Myocardial biopsy of Liwen procedure: representability and etiological diagnostic value of cardiac samples obtained by a novel technique in patients with hypertrophic cardiomyopathy / 中华心血管病杂志

Objective: To investigate the representability and etiological diagnostic value of myocardium samples obtained from patients with hypertrophic cardiomyopathy (HCM) by transthoracic echocardiography-guided percutaneous intramyocardial septal biopsy (myocardial biopsy of Liwen procedure). Methods: This study was a retrospective case-series analysis. Patients with HCM, who underwent myocardial biopsy of Liwen procedure and radiofrequency ablation in Xijing Hospital, Air Force Military Medical University from July to December 2019, were included. Demographic data (age, sex), echocardiographic data and complications were collected through electronic medical record system. The histological and echocardiographic features, pathological characteristics of the biopsied myocardium of the patients were analyzed. Results: A total of 21 patients (aged (51.2±14.5) years and 13 males (61.9%)) were enrolled. The thickness of ventricular septum was (23.3±4.5)mm and the left ventricular outflow tract gradient was (78.8±42.6)mmHg (1 mmHg=0.133 kPa). Eight patients (38.1%) were complicated with hypertension, 1 patient (4.8%) had diabetes, and 2 patients (9.5%) had atrial fibrillation. Hematoxylin-eosin staining of myocardial samples of HCM patients before radiofrequency ablation evidenced myocytes hypertrophy, myocytes disarray, nuclear hyperchromatism, hypertrophy, atypia, coronary microvessel abnormalities, adipocyte infiltration, inflammatory cell infiltration, cytoplasmic vacuoles, lipofuscin deposition. Interstitial fibrosis and replacement fibrosis were detected in Masson stained biopsy samples. Hematoxylin-eosin staining of myocardial samples of HCM patients after radiofrequency ablation showed significantly reduced myocytes, cracked nuclear in myocytes, coagulative necrosis, border disappearance and nuclear fragmentation. Quantitative analysis of myocardial specimens of HCM patients before radiofrequency ablation showed that there were 9 cases (42.9%) with mild myocardial hypertrophy and 12 cases (57.1%) with severe myocardial hypertrophy. Mild, moderate and severe fibrosis were 5 (23.8%), 9 (42.9%) and 7 (33.3%), respectively. Six cases (28.6%) had myocytes disarray. There were 11 cases (52.4%) of coronary microvessel abnormalities, 4 cases (19.0%) of adipocyte infiltration, 2 cases (9.5%) of inflammatory cell infiltration,6 cases (28.5%) of cytoplasmic vacuole, 16 cases (76.2%) of lipofuscin deposition. The diameter of cardiac myocytes was (25.2±2.8)μm, and the percentage of collagen fiber area was 5.2%(3.0%, 14.6%). One patient had severe replacement fibrosis in the myocardium, with a fibrotic area of 67.0%. The rest of the patients had interstitial fibrosis. The myocardial specimens of 13 patients were examined by transmission electron microscopy. All showed increased myofibrils, and 9 cases had disorder of myofibrils. All patients had irregular shape of myocardial nucleus, partial depression, mild mitochondrial swelling, fracture and reduction of mitochondrial crest, and local aggregation of myofibrillary interfascicles. One patient had hypertrophy of cardiomyocytes, but the arrangement of muscle fibers was roughly normal. There were vacuoles in the cytoplasm, and Periodic acid-Schiff staining was positive. Transmission electron microscopy showed large range of glycogen deposition in the cytoplasm, with occasional double membrane surround, which was highly indicative of glycogen storage disease. No deposition of glycolipid substance in lysozyme was observed under transmission electron microscope in all myocardial specimens, which could basically eliminate Fabry disease. No apple green substance was found under polarized light after Congo red staining, which could basically exclude cardiac amyloidosis. Conclusion: Myocardium biopsied samples obtained by Liwen procedure of HCM patients are representative and helpful for the etiological diagnosis of HCM.

