Carlos Quesada
Dr. Carlos Quesada is a board-certified physician in interventional cardiology, cardiovascular diseases, echocardiography, nuclear cardiology, cardiac computed tomography, vascular imaging, and internal medicine. He is currently a cardiology attending at Cedars-Sinai Medical Center and Cardiovascular Medical Group (Beverly Hills). Dr. Quesada earned his medical degree and graduated summa cum laude from Universidad La Salle (Mexico City) in 2007. As a medical student, he trained at the National Health Institutes, a group of public hospitals that provide high-level health care to the most underserved populations in Mexico. After medical school, he attended Baylor College of Medicine (Houston) and Albert Einstein College of Medicine (New York) to study the mechanisms responsible for orchestrating the healing response and the therapeutic targets for attenuation of adverse remodeling following cardiac injury. He also conducted research on genetic polymorphisms associated with cardiovascular diseases in the Mexican population. Dr. Quesada also completed a dual residency in internal medicine and global health equity at Brigham and Women’s Hospital (Boston), a Harvard teaching hospital. During this time, Dr. Quesada worked in Haiti, Rwanda, Mexico City, and Geneva. He also worked at the Harvard Global Equity Initiative supporting projects on noncommunicable diseases (NCDs). He co-founded Global Poverty Project 2030, a global initiative to support and promote the UN Sustainable Development Goals. In 2015, Dr. Quesada earned his M.P.H. degree from the Harvard T. H. Chan School of Public Health. In 2018, Dr. Quesada completed the Cardiovascular Disease Fellowship at the Ronald Reagan UCLA Medical Center (Los Angeles). He also completed the interventional and structural cardiology fellowship at the Mayo Clinic (Rochester). Dr. Quesada also serves as Editor-in-Chief of Guía EXARMED, a top general medicine treatise which aids in the training of medical students and primary care providers of lower- and middle-income regions within Mexico and Latin America.
Supervisors: Marco Antonio Martinez Rios, MD, FACC, FSCAI, Nikolaos G. Frangogiannis, MD, and Felicia M Knaul, PhD
Supervisors: Marco Antonio Martinez Rios, MD, FACC, FSCAI, Nikolaos G. Frangogiannis, MD, and Felicia M Knaul, PhD
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Papers by Carlos Quesada
-Heart failure in diabetics is associated with cardiac hypertrophy, fibrosis and diastolic dysfunction. Activation of transforming growth factor (TGF)-β/Smad3 signaling in the diabetic myocardium may mediate fibrosis and diastolic heart failure, while preserving matrix homeostasis. We hypothesized that Smad3 may play a key role in the pathogenesis of cardiovascular remodeling associated with diabetes and obesity.
METHODS AND RESULTS:
-We generated leptin-resistant db/db Smad3 null mice (dbSKO) and db/db Smad3 +/- animals (dbShet). Smad3 haploinsufficiency did not affect metabolic function in db/db mice, but protected from myocardial diastolic dysfunction, while causing left ventricular chamber dilation. Improved cardiac compliance and chamber dilation in dbShet animals was associated with decreased cardiomyocyte hypertrophy, reduced collagen deposition and accentuated matrix metalloproteinase (MMP) activity. Attenuation of hypertrophy and fibrosis in dbShet hearts was associated with reduced myocardial oxidative and nitrosative stress. dbSKO mice had reduced weight gain and decreased adiposity associated with attenuated insulin resistance, but also exhibited high early mortality, in part due to spontaneous rupture of the ascending aorta. Ultrasound studies showed that both lean and obese Smad3 null animals had significant aortic dilation. Aortic dilation in dbSKO mice occurred despite reduced hypertension, and was associated with perturbed matrix balance in the vascular wall.
CONCLUSIONS:
-Smad3 mediates diabetic cardiac hypertrophy, fibrosis and diastolic dysfunction, while preserving normal cardiac geometry and maintaining the integrity of the vascular wall.
