Liraglutide provides cardioprotection through the recovery of mitochondrial dysfunction and oxidative stress in aging hearts

Glucagon-like peptide-1 receptor (GLP-1R) agonists improve cardiovascular dysfunction via the pleiotropic effects behind their receptor action. However, it is unknown whether they have a cardioprotective action in the hearts of the elderly. Therefore, we examined the effects of GLP-1R agonist liraglutide treatment (LG, 4 weeks) on the systemic parameters of aged rats (24-month-old) compared to those of adult rats (6-month-old) such as electrocardiograms (ECGs) and systolic and diastolic blood pressure (SBP and DBP). At the cellular level, the action potential (AP) parameters, ionic currents, and Ca2+ regulation were examined in freshly isolated ventricular cardiomyocytes. The LG treatment of aged rats significantly ameliorated the prolongation of QRS duration and increased both SBP and DBP together with recovery in plasma oxidant and antioxidant statuses. The prolonged AP durations and depolarized membrane potentials of the isolated cardiomyocytes from the aged rats were normalized via recoveries in K+ channel currents with LG treatment. The alterations in Ca2+ regulation including leaky-ryanodine receptors (RyR2) could be also ameliorated via recoveries in Na+/Ca2+ exchanger currents with this treatment. A direct LG treatment of isolated aged rat cardiomyocytes could recover the depolarized mitochondrial membrane potential, the increase in both reactive oxygen and nitrogen species (ROS and RNS), and the cytosolic Na+ level, although the Na+ channel currents were not affected by aging. Interestingly, LG treatment of aged rat cardiomyocytes provided a significant inhibition of activated sodium-glucose co-transporter-2 (SGLT2) and recoveries in the depressed insulin receptor substrate 1 (IRS1) and increased protein kinase G (PKG). (AU)

USP13 reduces septic mediated cardiomyocyte oxidative stress and inflammation by inducing Nrf2

Background: Sepsis is a common cardiovascular complication that can cause heart damage. The regulatory role of ubiquitin-specific peptidase 13 (USP13) on erythroid 2–related factor 2 (Nrf2) has been reported, but its regulatory role in septic cardiomyopathy remains unclear. Methods: The Sprague Dawley (SD) rat model of septic myocardial injury was constructed by lipopolysaccharides (LPS). The serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels were detected, the mRNA and protein expression levels of Nrf2 and USP13 in tissues were detected by real-time quantitative reverse transcription PCR (qRT-PCR) and western blot (WB), and the expression of USP13 at the treatment time of 3 h, 6 h, and 12 h was also detected. The cell viability and USP13, Nrf-2 and heme oxygenase-1 (HO-1) expression levels of H9C2-treated cells by LPS and the oxidative stress level and inflammatory response of H9C2 cells were detected by enzyme-linked immunosorbent assay (ELISA) and WB. Results: The results showed that USP13 was downregulated in septic myocardial injury tissues, and the Nrf2 level was increased in vitro after the cells were treated with LPS. Overexpression of USP13 further induced Nrf2 to reduce apoptosis, oxidative stress, and expression of inflammatory factors. Conclusion: In conclusion, this study demonstrated that USP13 was downregulated in septic myocardial injury tissues, and USP13 overexpression increased Nrf2 levels and reduced apoptosis. Further studies showed that USP13 reduced LPS-induced oxidative stress and inflammation by inducing Nrf2 (AU)

RBM3 interacts with Raptor to regulate autophagy and protect cardiomyocytes from ischemia–reperfusion-induced injury

Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality worldwide. However, postinfarction pathogenesis remains unclear, and it is particularly important to identify new therapeutic targets. The RNA-binding motif protein RBM3 (also known as cold-inducible protein) is known to promote translation and is associated with tumor proliferation and neuroprotection. However, little is known about the biological effects of RBM3 on myocardial infarction. In the present study, we found that RBM3 expression was significantly upregulated in ischemia–reperfusion (I/R) condition and downregulation of RBM3 inhibited autophagy and promoted apoptosis in cardiomyocytes. We confirmed that RBM3 interacts with Raptor to regulate the autophagy pathway. Taken together, these findings illustrate the protective effects of RBM3 against I/R-induced myocardial apoptosis through the autophagy pathway. (AU)

Cordycepin alleviates myocardial ischemia/reperfusion injury by enhancing autophagy via AMPK-mTOR pathway