Fucoxanthin regulates Nrf2/Keap1 signaling to alleviate myocardial hypertrophy in diabetic rats / 南方医科大学学报

OBJECTIVE@#To investigate the protective effect of fucoxanthin (FX) against diabetic cardiomyopathy and explore the underlying mechanism.@*METHODS@#Rat models of diabetes mellitus (DM) induced by intraperitoneal injection of streptozotocin (60 mg/kg) were randomized into DM model group, fucoxanthin treatment (DM+FX) group and metformin treatment (DM+ Met) group, and normal rats with normal feeding served as the control group. In the two treatment groups, fucoxanthin and metformin were administered after modeling by gavage at the daily dose of 200 mg/kg and 230 mg/kg, respectively for 12 weeks, and the rats in the DM model group were given saline only. HE staining was used to examine the area of cardiac myocyte hypertrophy in each group. The expression levels of fibrotic proteins TGF-β1 and FN proteins in rat hearts were detected with Western blotting. In the cell experiment, the effect of 1 μmol/L FX on H9C2 cell hypertrophy induced by exposure to high glucose (HG, 45 mmol/L) was evaluated using FITC-labeled phalloidin. The mRNA expression levels of the hypertrophic factors ANP, BNP and β-MHC in H9C2 cells were detected using qRT-PCR. The protein expressions of Nrf2, Keap1, HO-1 and SOD1 proteins in rat heart tissues and H9C2 cells were determined using Western blotting. The DCFH-DA probe was used to detect the intracellular production of reactive oxygen species (ROS).@*RESULTS@#In the diabetic rats, fucoxanthin treatment obviously alleviated cardiomyocyte hypertrophy and myocardial fibrosis, increased the protein expressions of Nrf2 and HO-1, and decreased the protein expressions of Keap1 in the heart tissue (P < 0.05). In H9C2 cells with HG exposure, fucoxanthin significantly inhibited the enlargement of cell surface area, lowered the mRNA expression levels of ANP, BNP and β-MHC (P < 0.05), promoted Nrf2 translocation from the cytoplasm to the nucleus, and up-regulated the protein expressions its downstream targets SOD1 and HO-1 (P < 0.05) to enhance cellular antioxidant capacity and reduce intracellular ROS production.@*CONCLUSION@#Fucoxanthin possesses strong inhibitory activities against diabetic cardiomyocyte hypertrophy and myocardial fibrosis and is capable of up-regulating Nrf2 signaling to promote the expression of its downstream antioxidant proteins SOD1 and HO-1 to reduce the level of ROS.

Effect and mechanism of leonurine on pressure overload-induced cardiac hypertrophy in rats / 中国中药杂志

To investigate the effects of leonurine(Leo) on abdominal aortic constriction(AAC)-induced cardiac hypertrophy in rats and its mechanism. A rat model of pressure overload-induced cardiac hypertrophy was established by AAC method. After 27-d intervention with high-dose(30 mg·kg~(-1)) and low-dose(15 mg·kg~(-1)) Leo or positive control drug losartan(5 mg·kg~(-1)), the cardiac function was evaluated by hemodynamic method, followed by the recording of left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVESP), as well as the maximum rate of increase and decrease in left ventricular pressure(±dp/dt_(max)). The degree of left ventricular hypertrophy was assessed based on heart weight index(HWI) and left ventricular mass index(LVWI). Myocardial tissue changes and the myocardial cell diameter(MD) were measured after hematoxylin-eosin(HE) staining. The contents of angiotensin Ⅱ(AngⅡ) and angiotensin Ⅱ type 1 receptor(AT1 R) in myocardial tissue were detected by ELISA. The level of Ca~(2+) in myocardial tissue was determined by colorimetry. The protein expression levels of phospholipase C(PLC), inositol triphosphate(IP3), AngⅡ, and AT1 R were assayed by Western blot. Real-time quantitative PCR(qRT-PCR) was employed to determine the mRNA expression levels of β-myosin heavy chain(β-MHC), atrial natriuretic factor(ANF), AngⅡ, and AT1 R. Compared with the model group, Leo decreased the LVSP, LVEDP, HWI, LVWI and MD values, but increased ±dp/dt_(max) of the left ventricle. Meanwhile, it improved the pathological morphology of myocardial tissue, reduced cardiac hypertrophy, edema, and inflammatory cell infiltration, decreased the protein expression levels of PLC, IP3, AngⅡ, AT1 R, as well as the mRNA expression levels of β-MHC, ANF, AngⅡ, AT1 R, c-fos, and c-Myc in myocardial tissue. Leo inhibited AAC-induced cardiac hypertrophy possibly by influencing the RAS system.

