Browsing by Author "Cordova Alvestegui, Samuel Edmundo"

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    Angiotensin I-converting enzyme insertion/deletion polymorphism and adrenergic response to exercise in hypertensive patients.
    (2002) Braun Jones, Vivian Sandra; Chamorro Spikin, Gastón Alberto; Cordova Alvestegui, Samuel Edmundo; Fardella Bello, Carlos Enrique; Jalil Milad, Jorge Emilio; Lavandero, Sergio; Ocaranza Jeraldino, María Paz; Schumacher, Erwin
    BackgroundThe insertion/deletion ACE polymorphism (ACE I/D) regulates different levels of circulating and tissue ACE activities, which may induce diverse adrenergic responses to physiological stimuli. The aim of this study was to evaluate the influence of
  • Thumbnail Image
    Item
    New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review
    (2024) Jalil Milad, Jorge Emilio; Gabrielli Nervi, Luigi Arnaldo; Ocaranza Jeraldino, María Paz; MacNab, P.; Fernandez R.; Grassi Corrales, Bruno; Jofré Mendoza, Paulina Eugenia; Verdejo, H.; Acevedo, M.; Cordova Alvestegui, Samuel Edmundo; Sanhueza, Luis; Greig Undurraga, Douglas Patrick
    This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.
  • Thumbnail Image
    Item
    Reverse Remodeling in Human Heart Failure after Cardiac Resynchronization Therapy Is Associated With Reduced RHO-Kinase Activation
    (2021) Ocaranza Jeraldino, Maria Paz; Jalil Milad, Jorge Emilio; Altamirano Assad, Rodrigo Patricio; De León Soto, Ana María; Moya López, Jackeline Trinidad; Lonis Álvarez, María Alejandra; Gabrielli Nervi, Luigi Arnaldo; Mac Nab, Paul; Cordova Alvestegui, Samuel Edmundo; Paredes, Alejandro; Vergara Saavedra, Ismael Antonio; Bittner Braemer, Alex Gerhard; Sabat Sarras, Karime Alejandra; Pastorini, Karla
    ["Background: Reverse remodeling is a clinically relevant endpoint in heart failure with reduced ejection fraction (HFrEF). Rho-kinase (ROCK) signaling cascade activation correlates with cardiac remodeling and left ventricular (LV) systolic dysfunction in HFrEF patients. Cardiac resynchronization therapy (CRT) is effective in HFrEF, especially when there is a left bundle block, as this treatment may stimulate reverse remodeling, thereby improving quality of life and prolonging survival for patients with this severe condition. Here, we evaluate the hypothesis that ROCK activation is reduced after effective CRT in HFrEF.", "Methods: ROCK activation in circulating leukocytes was evaluated in 28 HFrHF patients, using Western blot (myosin light chain phosphatase subunit 1 phosphorylation, MYPT1p/t), before and three months after initiation of CRT. LV systolic function and remodeling were assessed by echocardiography.", "Results: Three months after CRT, LV ejection fraction increased an average of 14.5% (p < 0.001) in 13 patients (responders), while no change was observed in 15 patients (non-responders). End-systolic diameter decreased 16% (p < 0.001) in responders, with no change in non-responders. ROCK activation in PBMCs decreased 66% in responders (p < 0.05) but increased 10% in non-responders (NS). LV end-diastolic diameter was also 5.2 mm larger in non-responders vs. responders (p = 0.058). LV ejection fraction, systolic diameter, and ROCK activation levels were similar in both groups at baseline.", "Conclusion: In HFrEF patients, 3 months of effective CRT induced reverse myocardial remodeling, and ROCK activation was significantly decreased in circulating leukocytes. Thus, decreased ROCK activation in circulating leukocytes may reflect reverse cardiac remodeling in patients with heart failure."]