To estimate the cardioprotective mechanism of cordycepin on myocardial ischemia/reperfusion (I/R) injury. The left anterior descending artery of mice was ligated transiently to establish the myocardial I/R model. TTC/Evans Blue staining and TUNEL assay were performed to quantify the infarct size and apoptosis index. The cardiac function was evaluated by echocardiography. Neonatal rat ventricular cardiomyocytes (NRVCs) underwent hypoxia and reoxygenation (H/R). MTS and LDH were detected to measured cell viability and necrosis respectively. The results suggested that cordycepin could markedly decrease apoptosis, reduce infarct size, and improve cardiac function in mice subjected to I/R injury, alongside with enhanced autophagy. In NRVCs, cordycepin treatment obviously reduced ROS production. In addition, cordycepin partly promoted autophagy in the context of H/R injury by regulating AMPK/mTOR pathway. Our data demonstrated that cordycepin exerts cardio-protective effect and promotes cardiac functional recovery following myocardial I/R by enhancing autophagy via AMPK-mTOR signaling pathway. (AU)

Acute effects of swimming aerobic exercise on contractility and intracellular calcium handling in isolated right ventricular cardiomyocytes / Efectos agudos del ejercicio de natación aeróbica sobre la contractilidad y el manejo del calcio intracelular en cardiomiocitos aislados del ventrículo derecho / Efeitos agudos do exercício aeróbio de natação na contratilidade e no transiente de cálcio intracelular em cardiomiócitos isolados do ventrículo direito

Objectives: The acute adjustments on the contractile function and the intracellular calcium (Ca2+) handling in the cardiomyocytes of the right ventricle (RV) after an acute aerobic exercise session are not known. Our aim was to investigate the acute responses of the contractile function and the intracellular Ca2+ handling in isolated RV cardiomyocytes after a swimming exercise session.Methods: Ten-week-old female Wistar rats were randomly allocated into two groups: control (C; n = 5) and exercise (Ex; n = 7). It was performed a swimming exercise session for 30 minutes. with an overload of 4% relative to the body weight attached to the tail. The rats were sacrificed after the exercise session for the analysis of the RV contractile function parameters and the intracellular Ca2+ handling by the isolated cardiomyocyte technique.Results: Body and heart weights, as well as sarcomere length were similar between the groups. Also, it was not observed differences between the groups for RV cardiomyocyte contractile parameters. However, the systolic and diastolic intracellular Ca2+ concentration was significantly lower in the Ex group compared to C with maintenance of Ca2+ amplitude.Conclusion: An acute swimming aerobic exercise session promotes cardiomyocyte contractility maintenance even with systolic and diastolic intracellular Ca2+ concentration reduced in the RV cardiomyocytes, reflecting an improvement in the intracellular Ca2+ handling.(AU)

Objetivos: se desconocen los ajustes agudos de la función contráctil y el manejo del calcio (Ca2+) intracelular en los cardiomiocitos del ventrículo derecho (VD) tras una sesión de ejercicio aeróbico agudo. Nuestro objetivo fue investigar las respuestas agudas de la función contráctil y el manejo del Ca2+ intracelular en cardiomiocitos aislados del VD después de una sesión de ejercicio de natación.Métodos: se asignaron al azar ratas Wistar hembra de diez semanas de edad en dos grupos: control (C; n = 5) y ejercicio (Ex; n = 7). Se realizó una sesión de ejercicios de natación durante 30 minutos con una sobrecarga del 4% con respecto al peso corporal adherido a la cola. Las ratas fueron sacrificadas después de la sesión de ejercicio para el análisis de los parámetros de la función contráctil del VD y el manejo del Ca2+ intracelular mediante la técnica de cardiomiocitos aislados.Resultados: los pesos corporales y cardíacos, así como la longitud del sarcómero, fueron similares entre los grupos. Además, no se observaron diferencias entre los grupos para los parámetros contráctiles de los cardiomiocitos del VD. Sin embargo, la concentración de Ca2+ intracelular sistólica y diastólica fue significativamente menor en el grupo Ex en comparación con C con el mantenimiento de la amplitud de Ca2+.Conclusión: Una sesión de ejercicio aeróbico de natación aguda promueve el mantenimiento de la contractilidad de los cardiomiocitos incluso con una concentración de Ca2+ intracelular sistólica y diastólica reducida en los cardiomiocitos del VD, lo que refleja una mejora en el manejo del Ca2+ intracelular.(AU)