Stingless bee propolis, metformin, and their combination alleviate diabetic cardiomyopathy

Abstract Background and aim: Stingless bee propolis, a resinous compound processed by mandibular secretion of stingless bees, is used for maintenance of hygiene and stability of beehives. Research on stingless bee propolis shows therapeutic properties attributed to polyphenols exhibiting antioxidative, antihyperglycemic and antiischemic effect. However, the cardioprotective effect of stingless bee propolis on diabetic cardiomyopathy is unknown. Methods: Adult male Sprague Dawley rats were randomised to five groups: normal group, diabetic group, diabetic given metformin (DM+M), diabetic given propolis (DM+P) and diabetic given combination therapy (DM+M+P) and treated for four weeks. Body weight, fasting blood glucose, food and water intake were taken weekly. At the end of experiment, biomarkers of oxidative damage were measured in serum and heart tissue. Antioxidants in heart tissue were quantified. Part of left ventricle of heart was processed for histological staining including Haematoxylin and Eosin (H&E) stain for myocyte size and Masson's Trichrome (MT) stain for heart fibrosis and perivascular fibrosis. Results: Propolis alleviated features of diabetic cardiomyopathy such as myocyte hypertrophy, heart fibrosis and perivascular fibrosis associated with improvement in antioxidative status. Conclusion: This study reports beneficial effect of propolis and combination with metformin in alleviating histopathological feature of diabetic cardiomyopathy by modulating antioxidants, making propolis an emerging complementary therapy.

Agenesia Pericárdica Completa. Presentación de una caso y revisión de la literatura / Complete pericardial agenesis. Presentation of a case and review of the literature

Resumen Paciente masculino de 18 años, quien es valorado en el Servicio de Cardiología del Hospital Víctor Manuel Sanabria Martínez referido del primer nivel de atención por cuadro crónico de dolor torácico atípico acompañado de pectus excavatum y desplazamiento izquierdo del latido de punta a la exploración física. La radiografía de tórax posteroanterior evidencia una cardiomegalia moderada con levocardia máxima. El ecocardiograma transtorácico con función sistólica biventricular conservada, dilatación moderada del ventrículo derecho, sin signos de hipertensión pulmonar e imagen cardiaca de "corazón en lágrima". Angiotomografía computarizada de tórax con contraste que documenta malformación de la caja torácica con hundimiento de la región esternal, en relación con pectus excavatum. Corazón aumentado de tamaño en relación con cardiomegalia grado I y desplazamiento hacia el hemitórax izquierdo. No se observa pericardio en ninguna región. Aurícula derecha levemente dilatada con un ventrículo derecho con diámetro aumentado en su porción media y deformidad de su tracto de salida debido a la forma de la caja torácica, de tal manera que se corrobora el diagnóstico de una agenesia pericárdica completa.

Abstract An 18-year-old male patient who is evaluated in the Cardiology Department of the Víctor Manuel Sanabria Martínez Hospital, referred to the first level of attention due to chronic symptoms of atypical chest pain accompanied by pectus excavatum and left displacement of the peak beat. Chest X-ray Posteroanterior with moderate cardiomegaly with maximum levocardia. Transthoracic echocardiogram with preserved biventricular systolic function, moderate dilatation of the right ventricle, without signs of pulmonary hypertension and cardiac image of "tear heart". Thoracic Computed Angiotomography with contrast documenting malformation of the rib cage with sinking of the external region, in relation to pectus excavatum. Heart enlarged in relation to grade I cardiomegaly and displacement towards the left hemithorax. No pericardium is observed in any region. Slightly dilated right atrium with a right ventricle with an increased diameter in its middle portion and deformity of its outflow tract due to the shape of the rib cage. Corroborating the diagnosis of complete pericardial agenesis.

Correlação entre Cardiomegalia pela Radiografia de Tórax e Diâmetro do Ventrículo Esquerdo pela Ecocardiografia em Pacientes com Doença de Chagas / Correlation between Cardiomegaly on Chest X-Ray and Left Ventricular Diameter on Echocardiography in Patients with Chagas Disease

Resumo Fundamento Cardiomegalia pela radiografia de tórax (RXT) é preditor independente de morte em indivíduos com cardiomiopatia crônica da doença de Chagas (CCDC). Contudo, a correlação entre o aumento do índice cardiotorácico (ICT) na RXT e do diâmetro telediastólico do ventrículo esquerdo (DDVE) pela ecocardiografia (ECO) nessa população não está bem definida. Objetivos Analisar a relação entre cardiomegalia pela RXT e DDVE pela ECO em pacientes com doença de Chagas (DC) e sua aplicabilidade ao escore de Rassi. Métodos Estudo retrospectivo incluiu 63 pacientes ambulatoriais com DC avaliados por RXT e ECO. Cardiomegalia na RXT foi definida como ICT > 0,5. DDVE foi avaliado como variável contínua. Curva ROC foi utilizada para avaliar o potencial do DDVE para identificação de cardiomegalia pela RXT, com ponto de corte definido pela maior somatória de sensibilidade e especificidade. Resultados Idade mediana = 61 anos [intervalo interquartil: 48-68], 56% mulheres. CCDC foi identificada em 58 pacientes; 5 tinham a forma indeterminada da DC. Cardiomegalia foi detectada em 28 indivíduos. A área sob a curva ROC do DDVE para identificação de cardiomegalia foi de 0,806 (IC 95%: 0,692-0,919). O ponto de corte ótimo para DDVE foi de 60 mm (sensibilidade = 64%, especificidade = 89%). O uso do DDVE pela ECO em substituição ao ICT pela RXT alterou o escore de Rassi em 14 pacientes, e em 10 deles houve redução do risco presumido. Conclusão DDVE pela ECO é parâmetro adequado e com alta especificidade para distinguir entre presença e ausência de cardiomegalia na RXT na DC. (Arq Bras Cardiol. 2021; 116(1):68-74)

