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RESUMEN Introducción: Estudios recientes sugieren combinar los hallazgos de la resonancia magnética cardíaca (RMC) y los de la tomografía por emisión de positrones (PET) para incrementar la sensibilidad del diagnóstico de la sarcoidosis cardíaca (SC). Objetivo: Evaluar el valor complementario de la RMC y la PET en el diagnóstico de la SC. Material y métodos: Entre diciembre 2018 y Julio 2020, 6 pacientes (4 hombres y 2 mujeres) fueron referidos a nuestro servicio con sospecha de SC para evaluación de inflamación del miocardio. Se efectuó un estudio de perfusión miocárdica en reposo (13N Amonio) y de 18F-Fluordesoxiglucosa (FDG)-PET para evaluar inflamación y/o fibrosis. A todos los pacientes se les realizó previamente una RMC con gadolinio. Resultados: La edad media fue de 60 ± 9 años. El 50% de los pacientes presentaban antecedente de sarcoidosis sistémica y el otro 50% sospecha de SC aislada. Ninguno de los pacientes presentó inflamación activa del miocardio por PET. Con la combinación de los patrones-PET y el realce por RMC se reclasificó a los pacientes: 50% tuvo menos del 10% de probabilidad de padecer SC y el otro 50% se clasificó como posible. Ninguno de los pacientes recibió tratamiento inmunosupresor. Conclusión: En nuestra población de pacientes con sospecha de SC e inflamación, realizamos un estudio PET luego de la RMC para calcular probabilidades de padecer SC. En ausencia de un patrón oro, se sugiere que el diagnóstico de SC se base en probabilidades de acuerdo a patrones de imágenes y cuadro clínico específicos.
ABSTRACT Background: Recent studies suggest combining the findings of cardiac magnetic resonance (CMR) and positron emission tomography (PET) to increase sensitivity in the diagnosis of cardiac sarcoidosis (CS). Objective: To evaluate the complementary value of CMR and PET in the diagnosis of CS. Methods: From December 2018 to July 2020, 6 patients (4 males and 2 females) with suspected CS were referred to our facility for evaluation of myocardial inflammation. A resting 13N Ammonia myocardial perfusion test and a 18F Fluorodeoxyglucose (FDG) PET were performed to evaluate myocardial inflammation and/or fibrosis. All patients had a previous gadoliniumenhanced CMR. Results: The average age was 60 ± 9 years. Fifty percent of the patients had a history of systemic sarcoidosis and the remaining 50% had suspected isolated CS. None of the patients had active myocardial inflammation based on the PET findings. With the combination of PET patterns and enhanced CMR, the patients were reclassified as follows: 50% had less than 10% chance of having CS and the other 50% was classified as possible cases of CS. None of the patients received immunosuppressants. Conclusion: In our patient population with suspected CS and inflammation, we conducted a PET study following a CMR to assess the potential for CS. In the absence of a gold standard, it is suggested that the diagnosis of CS should be based on probabilities according to specific imaging patterns and clinical features.
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Objective:To investigate whether myocardial inflammation and apoptosis are involved in right ventricular dysfunction (RVD) induced by injurious mechanical ventilation with high tidal volume (VT) in rats.Methods:Total 30 adult male SD rats were randomly divided into the control group (CON group), the low VT ventilation group (LVT group) and the injurious mechanical ventilation group (HVT group), with 10 rats in each group. The CON group was maintained spontaneous breathing, the LVT group and HVT group were ventilated with different VT 6 mL/kg and 20 mL/kg for 4 hours, respectively. The right jugular vein and the left carotid artery were catheterized and connected with the PowerLab biological signal acquisition and analysis system to record heart rate (HR), mean arterial pressure (MAP), right ventricular systolic pressure (RVSP), the maximum rate of rising of right ventricular pressure (+dp/dt max). Echocardiography was performed to measure left ventricular end-diastolic diameter (LVEDd), right ventricular end-diastolic diameter (RVEDd), tricuspid annulus plane systolic migration (TAPSE) and myocardial performance index (MPI). The rats were sacrified by cervical dislocation. Specimens of right ventricle tissues were taken for hematoxylin-eosin (HE) staining, and morphological changes of right ventricle tissues were observed under light microscope. Real time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the mRNA and protein expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), caspase-3, apoptosis-related proteins Bax and Bcl-2.Results:HR, MAP, +dp/dt max gradually decreased, while RVSP gradually increased in different group with the increase of VT ventilation. There was no significant difference between the CON group and LVT group. However, there was a statistically significant difference with respect to these index in HVT group as compared to CON group and LVT group [HR (bpm): 397.6±5.7 vs. 433.0±4.8, 441.6±7.8; MAP (mmHg, 1 mmHg≈0.133 kPa): 102.0±2.4 vs. 108.5±2.2, 110.6±2.1; +dp/dt max (mmHg/s): 2 357.65±62.80 vs. 2 661.27±55.62, 2 679.43±75.13; RVSP (mmHg): 28.8±1.0 vs. 22.6±10.8, 21.9±0.4; all P < 0.05]. Echocardiography findings showed that RVEDd/LVEDd and MPI gradually increased, TAPSE gradually decreased in different group with the increase of VT ventilation. There was no significant difference between the LVT group and CON group. However, there was a statistically significant difference with respect to these indexes in HVT group as compared to the CON group and LVT group [RVEDd/LVEDd: 0.36±0.02 vs. 0.26±0.01, 0.23±0.02; MPI: 1.23±0.03 vs. 0.84±0.04, 0.86±0.03; TAPSE (mm): 1.65±0.03 vs. 1.88±0.02, 1.91±0.04; all P < 0.05]. Histopathological observation of the right ventricle tissue showed that myocardial cells of the rats in the CON group were orderly arranged and uniformed in size. In the LVT group, there was a small amount of inflammatory cell infiltration in the myocardial interstitium, while in the HVT group, the myocardial cell arrangement was obviously disordered, the structure was obviously damaged, and more inflammatory cell infiltration was found. RT-PCR and Western blotting analysis showed that the mRNA and protein expressions of IL-6, TNF-α, caspase-3 and Bax in HVT group were significantly higher than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt): IL-6 were 1.97±0.07 vs. 1.09±0.02, 1.02±0.03, TNF-α were 1.69±0.10 vs. 1.10±0.03, 1.05±0.04, caspase-3 were 1.82±0.09 vs. 1.08±0.02, 1.06±0.03, Bax were 2.19±0.14 vs. 1.07±0.03, 1.04±0.03; protein expression (gray value): IL-6 were 0.64±0.02 vs. 0.38±0.03, 0.31±0.04, TNF-α were 0.50±0.04 vs. 0.16±0.01, 0.15±0.01, caspase-3 were 0.58±0.02 vs. 0.29±0.01, 0.25±0.02, Bax were 0.50±0.03 vs. 0.21±0.01, 0.26±0.02; all P < 0.05], and the mRNA and protein expressions of Bcl-2 in the HVT group were lower than those in the LVT group and CON group [mRNA expression (2 -ΔΔCt): 1.23±0.05 vs. 1.43±0.05, 1.50±0.08; protein expression (gray value): 0.42±0.02 vs. 0.62±0.03, 0.65±0.03, all P < 0.05]. Conclusion:Myocardial inflammation and apoptosis may be involved in RVD induced by injurious mechanical ventilation.