Objetivo: os ajustes agudos na função contrátil e no transiente do cálcio (Ca2+) intracelular nos cardiomiócitos do ventrículo direito (VD) após uma sessão aguda de exercício aeróbio não são conhecidos. Desta forma objetivo foi investigar as respostas agudas da função contrátil e do no transiente Ca2+ intracelular em cardiomiócitos do VD isolados após uma sessão de exercício de natação.Métodos: Ratas Wistar com dez semanas de idade foram alocadas aleatoriamente em dois grupos: controle (C; n = 5) e exercício (Ex; n = 7). Foi realizada uma sessão de exercícios de natação por 30 minutos com uma sobrecarga de 4% em relação ao peso corporal preso à cauda. Os ratos foram sacrificados após a sessão de exercícios para análise dos parâmetros da função contrátil do VD e do transiente Ca2+ intracelular pela técnica de cardiomiócitos isolados.Resultados: Os pesos corporais e cardíacos, bem como o comprimento do sarcômero foram semelhantes entre os grupos. Além disso, não foram observadas diferenças entre os grupos para os parâmetros contráteis dos cardiomiócitos do VD. No entanto, a concentração de Ca2+ intracelular sistólica e diastólica foi significativamente menor no grupo Ex em comparação com C com manutenção da amplitude de Ca2+. Conclusão: Uma sessão aguda de exercício aeróbio de natação promove a manutenção da contratilidade dos cardiomiócitos mesmo com a concentração intracelular de Ca2+ sistólica e diastólica reduzida nos cardiomiócitos do VD, refletindo uma melhora no manuseio do Ca2+ intracelular.(AU)

MicroRNA-451a attenuates angiotensin II–induced cardiac fibrosis and inflammation by directly targeting T-box1

Hypertension or angiotensin II (Ang II) induces cardiac inflammation and fibrosis, thus contributing to cardiac remodeling. MicroRNAs (miRNAs) are considered crucial regulators of cardiac homeostasis and remodeling in response to various types of stress. It has been reported that miR-451a is involved in regulating ischemic heart injury. However, its role in Ang II-induced cardiac fibrosis remains unknown. Cardiac remodeling was induced in mice by infusion of low-dose Ang II (490 ng/kg/min) with a minipump for 2 weeks. Echocardiography and histological examinations were performed to evaluate cardiac function and pathological changes. We observed that miR-451a expression was the most significantly downregulated in the hearts of Ang II-infused mice and in both primary cardiac myocytes and fibroblasts. Overexpression of miR-451a in mice significantly attenuated Ang II–induced cardiac fibrosis and inflammation. Conversely, knockdown of miR-451a in mice aggravated this effect. Bioinformatics analysis and a luciferase reporter assay revealed that TBX1 was a direct target of miR-451a. Mechanistically, miR-451a directly targeted TBX1 expression, which inhibited TGF-β1 production in both cardiac myocytes and fibroblasts, inactivating of TGF-β1/SMAD2/3 signaling, inhibiting myofibroblast differentiation and proinflammatory cytokine expression, and leading to attenuation of cardiac fibrosis and inflammation. In conclusion, these results indicate that miR-451a acts as a novel regulator of Ang II–induced cardiac fibrosis and inflammation by directly targeting TBX1, and may be a promising therapeutic target for treating hypertensive cardiac diseases. (AU)

Resonancia magnética cardiaca en la miocardiopatía arritmogénica: ¿hay que actualizar los criterios de 2010? / Cardiac magnetic resonance in arrhythmogenic cardiomyopathy: is it time to update the 2010 criteria?

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Cicatriz miocárdica arritmogénica localizada mediante el uso combinado de la SPECT con 123I-MIBG y la RMN cardíaca / Arrhythmogenic myocardial scar localized through the combined use of 123I-MIBG SPECT and cardiac MRI

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¿Debe realizarse una toracocentesis para diagnosticar el derrame pleural de origen cardiaco? / Should thoracentesis be performed to diagnose pleural effusion of cardiac origin?