Abstract Background Cardiomegaly on chest X-ray is an independent predictor of death in individuals with chronic Chagas cardiomyopathy (CCC). However, the correlation between increased cardiothoracic ratio (CTR) on chest X-ray and left ventricular end-diastolic diameter (LVEDD) on echocardiography is not well established in this population. Objectives To assess the relationship between chest X-ray and LVEDD on echocardiography in patients with Chagas disease and its applicability to the Rassi score. Methods Retrospective study on 63 Chagas disease outpatients who underwent chest X-ray and echocardiography. Cardiomegaly on chest X-ray was defined as a CTR>0.5. LVEDD was analyzed as a continuous variable. ROC curve was used to evaluate the ability of LVEDD in detecting cardiomegaly by chest X-ray, with a cut-off point defined by the highest sum of sensitivity and specificity. Results Median age 61 years [interquartile range 48-68], 56% were women. CCC was detected in 58 patients, five patients had the indeterminate form of Chagas disease. Cardiomegaly was detected in 28 patients. The area under the ROC curve for LVEDD was 0.806 (95%CI: 0.692-0.919). The optimal cut-off for LVEDD was 60 mm (sensitivity = 64%, specificity = 89%). The use of LVEDD on echocardiography as a surrogate for CTR on chest X-ray changed the Rassi score values of 14 patients, with a reduction in the presumed risk in 10 of them. Conclusion LVEDD on echocardiography is an appropriate, highly specific parameter to distinguish between the presence and absence of cardiomegaly on chest X-ray in Chagas disease. (Arq Bras Cardiol. 2021; 116(1):68-74)

Chikusetsu saponin Ⅳa ameliorates myocardial hypertrophy of rats through regulating expression of miR199a-5p/Atg5 / 中国中药杂志

The present study investigated the effects of chikusetsu saponin Ⅳa(CHS Ⅳa) on isoproterenol(ISO)-induced myocardial hypertrophy in rats and explored the underlying molecular mechanism. ISO was applied to establish a rat model of myocardial hypertrophy, and CHS Ⅳa(5 and 15 mg·kg~(-1)·d~(-1)) was used for intervention. The tail artery blood pressure was measured. Cardiac ultrasound examination was performed. The ratio of heart weight to body weight(HW/BW) was calculated. Morphological changes in the myocardial tissue were observed by HE staining. Collagen deposition in the myocardial tissue was observed by Masson staining. The mRNA expression of myocardial hypertrophy indicators(ANP and BNP), autophagy-related genes(Atg5, P62 and beclin1), and miR199 a-5 p was detected by qRT-PCR. Atg5 protein expression was detected by Western blot. The results showed that the model group exhibited increased tail artery blood pressure and HW/BW ratio, thickened left ventricular myocardium, enlarged myocardial cells, disordered myocardial fibers with widened interstitium, and a large amount of collagen aggregating around the extracellular matrix and blood vessels. ANP and BNP were largely expressed. Moreover, P62 expression was up-regulated, while beclin1 expression was down-regulated. After intervention by CHS Ⅳa at different doses, myocardial hypertrophy was ameliorated and autophagy activity in the myocardial tissue was enhanced. Meanwhile, miR199 a-5 p expression declined and Atg5 expression increased. As predicted by bioinformatics, Atg5 was a target gene of miR199 a-5 p. CHS Ⅳa was capable of preventing myocardial hypertrophy by regulating autophagy of myocardial cells through the miR-199 a-5 p/Atg5 signaling pathway.

