Presentation of a case with Wellens syndrome

This case report is about a 56-year-old male, farm worker with a history of being a smoker and suffering from high blood pressure, who was admitted at the Cardiology Care Department with the diagnosis of coronary artery disease –unstable angina–, because of chest pain related to physical effort and changes in the appearance threshold. Rest-electrocardiogram, painless, shows deep, symmetric negative T waves in anterior wall, without enzyme elevation; but during admission the patient evolves quickly, clinically and electrically, to an extensive anterior wall acute myocardial infarction, without responding to the fibrinolytic reperfusion therapy, and showing a ventricular tachycardia degenerating into ventricular fibrillation. There was no response to the maneuvers of cardiovascular resuscitation, thus, he dies. It is diagnosed postmortem as a Wellens syndrome, because necropsy showed severe atherosclerotic disease of the proximal segment of the left anterior descending coronary artery with extensive anterior transmural infarction

Anais do V Encontro Brasileiro de Educomunicação: Educação midiática e políticas públicas

A presente coletânea, que chega ao público através de um suporte digital, tem como objetivo disponibilizar os papers, bem como os relatos de experiências educomunicativas apresentados durante o V ENCONTRO BRASILEIRO DE EDUCOMUNICAÇÃO, que teve como tema central: “Educação Midiática e Políticas Públicas”. O evento foi realizado em São Paulo, entre 19 e 21 de setembro de 2013, a partir de uma parceria entre o NCE/USP - Núcleo de Comunicação e Educação da USP, a Licenciatura em Educomunicação da ECA/USP, a ABPEducom – Associação Brasileira de Pesquisadores e Profissionais da Educomunicação e a FAPCOM – Faculdade Paulus de Tecnologia e Comunicação, que ofereceu seu campus, na Vila Mariana, para os atos do evento. Os presentes anais disponibilizam o texto de abertura, de autoria do coordenador geral do evento, denominado “Educação midiática e políticas públicas: vertentes históricas da emergência da Educomunicação na América Latina”. Na sequência, apresentam 61 papers sobre aspectos específicos da temática geral, resultantes de pesquisas na área, seguidos de 27 relatos de práticas educomunicativas, em nível nacional

Osteopontin & β2-adrenergic receptor signaling in cardiac fibrosis

Objective: Test the role of osteopontin in anti-fibrotic β2AR signaling in cardiac myocytes. Background: Cardiac β2-adrenergic receptors (ARs) are known to inhibit collagen production and fibrosis in cardiac fibroblasts and myocytes. β2AR is a Gs protein-coupled receptor (GPCR) and, upon its activation, stimulates generation of cyclic 3`, 5`-adenosine monophosphate (cAMP). cAMP has two effectors: protein kinase A (PKA) and the exchange protein directly activated by cAMP (Epac). Epac1 inhibits cardiac fibroblast activation and fibrosis. Osteopontin (OPN) is a ubiquitous pro-inflammatory and pro-fibrotic cytokine, including in the heart. Methods: We used the H9c2 cardiac myocyte cell line & the real-time qPCR, co-immunoprecipitation/western blotting, and ELISA techniques. Results: The cardiotoxic hormone aldosterone upregulates OPN via the mineralocorticoid receptor (MR) in H9c2 cardiomyocytes. This is prevented by β2AR-activated GPCR-kinase (GRK)-5. GRK5 directly phosphorylates and inhibits the MR in cardiomyocytes. Additionally, CRISPR-mediated OPN deletion enhances β AR-dependent cAMP generation in H9c2 cardiomyocytes and upregulates Epac1. OPN deletion also enables the β AR to completely abrogate transforming growth factor (TGF)-β-dependent fibrosis in H9c2 cardiomyocytes. Mechanistically, OPN interacts with Gsa subunits to facilitate recruitment of GRK2, the major GRK phosphorylating and desensitizing the cardiac β2AR. This, in turn, augments the GRK2-dependent functional desensitization of the β2AR, thereby opposing this receptor`s anti-fibrotic cAMP/Epac1 signaling. Conclusion: We have uncovered a direct inhibitory effect of OPN in cardiac β2AR`s anti-fibrotic signaling via facilitation of GRK2-mediated receptor desensitization. Thus, OPN blockade could be of value in the treatment and/or prevention of cardiac fibrosis. Grants: PFRDG FY2018-19 #33546

Infarto agudo de miocardio después de la administración subcutánea de sumatriptán

Sumatriptan is a drug used for migraine which can produce coronary vasoconstriction. The case of a 50-year-old male with no history of cardiovascular disease who suffered an acute myocardial infarction, of non-atherosclerotic cause, as a result of the subcutaneous administration of this drug is reported. The patient did not show complications after drug withdrawal.El sumatriptán es un medicamento que se utiliza para la migraña y puede producir vasoconstricción coronaria. Se presenta un caso con infarto agudo de miocardio de causa no ateroesclerótica, secundaria a la administración subcutánea de este fármaco, en un hombre de 50 años de edad, sin antecedentes de enfermedad cardiovascular. El paciente evolucionó sin complicaciones después de la retirada del sumatriptán