KEYWORDS:
TGF-beta; cardiac remodeling; diabetic cardiomyopathy; fibrosis; obesity
METHODS AND RESULTS:
Wildtype and CXCR3 null mice underwent reperfused infarction protocols. CXCL10 was markedly induced in the infarct; in contrast, expression of the other two CXCR3 ligands, CXCL9 and CXCL11 was extremely low. CXCR3 loss did not affect scar size, geometric ventricular remodeling, collagen deposition, and systolic dysfunction of the infarcted heart. CXCR3 null mice had increased peak neutrophil recruitment and delayed myofibroblast infiltration in the infarcted heart, but exhibited comparable myocardial expression of pro-inflammatory cytokines and chemokines. In vitro, CXCL10 did not modulate Transforming Growth Factor (TGF)-β signaling, but inhibited basic fibroblast growth factor (bFGF)-induced cardiac fibroblast migration in both wildtype and CXCR3 null cells. Treatment of fibroblasts with heparinase and chondroitinase to cleave glycosaminoglycan chains abrogated the inhibitory effects of CXCL10 on cell migration.
CONCLUSIONS:
CXCR3 signaling does not critically regulate cardiac remodeling and dysfunction following myocardial infarction. The anti-fibrotic effects of CXCL10 in the healing infarct and in isolated cardiac fibroblasts are CXCR3-independent and may be mediated through proteoglycan signaling. Thus, administration of CXCR3-defective forms of CXCL10 may be an effective anti-fibrotic strategy in the remodeling myocardium without activating a potentially injurious, CXCR3-driven T cell response.
-Heart failure in diabetics is associated with cardiac hypertrophy, fibrosis and diastolic dysfunction. Activation of transforming growth factor (TGF)-β/Smad3 signaling in the diabetic myocardium may mediate fibrosis and diastolic heart failure, while preserving matrix homeostasis. We hypothesized that Smad3 may play a key role in the pathogenesis of cardiovascular remodeling associated with diabetes and obesity.
METHODS AND RESULTS:
-We generated leptin-resistant db/db Smad3 null mice (dbSKO) and db/db Smad3 +/- animals (dbShet). Smad3 haploinsufficiency did not affect metabolic function in db/db mice, but protected from myocardial diastolic dysfunction, while causing left ventricular chamber dilation. Improved cardiac compliance and chamber dilation in dbShet animals was associated with decreased cardiomyocyte hypertrophy, reduced collagen deposition and accentuated matrix metalloproteinase (MMP) activity. Attenuation of hypertrophy and fibrosis in dbShet hearts was associated with reduced myocardial oxidative and nitrosative stress. dbSKO mice had reduced weight gain and decreased adiposity associated with attenuated insulin resistance, but also exhibited high early mortality, in part due to spontaneous rupture of the ascending aorta. Ultrasound studies showed that both lean and obese Smad3 null animals had significant aortic dilation. Aortic dilation in dbSKO mice occurred despite reduced hypertension, and was associated with perturbed matrix balance in the vascular wall.
CONCLUSIONS:
-Smad3 mediates diabetic cardiac hypertrophy, fibrosis and diastolic dysfunction, while preserving normal cardiac geometry and maintaining the integrity of the vascular wall.
KEYWORDS:
TGF-beta; cardiac remodeling; diabetic cardiomyopathy; fibrosis; obesity
METHODS AND RESULTS:
Wildtype and CXCR3 null mice underwent reperfused infarction protocols. CXCL10 was markedly induced in the infarct; in contrast, expression of the other two CXCR3 ligands, CXCL9 and CXCL11 was extremely low. CXCR3 loss did not affect scar size, geometric ventricular remodeling, collagen deposition, and systolic dysfunction of the infarcted heart. CXCR3 null mice had increased peak neutrophil recruitment and delayed myofibroblast infiltration in the infarcted heart, but exhibited comparable myocardial expression of pro-inflammatory cytokines and chemokines. In vitro, CXCL10 did not modulate Transforming Growth Factor (TGF)-β signaling, but inhibited basic fibroblast growth factor (bFGF)-induced cardiac fibroblast migration in both wildtype and CXCR3 null cells. Treatment of fibroblasts with heparinase and chondroitinase to cleave glycosaminoglycan chains abrogated the inhibitory effects of CXCL10 on cell migration.