Mouse strain-specific responses of mitochondrial respiratory function and cardiac hypertrophy to isoproterenol treatment / 生理学报

Cardiac hypertrophy is a common pathological process of various cardiovascular diseases and eventually develops into heart failure. This paper was aimed to study the different pathological characteristics exhibited by different mouse strains after hypertrophy stimulation. Two mouse strains, A/J and FVB/nJ, were treated with isoproterenol (ISO) by osmotic pump to induce cardiac hypertrophy. Echocardiography was performed to monitor heart morphology and function. Mitochondria were isolated from hearts in each group, and oxidative phosphorylation function was assayed in vitro. The results showed that both strains showed a compensatory enhancement of heart contractile function after 1-week ISO treatment. The A/J mice, but not the FVB/nJ mice, developed significant cardiac hypertrophy after 3-week ISO treatment as evidenced by increases in left ventricular posterior wall thickness, heart weight/body weight ratio, cross sectional area of cardiomyocytes and cardiac hypertrophic markers. Interestingly, the heart from A/J mice contained higher mitochondrial DNA copy number compared with that from FVB/nJ mice. Functionally, the mitochondria from A/J mice displayed faster O

Achados cardiovasculares incidentais em tomografias de tórax solicitadas para suspeita de COVID-19 / Incidental cardiovascular findings on chest CT scans requested for suspected COVID-19

Resumo Contexto As tomografias de tórax são frequentemente solicitadas como exames complementares para avaliação de suspeita clínica de afecção pulmonar pelo novo coronavírus 19 (COVID-19). Objetivos Nosso objetivo foi analisar a prevalência dos achados cardiovasculares incidentais em tomografias de tórax solicitadas para avaliar sinais radiológicos sugestivos de COVID-19. Métodos Por meio de um estudo transversal, descritivo e retrospectivo, foram revisadas 1.444 tomografias de tórax realizadas no setor de radiologia do Hospital de Clínicas Gaspar Vianna, no período de 1° de março a 30 de julho de 2020, com a descrição da prevalência de imagens sugestivas de pneumonia viral pelo COVID-19, além de achados pulmonares e cardiovasculares incidentais. Resultados A média de idade dos pacientes foi 50,6±16,4 anos, sendo o sexo feminino o mais frequente. A tomografia sem contraste foi o método mais utilizado (97,2%), e opacidades em vidro fosco foram identificadas em 56,0% dos casos. Achados incidentais cardiovasculares ocorreram em 51,2% (intervalo de confiança 48,7%-53,8%) das tomografias, prevalecendo calcificação da parede aórtica (21,8%), cardiomegalia (10,5%), e calcificação coronária (5,0%). Nas tomografias com contraste, evidenciaram-se aneurismas de aorta (9,7%), dissecção de aorta (7,3%) e úlceras de aorta torácica (2,4%). Conclusões Achados cardiovasculares incidentais ocorreram em aproximadamente metade das tomografias de tórax de pacientes com suspeita de COVID-19, mais especificamente, calcificações da parede da aorta, cardiomegalia e calcificação coronária.

Abstract Background Computed tomography scans of the chest are often requested as a complementary examination to investigate a clinical suspicion of pulmonary disease caused by the novel coronavirus 19 (COVID-19). Objectives Our objective was to analyze the prevalence of incidental cardiovascular findings on chest CT scans requested to assess radiological signs suggestive of COVID-19 infection. Methods This cross-sectional, descriptive, and retrospective study reviewed 1,444 chest tomographies conducted in the Radiology department of the Hospital de Clínicas Gaspar Vianna, from March 1 to July 30, 2020, describing the prevalence of images suggestive of viral pneumonia by COVID-19 and incidental pulmonary and cardiovascular findings. Results The mean age of the patients was 50.6 ± 16.4 years and female sex was more frequent. Computed tomography without contrast was the most frequently used method (97.2%). Aortic and coronary wall calcification and cardiomegaly were the most prevalent cardiovascular findings. CT angiography revealed aortic aneurysms (9.7%), aortic dissection (7.3%) and thoracic aortic ulcers (2.4%). Conclusions Incidental cardiovascular findings occurred in about half of the chest CT scans of patients with suspected COVID-19, especially aortic calcifications, cardiomegaly, and coronary calcification.