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Chronic inhalation of 2, 2-dichlorovinyl dimethyl phosphate (DDVP) induces organ pathology in the adult albino rats

The acute toxic effects of the acetyl cholinesterase-inhibiting pesticide, DDVP, following oral and dermal exposure are well recorded in literature. The ability of DDVP to easily vaporize makes the aero-nasal route a possible means of exposure, albeit chronically. This study aimed to describe the pathology, if any, of the heart, kidney and liver following chronic exposure to various concentrations of DDVP via inhalation.Sixty male Wistar rats were divided into 6 groups (A-F) of 10 rats each. Rats in Group A were exposed to distilled water only, while rats in groups B, C, D, E and F were exposed to 20, 40, 60, 80 and 100% v/v concentrated fumes of DDVP respectively. Duration of inhalational exposure was for 90 days. The heart, liver and kidney of the rats in the groups were extracted for routine histopathology. Organ pathologies were semi-quantitatively scored and analyzed across and between the 6 groups.Generally, lesions were of progressive severity with increasing concentrations of DDVP. Across the organs, pathology was related to altered vascular and degenerative changes. Specifically, the heart, kidney and liver showed shredding of cardiomyocytes, sloughing of renal tubular epithelial cells with dilated tubular lumina, and hepatocellular degeneration and necrosis respectively. Inflammatory changes were limited to the livers of rats exposed to 80 and 100% v/v DDVP.It was concluded that DDVP induced altered vascular and degenerative changes following chronic exposure via inhalation. Safer alternatives to aerosolized DDVP-containing insecticides are recommended for the control of arthropod vectors in enclosures

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An unusual tumour: Hamartoma of mature cardiac myocytes / Hamartoma de miocitos cardiacos maduros: un tumor inusual

Heart neoplasms are uncommon and usually benign. Hamartoma of mature cardiac myocytes is an unusual lesion with only a few reported cases. It is a heterogeneous mixture of well-differentiated myocytes, fibroblasts, adipocytes and blood vessels. We present a case of hamartoma of mature cardiac myocytes and a concise review of the pertinent literature. A multi-lobulated polypoid tumour attached to the wall of the right atrium was found during an autopsy of a young woman. Microscopy revealed cardiomyocytes, fibrous connective tissue and well-differentiated adipocytes. The immunohistochemical study had a positive immunoreactivity for desmin, muscle-specific actin (HHF-35) and CD34 markers, showing the different types of mesenchymal cells involved. This combination of markers has not been previously used. Other tumours, such as cardiac rhabdomyoma and cardiac myxoma were ruled out due to the differences in histological characteristics and clinical presentation

Las neoplasias cardiacas son inusuales, y la mayoría benignas. El hamartoma de miocitos cardiacos maduros es una lesión inusual con pocos casos reportados en la literatura; está conformado por una mezcla heterogénea de miocitos, fibroblastos, adipocitos y vasos sanguíneos bien diferenciados. El objetivo de este artículo es describir un caso de hamartoma de miocitos cardiacos maduros y hacer una breve revisión de la literatura. Se trata de una mujer de 23 años en cuya autopsia se encontró una lesión tumoral polipoide multilobulada fija a la pared del atrio derecho. Microscópicamente se observaron miocitos cardiacos, tejido fibroconectivo y adipocitos bien diferenciados. El estudio de inmunohistoquímica confirmó la histogénesis de la lesión, ya que hubo inmunoreactividad positiva para los marcadores desmina, actina músculo específica/HHF-35 y CD34, marcadores que no habían sido usados en conjunto en la misma muestra en publicaciones previas. Se descartaron otros tumores como el rabdomioma cardiaco y el mixoma cardiaco por las características histológicas y la presentación clínica de estos que difieren con nuestro caso

Changes in the activity of some metabolic enzymes in the heart of SHR rat incurred by transgenic expression of CD36

Hypertension, dyslipidemia, and insulin resistance in the spontaneously hypertensive rat (SHR) can be alleviated by rescuing CD36 fatty acid translocase. The present study investigated whether transgenic rescue of CD36 in SHR could affect mitochondrial function and activity of selected metabolic enzymes in the heart. These analyses were conducted on ventricular preparations derived from SHR and from transgenic strain SHR-Cd36 that expresses a functional wild-type CD36. Our respirometric measurements revealed that mitochondria isolated from the left ventricles exhibited two times higher respiratory activity than those isolated from the right ventricles. Whereas, we did not observe any significant changes in functioning of the mitochondrial respiratory system between both rat strains, enzyme activities of total hexokinase, and both mitochondrial and total malate dehydrogenase were markedly decreased in the left ventricles of transgenic rats, compared to SHR. We also detected downregulated expression of the succinate dehydrogenase subunit SdhB (complex II) and 70 kDa peroxisomal membrane protein in the left ventricles of SHR-Cd36. These data indicate that CD36 may affect in a unique fashion metabolic substrate flexibility of the left and right ventricles