CONCLUSIONS:
CXCR3 signaling does not critically regulate cardiac remodeling and dysfunction following myocardial infarction. The anti-fibrotic effects of CXCL10 in the healing infarct and in isolated cardiac fibroblasts are CXCR3-independent and may be mediated through proteoglycan signaling. Thus, administration of CXCR3-defective forms of CXCL10 may be an effective anti-fibrotic strategy in the remodeling myocardium without activating a potentially injurious, CXCR3-driven T cell response.
Cardiac fibroblasts are key effector cells in the pathogenesis of cardiac fibrosis. Transforming growth factor (TGF)-beta/Smad3 signaling is activated in the border zone of healing infarcts and induces fibrotic remodeling of the infarcted ventricle contributing to the development of diastolic dysfunction.
OBJECTIVE:
The present study explores the mechanisms responsible for the fibrogenic effects of Smad3 by dissecting its role in modulating cardiac fibroblast phenotype and function.
METHODS AND RESULTS:
Smad3 null mice and corresponding wild-type controls underwent reperfused myocardial infarction protocols. Surprisingly, reduced collagen deposition in Smad3-/- infarcts was associated with increased infiltration with myofibroblasts. In vitro studies demonstrated that TGF-beta1 inhibited murine cardiac fibroblast proliferation; these antiproliferative effects were mediated via Smad3. Smad3-/- fibroblasts were functionally defective, exhibiting impaired collagen lattice contraction when compared with wild-type cells. Decreased contractile function was associated with attenuated TGF-beta-induced expression of alpha-smooth muscle actin. In addition, Smad3-/- fibroblasts had decreased migratory activity on stimulation with serum, and exhibited attenuated TGF-beta1-induced upregulation of extracellular matrix protein synthesis. Upregulation of connective tissue growth factor, an essential downstream mediator in TGF-beta-induced fibrosis, was in part dependent on Smad3. Connective tissue growth factor stimulation enhanced extracellular matrix protein expression by cardiac fibroblasts in a Smad3-independent manner.
CONCLUSIONS:
Disruption of Smad3 results in infiltration of the infarct with abundant hypofunctional fibroblasts that exhibit impaired myofibroblast transdifferentiation, reduced migratory potential, and suppressed expression of fibrosis-associated genes."
2a. edición; 2013
ISBN 978607443353-1
Intersistemas
La obra está dividida en 22 áreas de conocimiento indispensable cuyos conceptos están distribuidos aleatoriamente con el fin de simular y adiestrar al lector de la forma más cercana a un examen real. Esta aleatoriedad ayuda a evitar que el lector conozca la respuesta correcta sólo por simple correlación de palabras o temas adyacentes. Ventajas: a) obtener una mejor comprensión de los temas en los que muestras fortalezas o debilidades; b) realizar un repaso de "última hora" antes del Examen; c) conocer los signos y síntomas de los pacientes clásicos "de examen"; d) mejorar tu participación en los interrogatorios habituales del "pase de visita"; e) utilizar mejor tu memoria para los conceptos que realmente importan (diagnóstico y tratamiento de primera elección), sobre otros menos relevantes para exámenes.
4a. edición; 2013
21 x 27 cm; Pasta dura
Intersistemas
Su objetivo sigue siendo apoyar a los médicos que se preparan para el examen de ingreso al entrenamiento en residencias médica. Los autores son médicos que recientemente obtuvieron los más altos puntajes en el Examen Nacional de Aspirantes a Residencias Médicas (ENARM®)
Algunas actualizaciones en esta edición 2013:
Cardiología:
Actualización de los capítulos referentes a los síndromes coronarios agudos (infarto miocárdico con y sin elevación del segmento ST) conforme a las más recientes recomendaciones de la American Heart Association
Refinamiento de los lineamientos y algoritmos de reanimación cardiovascular en pacientes pediátricos y adultos
Novedades en el diagnóstico y manejo de pacientes en endocarditis y enfermedades venosas
Neumología:
Las recomendaciones más recientes de la Global Initiative for Asthma (GINA)
Infectología:
Nueva definición de fiebre de origen a determinar y esquema diagnóstico, así como las causas más frecuentes en México
Otorrinolaringología:
Actualizaciones en temas como sinusitis, rinitis alérgica, fracturas nasales y neoplasias benignas y malignas
Pediatría:
Reestructuración y expansión de la información referente a crecimiento y desarrollo