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Objective To observe the effect of myocardial transcription factor MRTF-A on myocardium inflammation and its mechanism.Methods Totally 30 rats were randomly divided into the sham,ischemia-reperfusion (myocardial ischemia 30 min and reperfusion 2 h),and MRTF-A groups(myocardial ischemia 30 min and reperfusion 2 h & Lentivirus infection MRTF-A) (n=10 each group).Serum myocardial enzyme activity was detected by biochemical analysis,myocardial infarct size detected by TTC,and degree of myocardial injury was measured by HE staining.The TLR4 and TRIF expression was analyzed by immunohistochemistry and qPCR.Results Compared with the sham group,the MRTF-A group significantly increased the activity of serum myocardial enzymes CK-MB and LDH (P＜0.05).The infarct area of myocardial tissue was gray-white,and the infarct area was (54.31±3.07)％ (P ＜ 0.05).Myocardial fibrosis was disorder,myocardial cell was swollen and burst,and inflammatory cell infiltration was obvious.Protein and mRNA expressions of TRL4 and TRIF were significantly up-regulated (P＜0.05).Compared with the ischemia-reperfusion group,the levels of CK-MB and LDH were significantly reduced after myocardial infection with MRTF-A (P＜0.05).The myocardial infarction area was significantly reduced to (16.74±4.26)％ (P＜ 0.05).The myocardial structure was nearly normal with mild edema.Protein and mRNA expression of TRL4 and TRIF decreased significantly (P＜0.05).Conclusions The overexpression of transcription factor MRTF-A in myocardial cells alleviates the myocardial ischemia reperfusion injury by inhibiting the TLR4/TRIF signaling pathway and reducing the serum myocardial enzyme activity and myocardial damage.
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AIM: To study the effect of ligustrazine on the cardiacmyocyte lesion in rats with type 2 diabetes mellitus.METHODS: Male Wistar rats were injected with STZ via tail vein under high-glucose and high-fat feeding for 4 weeks to establish the animal model of type 2 diabetes mellitus.Ligustrazine at different doses was used to treat the diabetic rats.The body weight, blood glucose and the morphology of heart tissues were observed.The myocardial levels of IL-1β, IL-6 and TNF-α were detected by ELISA, and the protein expression of IKKβ and NF-κB in the myocardium was determined by Westeren blotting.RESULTS: Ligustrazine at high dose alleviated the body weight reduction and blood glucose elevation cause by diabetes, and reduced pro-inflammatory factors IL-1β, TNF-α and IL-6.Moreover, the protein expression of IKKβ and NF-κB was significant decreased by ligustrazine.CONCLUSION: Ligustrazine inhibits the myocardial inflammation caused by diabetes through anti-inflammatory pathway.
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Aim To study the protective effect of total flavones of rhododendra pharmacological preconditioning(TFR-PP)on myocardial ischemia and reperfusion injury and its mechanisms involved in myocardial inflammation in rats.Methods In model group the isolated perfused rat hearts set up by Langendorff system were subjected to 30 min ischemia followed by 40 min reperfusion. The hearts in TFR-PP groups were subjected to three cycles of 5 min perfusion with and without TFR before 30 min ischemia followed by 40 min reperfusion. In all groups the activities of lactate dehydrogenase (LDH), creatine phosphokinase (CK), and myeloperoxidase (MPO) in myocardium, the expressions of nuclear factor-kappa B (NF-?B), tumor necrosis factor-alpha(TNF-?), and intercellular adhersion molecule-1 (ICAM-1) were measured, and the myocardial pathomorphological changes were examined.Results TFR-PP(25、50、100 mg?L-1) could inhibit markedly the reductions of LDH and SOD activities in myocardium induced by ischemia and reperfusion injury.100 mg?L-1 TFR-PP also significantly improved the pathomorphological changes of injury. TFR-PP (25、50、100 mg?L-1) could inhibit the expressions of NF-?B, TNF-? and ICAM-1 to varying degrees.Conclusion TFR-PP has marked protective effect on ischemia and reperfusion injury in isolated rat heart via inhibiting the inflammation of myocardium.