Metodología de la PET/TC con 18F-FDG cardíaca para el diagnóstico de la endocarditis protésica y de dispositivos intracardíacos / Cardiac 18F-FDG PET/CT procedure for the diagnosis of prosthetic endocarditis and intracardiac devices

La endocarditis infecciosa (EI) es una patología grave y con mal pronóstico cuya mortalidad no se ha modificado significativamente a pesar de los avances en su diagnóstico y tratamiento en los últimos 30años. La capacidad diagnóstica de los criterios de Duke modificados en la endocarditis protésica y/o de dispositivos no supera el 50%, por lo que se hacen necesarias nuevas herramientas para el diagnóstico de esta entidad en dicho contexto. La 18F-FDG PET/aTC combina una técnica con gran sensibilidad para detectar actividad inflamatoria-infecciosa y una técnica con gran resolución anatómica para valorar las lesiones estructurales asociadas a la endocarditis. Con una sensibilidad diagnóstica entre el 91 y el 97%, esta técnica híbrida se ha convertido en una herramienta de diagnóstico útil en la sospecha de EI de pacientes con válvulas protésicas o dispositivos, convirtiéndose en un criterio mayor en el algoritmo diagnóstico de las guías actuales. Esta excelente capacidad diagnóstica depende de forma directa de la calidad de la exploración obtenida y del conocimiento a la hora de interpretar las imágenes. El objetivo de esta revisión es describir y estandarizar la metodología de la 18F-FDG-PET/aTC cardíaca en el diagnóstico de endocarditis protésica y de dispositivos intracardíacos, haciendo especial énfasis en las particularidades de la preparación del paciente, de la adquisición de los estudios PET y TC, y del posterior posprocesado e interpretación de las imágenes

Infective endocarditis (IE) is a serious condition with a poor prognosis, its mortality unchanged significantly despite diagnostic and therapeutic advances in the last 30years. The diagnostic ability of the modified Duke criteria in prosthetic endocarditis and/or devices does not exceed 50%, so new tools are necessary for the diagnosis of this entity in this context. The 18F-FDG PET/CTA combines a highly sensitive technique to detect inflammatory-infectious activity with a technique with high anatomical resolution to assess the structural lesions associated with endocarditis. With a diagnostic sensitivity between 91-97%, this hybrid technique has become a useful diagnostic tool for patients with prosthetic valves or devices and suspicion of IE, becoming a major criterion in the diagnostic algorithm of current guidelines. This excellent diagnostic ability depends directly on the quality of the obtained exploration and the knowledge at the time of interpreting the images. The aim of this review is to describe and standardize the methodology of cardiac 18F-FDG PET/CTA in the diagnosis of endocarditis in prosthetic valves and intracardiac devices, with special emphasis on the particularities of the patient's preparation, the PET and CT acquisition procedures, and the subsequent imaging postprocessing and interpretation

ICaL and Ito mediate rate-dependent repolarization in rabbit atrial myocytes

Rate-dependent repolarization (RDR) of action potential (AP) in cardiomyocyte plays a critical role in the genesis of arrhythmias and RDR in atrium has been linked with atrial fibrillation. However, detailed studies focusing on the role of RDR in rabbit atrium are scant. In this study, atrial cells were isolated from rabbit heart and rate-dependent property was explored in single atrial cell to elucidate the underlying mechanism. Our results indicated that rate-dependent prolongation was evident at the action potential duration at 20% (APD20) and 50% (APD50) repolarization but not at 90% repolarization (APD90) under control condition. Using transient outward potassium current (Ito) inhibitor 4-Aminopyridine (4-AP, 2 mM) effectively eliminated the changes in APD20 and APD50, and unmasked the rate-dependent reduction of APD90 which could be diminished by further adding L-type calcium current (ICaL) inhibitor nifedipine (30 μM). However, using the selective late sodium current (INaL) inhibitor GS-458967 (GS967, 1 μM) caused minimal effect on APD90 of atrial cells both in the absence and presence of 4-AP. In consistence with results from APs, Ito and ICaL displayed significant rate-dependent reduction because of their slow reactivation kinetics. In addition, the magnitude of INaL in rabbit atrium was so small that its rate-dependent changes were negligible. In conclusion, our study demonstrated that Ito and ICaL mediate RDR of AP in rabbit atrium, while minimal effect of INaL was seen