The role of left atrial enlargement and age in the prediction of recurrence in embolic strokes of undetermined source / El papel del crecimiento auricular izquierdo y la edad como predictores de recurrencia en infarto cerebral embólicos de origen indeterminado

Abstract Objectives: Left atrial disease is an independent risk factor for ischemic stroke and can be used to predict atrial fibrillation (AF). We examine whether left atrial enlargement (LAE) could predict stroke recurrence in patients with embolic stroke of undetermined source (ESUS). Materials and methods: Sixty-four patients with a confirmed diagnosis of ESUS were followed for a median of 22 months. Clinical data and echocardiogram findings were recorded. The echocardiogram interpretation was performed centrally and blindly. The Brown ESUS – AF score was used to categorize patients into high (human resource planning [HRP]: score > 2) and low-risk patients (non-HRP score 0-1). Stroke recurrence was the primary outcome. Results: The median age was 62 years (range: 22-85 years); and 33 (51.6%) were men. The median initial NIHSS score was three points (range: 0-27). Twelve (18.8%) patients were categorized as HRP. We found a significant tendency toward recurrence among HRP versus non-HRP patients. Three (25%) HRP versus 2 (3.8%) non-HRP experienced recurrence (OR: 8.3 95% CI 1.2-57; p=0.042); this association was related to severe atrial dilatation (OR: 14.5 95% CI 0.78-277, p = 0.02) and age > 75 years (OR: 12.7 95% CI 1.7-92.2, p = 0.03). We found no differences in recurrence in a univariate analysis. Conclusions: Patients with severe LAE who are 75 years old or older have a significant tendency to experience stroke recurrence.

Resumen Objetivos: La patología atrial izquierda es factor de riesgo independiente para infarto cerebral y puede utilizarse para predecir fibrilación auricular. Examinamos si el crecimiento aurícular izquierdo puede predecir recurrencia en pacientes con infarto embolico de origen indeterminado (ESUS). Materiales y métodos: Sesenta y cuatro pacientes con diagnóstico confirmado de ESUS fueron seguidos por una mediana de seguimiento de 22 meses. Registramos los datos clínicos y ecocardiográficos. La interpretación ecocardiográfica fue centralizada y cegada. La escala de Brown ESUS – AF fue utilizada para categorizar a los pacientes en riesgo alto (HRP puntaje > 2) y bajo riesgo (no-HRP: puntaje 0-1). El descenlace primario fue recurrencia de infarto cerebral. Resultados: Mediana de edad fue de 62 años (rango: 22-85 años); 33 (51.6%) fueron hombres. La mediana inicial de la escala de NIHSS fue de 3 putnos (rango de 0 a 27). 12 (18.8%) pacientes fueron de alto riesgo (HRP) y 52 (81.3%) de bajo riesgo (non- HRP). El grupo HRP mostró tendencia significatica hacia mayor recurrencia. Tres (25%) HRP versus 2 (3.8%) no-HRP experimentaron recurrencia (OR: 8.3 IC 95% 1.2-57; p = 0.042); esta asociación se relacionó con dilatación auricular severa (OR: 14.5 IC 95% 0.78-277, p = 0.02) y edad > 75 años (OR: 12.7 IC 95% 1.7-92.2, p = 0.03). En el análisis multivarioado, no encontramos significativas. Conclusiones: El crecimiento auricular izquierdo severo y la edad mayor de 75 años mostraron tendencia significativa a recurrencia de infarto cerebral.

Factores moleculares implicados en insuficiencia cardiaca / Molecular factors involved in heart failure

La insuficiencia cardiaca se define como un síndrome caracterizado por la incapacidad de proveer las necesidades metabólicas del organismo, presentando disnea y fatiga. Hasta ahora, se ha descrito la participación de varias moléculas involucradas en los mecanismos de señalización intracelular que conducen a la insuficiencia cardiaca y estimulan la síntesis de algunas proteínas, como colágeno, la cual induce a una hipertrofia cardiaca(AU)

Heart failure is defined as a syndrome characterized by the inability to meet the metabolic needs of the organism, causing dyspnea and fatigue.Descriptions are available of the involvement of several molecules in cell signaling mechanisms which lead to heart failure and prompt the synthesis of some proteins, such as collagen, inducing cardiac hypertrophy(AU)

Criterios tomográficos sugestivos de evolución a complicaciones en pacientes con neumonía por 2019-nCoV / Tomographic criteria suggestive of evolution to complications in patients with 2019-nCoV pneumonia

