8.29). Conclusions: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection (Rev Med Chile 2008; 136: 442-50).
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    Xanthine-oxidase inhibitors and statins in chronic heart failure: Effects on vascular and functional parameters
    (ELSEVIER SCIENCE INC, 2011) Greig, Douglas; Alcaino, Hernan; Castro, Pablo F.; Garcia, Lorena; Verdejo, Hugo E.; Navarro, Mario; Lopez, Rafael; Mellado, Rosemarie; Tapia, Fabiola; Gabrielli, Luigi A.; Nogerol, Camilo; Chiong, Mario; Godoy, Ivan; Lavandero, Sergio
    BACKGROUND: Increased oxidative stress in heart failure (HF) leads to inflammation and endothelial dysfunction (ED). Both statins and allopurinol have known anti-oxidant properties, but their utility in HF has not been fully assessed.