Muerte súbita en paciente con síndrome LEOPARD

LEOPARD or Moynahan syndrome, also called multiple lentigines, is a rare genetic disease which causes multiple visceral abnormalities, including heart abnormalities, and may trigger sudden death. The case of a 26-year-old woman with a history of hypertrophic cardiomyopathy since early childhood is reported. She was referred to consultation due to loss of consciousness, associated with moderate exertion, and a resuscitated sudden death episode. The study revealed the presence of LEOPARD syndrome with subvalvular pulmonary stenosis and left ventricular hypertrophic cardiomyopathy, both of which cause sudden cardiac death.El síndrome LEOPARD o de Moynahan, también llamado lentiginosis múltiple, es una rara enfermedad de origen genético que origina múltiples anomalías viscerales, que incluye al corazón, y puede ser causa de muerte súbita. Se presenta el caso de una mujer de 26 años de edad, con antecedentes de miocardiopatía hipertrófica diagnosticada desde la infancia temprana que es remitida por pérdida de la conciencia relacionada con esfuerzos físicos moderados y muerte súbita recuperada. El estudio demostró la presencia de un síndrome LEOPARD con estenosis pulmonar subvalvular y miocardiopatía hipertrófica del ventrículo izquierdo como causa de la muerte súbita de origen cardíaco

Presentación de un caso con síndrome de Wellens

This case report is about a 56-year-old male, farm worker with a history of being a smoker and suffering from high blood pressure, who was admitted at the Cardiology Care Department with the diagnosis of coronary artery disease –unstable angina–, because of chest pain related to physical effort and changes in the appearance threshold. Rest-electrocardiogram, painless, shows deep, symmetric negative T waves in anterior wall, without enzyme elevation; but during admission the patient evolves quickly, clinically and electrically, to an extensive anterior wall acute myocardial infarction, without responding to the fibrinolytic reperfusion therapy, and showing a ventricular tachycardia degenerating into ventricular fibrillation. There was no response to the maneuvers of cardiovascular resuscitation, thus, he dies. It is diagnosed postmortem as a Wellens syndrome, because necropsy showed severe atherosclerotic disease of the proximal segment of the left anterior descending coronary artery with extensive anterior transmural infarction.Se presenta el caso de un varón de 56 años de edad, obrero agrícola, con antecedentes de ser fumador y padecer de hipertensión arterial; que ingresa en el Servicio de Cardiología con el diagnóstico de cardiopatía isquémica –angina inestable–, por presentar dolor precordial relacionado con el esfuerzo físico y cambios en su umbral de aparición. El electrocardiograma en reposo, sin dolor, muestra ondas T negativas profundas, simétricas, en cara anterior, sin elevación enzimática; y durante el ingreso evoluciona de forma rápida, clínica y eléctricamente, a un infarto agudo de miocardio anterior extenso, sin respuesta a la terapia de reperfusión con fibrinolíticos, y aparición de una taquicardia ventricular que degenera en fibrilación ventricular, sin respuesta a las maniobras de reanimación cardiovascular, por lo que fallece. Se diagnostica post mortem como un síndrome de Wellens, pues la necropsia demostró enfermedad aterosclerótica grave del segmento proximal de la arteria coronaria descendente anterior con infarto transmural anterior extenso

Fragmentación del QRS y muerte súbita en paciente con displasia arritmogénica del ventrículo derecho

The arrhythmogenic right ventricular dysplasia or cardiomyopathy is a genetic heart disease whose diagnosis is often a challenge for the clinician. It is one of the most common causes of sudden cardiac death in adolescence and in young adults. We present the case of a patient with a history of malignant ventricular arrhythmias and recovered sudden cardiac death due to arrhythmogenic right ventricular dysplasia, with QRS fragmentation in the right precordial leads, as a marker of the presence of a suitable substrate for the emergence of spontaneous ventricular fibrillation. The pathogenesis, diagnosis and treatment of this disease are discussed.La miocardiopatía o displasia arritmogénica del ventrículo derecho es una cardiopatía de origen genético cuyo diagnóstico supone, a menudo, un reto para el clínico. Es una de las causas más comunes de muerte súbita cardíaca en la adolescencia y en los adultos jóvenes. Se presenta el caso de un paciente con historia de arritmias ventriculares malignas y de muerte súbita cardíaca recuperada, por displasia arritmogénica del ventrículo derecho, con fragmentación del QRS en las derivaciones precordiales derechas, como marcador de la presencia de un sustrato propicio para el surgimiento de la fibrilación ventricular espontánea. Se comenta la patogenia, el diagnóstico y el tratamiento de esta enfermedad