Introducción: El nuevo coronavirus (2019-nCoV), puede causar una infección respiratoria leve, moderada o grave, incluso la muerte. Objetivos: Determinar los criterios tomográficos (TAC) inductivos de complicaciones en pacientes con neumonía por 2019-nCoV. Materiales y métodos: Estudio observacional, analítico de casos y controles, de 123 pacientes afectos de neumonía por 2019-nCoV a quienes se les realizó tomografía simple de tórax. Los datos se expresan en medias y proporciones. Se calculó el Odds Ratio, el coeficiente de Cramer, la prueba de chi cuadrado y la "t" de Student para la comparación de los grupos, considerando una p< 0,05 como significativa. Resultados: Rango etario de 23 a 87 (57,1±13,9) años. 70 (56,9%) fueron varones. El infiltrado alveolar del parénquima pulmonar consolidativo o en bloque se encontró en 38 (30,9%), en 80 (55%) vidrio esmerilado y en 5 (4,1%) pseudo nodular. En 54 (43,9%) fue difusa, bilateral en 80 (65%), engrosamiento parietal en 55 (44,7%). El derrame pleural en 15 (12,2%), cardiomegalia en 11 (8,9%), y ambas en 15 (12,2%) y ninguna en 82 (66,7%). Fueron significativos el tipo de infiltrado (p= 0,000 R2= 0,79), el tipo de distribución (p= 0,038 R2= 0,69), el engrosamiento parietal (p= 0,000 R2= 0,71). Conclusión: La TAC de tórax simple presenta imágenes que sugieren una evolución a algún tipo de complicación en pacientes afectos por neumonía por 2019-nCoV.

Introduction: The new coronavirus (2019-nCoV) can cause a mild, moderate or severe respiratory infection, even death. Objectives: To determine the complication-inducing tomographic (CT) criteria in patients with 2019-nCoV pneumonia. Materials and methods: An observational, analytical casecontrol study of 123 patients with 2019-nCoV pneumonia who underwent a chest CT scan. The data are expressed in means and proportions. Odds Ratio, Cramer's coefficient, chi-square test and Student's "t" were calculated for the comparison of groups, considering p <0.05 as significant. Results: Age range from 23 to 87 (57.1 ± 13.9) years. 70 (56.9%) were male. The infiltrate of the pulmonary parenchyma en bloc was found in 38 (30.9%), in 80 (55%) ground glass and in 5 (4.1%) pseudo nodular. In 54 (43.9%) it was diffuse, bilateral in 80 (65%), and parietal thickening in 55 (44.7%). Pleural effusion in 15 (12.2%), cardiomegaly in 11 (8.9%), and both in 15 (12.2%) and none in 82 (66.7%). The type of infiltrate (p = 0.000 R2 = 0.79), the type of distribution (p = 0.038 R2 = 0.69), the wall thickening (p = 0.000 R2 = 0.71) were significant. Conclusion: Chest CT shows images that suggest an evolution to some type of complication in patients with 2019-nCoV pneumonia.

Cardiac Alterations in Patients with Familial Lipodystrophy / Alterações Cardiovasculares em Pacientes Portadores de Lipodistrofia Familiar

Abstract Familial lipodystrophy is a rare genetic condition in which individuals have, besides metabolic changes and body fat deposits, a type of cardiomyopathy that has not been well studied. Many of the patients develop cardiovascular changes, the most commonly reported in the literature being the expression of a type of hypertrophic cardiomyopathy. This article, presented as a bibliographic review, reviews the clinical and cardiovascular imaging aspects in this scenario of cardiomyopathy in a rare metabolic disease, based on the latest scientific evidence published in the area. Despite the frequent association of congenital lipodystrophy and ventricular hypertrophy described in the literature, the pathophysiological mechanisms of this cardiomyopathy have not yet been definitively elucidated, and new information on cardiac morphological aspects is emerging in the aegis of recent and advanced imaging methods, such as cardiac magnetic resonance.

Resumo A lipodistrofia familiar é uma condição genética rara na qual indivíduos apresentam, além das alterações metabólicas e de depósitos de gordura físicos, um tipo de cardiomiopatia pouco estudada. Muitos dos pacientes desenvolvem alterações cardiovasculares, sendo a mais comumente reportada em literatura, a expressão de um tipo de cardiomiopatia hipertrófica. Este artigo, apresentado como uma revisão bibliográfica, revisa os aspectos clínicos e de imagem cardiovascular neste cenário de cardiomiopatia em doença metabólica rara, com base nas últimas evidências científicas publicadas na área. Apesar da frequente associação de lipodistrofia congênita e hipertrofia ventricular descrita em literatura, os mecanismos fisiopatológicos desta cardiomiopatia ainda não estão definitivamente elucidados, e novas informações do aspecto morfológico cardíaco surgem à égide de recentes e avançados métodos de imagem como a ressonância cardíaca magnética.

Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy / 生物医学工程学杂志

This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). , norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.