Saffron (Crocus sativus) pretreatment confers cardioprotection against ischemia-reperfusion injuries in isolated rabbit heart

Restoration of blood flow to the ischemic myocardium is imperative to avoid demise of cardiomyocytes, but is paradoxically associated with irreversible damage to cardiac tissues due to the excessive generation of reactive oxygen species (ROS). We have previously reported that saffron, a natural antioxidant, attenuated ischemia-reperfusion (IR) injuries in vitro; however, its role in a meaningful cardiac recovery remains unknown. Here, we show that saffron supplement (oral administration for 6 weeks) reduced myocardial damage and restored cardiac function in an IR model of rabbit hearts. This was evidenced by improved left ventricle pressure, heart rate and coronary flow, and left ventricle end diastolic pressure (LVEDP) in IR hearts (isolated from rabbits pre-exposed to saffron (S/IR)). Electrophysiological recordings revealed a significant decline in both premature ventricle contraction and ventricle tachycardia/fibrillation in S/IR compared to IR hearts. This was paralleled by increased expression of the contractile proteins α-actinin and Troponin C in the myocardium of S/IR hearts. Histological examination combined to biochemical analysis indicated that hearts pre-exposed to saffron exhibited reduced infarct size, lower lipid peroxidation, with increased glutathione peroxidase activity, and oxidation of nitro blue tetrazolium (by reactive oxygen species). Furthermore, in contrast with IR hearts, saffron pretreatment induced restoration of the phosphorylation level of the survival proteins Akt and 4EBP1 and reduced activity of p38. Collectively, our data demonstrate that the natural antioxidant saffron plays a pivotal role in halting IR-associated cardiac injuries and emerges as a novel preventive tool for ischemic heart disease (AU)

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Muerte súbita en varón joven / Sudden death in a young adult

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Ritme idioventricular accelerat transitori en un nounat afectat d’acidèmia metilmalònica / Ritmo idioventricular acelerado en un neonato afecto de acidemia metilmalónica / Transient accelerated idioventricular rhythm in a newborn with methylmalonic academia

Introducció: el ritme accelerat idioventricular (RIVA) és una disrítmia originada a nivell dels feixos de His, de les fibres de Purkinje o dels miòcits ventriculars, molt rara en infants i nadons. Cas clínic: es presenta el cas d'un nounat a terme amb la presència de RIVA els primers dies de vida, sense repercus-sió hemodinàmica, i que s'autolimita als dos mesos d'edat. Posteriorment es va diagnosticar d'acidèmia metilmalònica tipus mut0, i es va iniciar el tractament amb dieta específica, carnitina i vitamina B12, amb bon control metabòlic. En el seguiment presenta extrasístoles ventriculars aïllades i un desenvolupament físic i psicomotor correctes. Comentaris: la identificació d'aquesta disrítmia pot ser difícil i és de gran transcendència, ja que planteja el diagnòstic diferencial principalment amb la taquicàrdia ventricular. El seu pronòstic generalment és benigne i tendeix a la resolució espontània; per tant, els fàrmacs antiarítmics no estan indicats. La coexistència de RIVA i acidèmia metilmalònica en un mateix pacient no ha estat descrita fins al moment

Introducción. El ritmo acelerado idioventricular (RIVA) es una disritmia originada a nivel de los haces de His, de las fibras de Purkinje o de los miocitos ventriculares, muy rara en niños y neonatos. Caso clínico. Se presenta el caso de un recién nacido a término con la presencia de RIVA los primeros días de vida, sin repercusión hemodinámica, y que se autolimita a los dos meses de edad. Posteriormente se diagnosticó de acidemia metilmalónica tipo mut0, y se inició el tratamiento con dieta específica, carnitina y vitamina B12, con buen control metabólico. En el seguimiento presenta extrasístoles ventriculares aisladas y un desarrollo físico y psicomotor correctos. Comentarios. La identificación de esta disritmia puede ser difícil y es de gran trascendencia, puesto que plantea el diagnóstico diferencial principalmente con la taquicardia ventricular. Su pronostico es, generalmente, benigno y tiende a la resolución espontánea; por tanto, los fármacos antiarrítmicos no están indicados. La coexistencia de RIVA y acidemia metilmalónica no ha sido descrita hasta el momento en un mismo paciente (AU)

Introduction. The accelerated idioventricular rhythm (AIVR) is a very rare pediatric dysrhythmia originated in the bundles of His, Purkinje fibers, or ventricular myocytes. Case report. A term newborn presented with AIVR in the first days of life; he was hemodynamically stable, and the arrhythmia resolved by two months of age. The infant was subsequently diagnosed with mut0 methylmalonic acidemia, and was started on specific diet, carnitine, and vitamin B12, with good response. On follow-up, the infant was found to have isolated ventricular extrasystoles and normal physical and psychomotor development. Comments. The identification of this dysrhythmia can be difficult; its prompt recognition is critical due to its differential diagnosis with ventricular tachycardia. The prognosis is usually benign, with spontaneous resolution in most cases; thus, antiarrhythmic agents are not indicated. The coexistence of AIVR and methylmalonic academia has not been previously described (AU)

Técnicas paramétricas de caracterización tisular del miocardio mediante resonancia magnética (parte 1): mapas de T1 / Parametric techniques for characterizing myocardial tissue by magnetic resonance imaging (part 1): T1 mapping

El desarrollo de fibrosis miocárdica es un proceso común en la aparición de disfunción ventricular en muchas enfermedades cardiacas. La resonancia magnética permite valorar la anatomía y la función cardiaca con precisión, y su papel en la caracterización macroscópica de la fibrosis miocárdica mediante las técnicas de realce tardío ha sido ampliamente validado en clínica. En fechas recientes se ha demostrado que las técnicas de mapeo T1 miocárdico permiten la cuantificación en términos absolutos de la fibrosis difusa y de la expansión del espacio extracelular miocárdico. Sin embargo, se necesitan estudios adicionales que consigan validar la utilidad de esta técnica en la detección temprana del remodelado tisular en un momento en que la instauración de un tratamiento precoz permita mejorar el pronóstico de los pacientes. Este artículo revisa el estado actual de las técnicas de mapeo T1 del miocardio, sus aplicaciones clínicas y sus limitaciones (AU)

The development of myocardial fibrosis is a common process in the appearance of ventricular dysfunction in many heart diseases. Magnetic resonance imaging makes it possible to accurately evaluate the structure and function of the heart, and its role in the macroscopic characterization of myocardial fibrosis by late enhancement techniques has been widely validated clinically. Recent studies have demonstrated that T1-mapping techniques can quantify diffuse myocardial fibrosis and the expansion of the myocardial extracellular space in absolute terms. However, further studies are necessary to validate the usefulness of this technique in the early detection of tissue remodeling at a time when implementing early treatment would improve a patient's prognosis. This article reviews the state of the art for T1 mapping of the myocardium, its clinical applications, and its limitations (AU)

Efecto cardioprotector de la ranolazina en el proceso de isquemia-reperfusión en cardiomiocitos de rata adultos / Cardioprotective effect of ranolazine in the process of ischemia-reperfusion in adult rat cardiomyocytes