Transforming growth factor-β-activated kinase 1 and pathological myocardial hypertrophy / 生理学报

The transforming growth factor-β-activated kinase 1 (TAK1) is a member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family. TAK1 plays important roles in many biological functions. Cardiac hypertrophy can be identified as physiological or pathological myocardial hypertrophy. TAK1 not only participates in the development of normal myocardium, but also plays an important role in regulating the occurrence and development of pathological myocardial hypertrophy. Angiotensin II (Ang II) or pressure overload induces pathological cardiac hypertrophy through different ways, such as hypoxia-inducible factor-1α (HIF-1α)-mediated transcriptional expression of TAK1, or transforming growth factor-β1 (TGF-β1)-, thyroid hormone-, ubiquitin protease-mediated TAK1 phosphorylation or ubiquitination. This article reviews the role of TAK1 in the occurrence and development of pathological myocardial hypertrophy and discusses the potential of TAK1 as an important target for the prevention and treatment of clinical myocardial hypertrophy.

MicroRNA-23a knockdown attenuates angiotensin Ⅱ induced hypertrophy in rat H9c2 cells via activating PTEN and AMPK pathway / 中华心血管病杂志

Objective: To investigate if microRNA (miR) -23a knockdown could attenuate angiotensin Ⅱ(AngⅡ) induced cardiac hypertrophy by activating phosphatase and tensin homolog deleted on chromosome ten(PTEN) and AMP-activated protein kinase(AMPK) pathway. Methods: Rat H9c2 cells were cultured in DMEM high glucose medium and put in 5% CO(2) incubator at 37 ℃(normal group). After 48 hours of culture, H9c2 cells were stimulated with 10 nmol/L AngⅡ to establish cell hypertrophy model (AngⅡgroup). The H9c2 cells were inoculated in a 6-well cell culture plate and cultured in an incubator at 37 ℃. When the confluence degree of cell growth was about 70%, the cells were transfected with different reagents, and 24 hours after transfection, 10 nmol/L AngⅡ was used to interfere with the cells. The H9c2 cells were divided into different groups according to the reagents, namely AngⅡ+anti-miR group(transfected with miR-23a inhibitor), Ang Ⅱ+NC group(transfected with miR-23a inhibitor negative control), Ang Ⅱ+anti-miR+si-PTEN group(cotransfected with miR-23a inhibitor and PTEN small interference RNA(siRNA)), and AngⅡ+anti-miR+si-NC group(cotransfected with miR-23a inhibitor and PTEN siRNA negative control). The surface area of single cell was measured by Image J software.The mRNA expression levels of α-actin 1 (ACTA1) and β-myosin heavy chain (β-MHC) and miR-23a were detected by quantitative real-time PCR(qRT-PCR). The expression levels of PTEN and AMPK signal pathway related proteins were detected by Western blot. In order to verify whether miR-23a targets PTEN gene, double luciferase reporter gene experiment was performed. The luciferase reporter gene vector recombinant plasmids of wild type pGL-WT-PTEN and mutant pGL-MUT-PTEN were constructed and prepared after normal sequencing. H9c2 cells was inoculated into 24-well cell culture plate and cultured overnight in 37 ℃ incubator. The cells were co-transfected with miR-23a mimic or miR-23a mimic negative control and wild type or mutant reporter gene recombinant plasmid. Forty-eight hours after transfection, firefly luciferase activity and sea kidney luciferase activity were measured, and the ratio of them was recorded as relative luciferase activity. Results: Compared with the normal group, the cell surface area, the mRNA expression levels of ACTA1, β-MHC and miR-23a were significantly higher, while the protein expression levels of PTEN and p-AMPK were significantly lower in the Ang Ⅱ group(all P<0.05). The results of double luciferase reporter gene assay showed that the relative luciferase activity of cells co-transfected with miR-23a mimic and wild-type reporter gene recombinant plasmid was lower than that of miR-23a mimic negative control (P<0.05), and PTEN served as the target gene of miR-23a. In AngⅡ+anti-miR group the mRNA expression levels of miR-23a, ACTA1 and β-MHC were lower, and the cell surface area was smaller, while the protein expression levels of PTEN and p-AMPK were higher than that in AngⅡ group and AngⅡ+NC group(all P<0.05). Compared with AngⅡ+anti-miR group, the cell surface area was bigger, the expression of ACTA1 and β-MHC mRNA was up-regulated, and the protein expression levels of PTEN and p-AMPK were down-regulated in Ang Ⅱ+anti-miR+si-PTEN group(all P<0.05). Conclusion: Inhibition of miR-23a can attenuate Ang Ⅱ-induced hypertrophy in H9c2 cells through targeting PTEN and activating AMPK signaling pathway.