Introducción y objetivos: La ranolazina se emplea como tratamiento complementario de la angina en pacientes sintomáticos insuficientemente controlados con los tratamientos antianginosos de primera línea. La ranolazina inhibe los canales de sodio operados por voltaje, lo cual indica su posible intervención en el proceso de reperfusión al prevenir la sobrecarga de sodio y calcio que se produce durante la isquemia. En este estudio, se ha caracterizado el efecto de la ranolazina en la homeostasis del calcio en miocitos cardiacos adultos de ratas a las que se aplicó un protocolo de isquemia y reperfusión simuladas. Métodos: Se evaluaron los efectos de la ranolazina en los cambios de la concentración de calcio intracelular en diferentes momentos empleando electroestimulación de campo. El estudio del calcio intracelular se llevó a cabo mediante microfluorimetría utilizando el indicador fluorescente Fura-2 y por microscopia confocal utilizando el indicador Fluo-3. Resultados: Se observó que los cardiomiocitos a los que se aplicaba la isquemia-reperfusión mostraban un aumento de la concentración de calcio diastólica y una disminución de la amplitud de los transitorios de calcio intracelular. La aplicación de la ranolazina durante la isquemia mejoró significativamente la regulación del calcio evitando la sobrecarga de calcio intracelular, reduciendo la concentración de calcio diastólica, aumentando la carga de calcio en el retículo sarcoplásmico y preservando la amplitud del transitorio de calcio intracelular, lo cual se reflejaba en una recuperación satisfactoria en el proceso de acoplamiento de excitación-contracción durante la reperfusión. Sin embargo, estos efectos de la ranolazina no se produjeron cuando el fármaco se aplicó solo durante la reperfusión o cuando se aplicó tanto en la isquemia como en la reperfusión. Conclusiones: La ranolazina muestra unos efectos favorables en los cardiomiocitos expuestos a isquemia-reperfusión, pero solo cuando se aplica durante la isquemia. Este efecto se alcanza mejorando la regulación del calcio durante la isquemia (AU)

Introduction and objectives: Ranolazine is used as a complementary treatment for angina in symptomatic patients who are inadequately controlled with first-line antianginal therapies. Ranolazine inhibits sodium voltage-dependent channels, suggesting their possible involvement in the reperfusion process by preventing the sodium and calcium overload that occurs during ischemia. In this study, we characterized the effect of ranolazine on calcium homeostasis in isolated adult cardiac myocytes from rats subjected to a simulated ischemia and reperfusion protocol. Methods: The effects of ranolazine on changes in intracellular calcium concentration were evaluated at different times using field electrostimulation. The study of intracellular calcium was performed using microfluorimetry with the fluorescent indicator, Fura-2, and by confocal microscopy with the indicator, Fluo-3. Results: We found that cardiomyocytes subjected to ischemia-reperfusion showed an increase in the diastolic calcium concentration and a decrease in the amplitude of intracellular calcium transients. The application of ranolazine during ischemia significantly improved intracellular calcium handling, preventing intracellular calcium overload, decreasing the diastolic calcium concentration, increasing the sarcoplasmic reticulum calcium load, and preserving the amplitude of the intracellular calcium transient, which was reflected by successful recovery in the process of excitation-contraction coupling during reperfusion. However, these effects of ranolazine did not occur when it was applied during reperfusion or when applied in both ischemia and reperfusion. Conclusions: Ranolazine shows beneficial effects in cardiomyocytes exposed to ischemia/reperfusion but only when applied during ischemia. This effect is achieved through its improvement of calcium handling during ischemia (AU)

Hallazgos de imagen de las masas cardíacas (parte I): protocolo de estudio y tumores benignos / Imaging findings in cardiac masses (Part I ): study protocol and benign tumors

Las masas cardíacas son un reto diagnóstico porque las decisiones terapéuticas se basan en los hallazgos de las técnicas de imagen. La ecocardiografía, la resonancia magnética (RM) y la tomografía computarizada (TC) son fundamentales para la detección, caracterización, estadificación y planificación del tratamiento. La mayoría de los tumores primarios son benignos; los más frecuentes son el mixoma, el fibroelastoma papilar y el lipoma. La localización del tumor y sus características en la TC y la RM orientan el diagnóstico etiológico en la mayor parte de los casos. Se describen los protocolos de estudio de TC y RM de las masas cardíacas, así como los hallazgos morfológicos, las localizaciones preferentes y las características más útiles para caracterizar las masas cardíacas benignas y establecer el diagnóstico diferencial con los tumores cardíacos malignos y las lesiones pseudotumorales no neoplásicas (AU)

Cardiac masses represent a diagnostic challenge because decisions about treatment are based on imaging techniques. Echocardiography, magnetic resonance (MR) and computed tomography (CT) are fundamental for the detection, characterization, and staging of cardiac masses as well as for planning their treatment. Most primary cardiac tumors are benign; myxomas, papillary fibroelastomas, and lipomas are the most common. The location of the tumors and its characteristics on CT and MR orient the etiologic diagnosis in most cases. This article describes the protocols for CT and MR studies of cardiac masses as well as the morphologic findings, predominant locations, and most useful characteristics for characterizing benign cardiac masses and establishing the differential diagnosis with malignant cardiac tumors and non-neoplastic pseudotumors (AU)