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La estenosis aórtica es la valvulopatía más frecuente en los países desarrollados. La etiología degenerativa es la principal, esto está íntimamente relacionado con una tendencia exponencial en la longevidad de la población actual; por lo que sería correcto esperar un aumento en la casuística de esta patología. El reemplazo valvular aórtico, ya sea percutáneo o quirúrgico, es la estrategia casi única de manejo. Las guías de manejo de las distintas sociedades científicas, actualmente, norman la realización del reemplazo valvular como indicación principal en aquellos pacientes portadores de estenosis aórtica severa que, además, presenten síntomas o bien presenten datos de reducción en su fracción de eyección. Sin embargo, varios estudios han demostrado el beneficio de no retrasar la intervención de estos pacientes y por el contrario realizar la intervención valvular de forma temprana.
Aortic stenosis is currently the most common valve disease in developed countries. Degenerative ethology is the main one, this being intimately related to the exponential trend towards longevity in the current population. Aortic valve replacement, either percutaneous or open, is almost the only management strategy. The current management guidelines of the different scientific societies regulate the performance of valve replacement in patients with severe aortic stenosis who also present symptoms or data of reduced ejection fraction. However, several studies have shown the benefit of not delaying the management of these patients and, on the contrary, performing valve intervention early.
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ABSTRACT Objective Acrylamide is a toxic compound widely used in industrial sectors. Acrylamide causes reactive oxygen species formation and the subsequent lipid peroxidation reaction, which plays an important role in the pathogenesis of oxidative damage. Taxifolin is a flavonoid with antioxidant properties that inhibit reactive oxygen species formation. In this study, we aimed to investigate the preventive effect of taxifolin on acrylamide-induced oxidative heart damage. Methods The rats were divided into three groups: Acrylamide, Acrylamide+Taxifolin , and Healthy group. Water and food intake and body weight alterations were recorded daily. Malondialdehyde, total glutathione, nuclear factor kappa-B, total oxidant status, and total antioxidant status levels were analyzed from the heart tissue. Troponin-I levels, the parameter known as a cardiac biomarker, were analyzed from the blood sample. The cardiac histopathologic examination was also performed. Results In the Acrylamide group animals, the malondialdehyde, nuclear factor kappa-B, total oxidant status, and troponin-I levels were significantly higher compared to the ones of Acrylamide+Taxifolin and Healthy groups. The levels of total glutathione and total antioxidant status were significantly lower compared to Acrylamide+Taxifolin and Healthy groups'. Additionally, in the Acrylamide group, body weight gain, food and water intake, significantly declined compared to the Acrylamide+Taxifolin and Healthy groups. However, in the Acrylamide+Taxifolin group, taxifolin supplementation brought these values close to Healthy group ones. Furthermore, taxifolin treatment ameliorated structural myocardial damage signs induced by acrylamide. Conclusion Acrylamide exposure significantly induced oxidative damage to rat heart tissue. Taxifolin was able to improve the toxic consequences of acrylamide biochemically and histopathologically, possibly due to its antioxidant properties.
RESUMO Objetivo A acrilamida é um composto tóxico amplamente utilizado em setores industriais. Ela causa a formação de reativas de oxigênio e subsequente reação de peroxidação lipídica, que desempenham um papel importante na patogênese do dano oxidativo. A taxifolina é um flavonóide com propriedades antioxidantes que inibe a formação de reativas de oxigênio. Neste estudo, o objetivo foi investigar o efeito preventivo da taxifolina no dano cardíaco oxidativo induzido por acrilamida. Métodos Os ratos foram divididos em três grupos: Acrilamida, Acrilamida+Taxifolina e grupo Saudável. Ingestão de água e comida e alterações de peso corporal dos animais foram registradas diariamente. Malondialdeído, glutationa total, fator nuclear kappa-B, estado oxidante total e estado antioxidante total foram analisados no tecido cardíaco dos ratos. Os níveis de troponina-I, - parâmetro conhecido como biomarcador cardíaco, foram analisados a partir de amostra de sangue. Um exame histopatológico cardíaco também foi realizado. Resultados Nos animais do grupo Acrilamida, os níveis de malondialdeído, fator nuclear kappa-B, estado oxidante total e troponina-I foram significativamente maiores em comparação com os do grupo Acrilamida+Taxifolina e Saudável. Os níveis de glutationa total e estado antioxidante total foram significativamente mais baixos em comparação com grupos Acrilamida+Taxifolina e Saudável. Além disso, no grupo Acrilamida, o ganho de peso corporal e a ingestão de alimentos e água diminuíram significativamente em comparação com os animais dos grupos Acrilamida+Taxifolina e Saudável. No entanto, no grupo Acrilamida+Taxifolina, a suplementação com taxifolina aproximou esses valores aos do grupo Saudável. Além disso, o tratamento com taxifolina melhorou os sinais de dano miocárdico estrutural induzidos pela acrilamida. Conclusão A exposição à acrilamida induziu significativamente o dano oxidativo do tecido cardíaco dos ratos. A taxifolina foi capaz de melhorar as consequências tóxicas da acrilamida bioquímica e histopatologicamente, possivelmente devido às suas propriedades antioxidantes.
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Animals , Male , Rats , Flavonoids/therapeutic use , Oxidative Stress/drug effects , Acrylamide/adverse effects , Acrylamide/toxicity , Heart/drug effectsABSTRACT
Objective:To explore the establishment of radiation-induced heart damage (RIDH) SD rat models caused by irradiation of 15Gy/3f and the changes in early detection indicators, and evaluate the effect of irradiation combined with recombinant human endostatin (Endostar).Methods:75 adult male SD rats were randomly divided into the blank control group (C group), Endostar group (E group), 25Gy irradiation group (MHD 25 group), 15Gy irradiation group (MHD 15 group) and 15Gy irradiation combined with Endostar group (MHD 15+ E group), respectively. Blood sample was taken to measure the CK, CK-MB, LDH and CRP at 24h, 48h and 15d after corresponding interventions. After cardiac echocardiography at 1, 3 and 6 months, 5 rats in each group were randomly sacrificed and myocardial tissues were collected for HE and Masson staining. Two-way ANOVA was employed for statistical analysis. Results:Compared with group C, myocardial fibrosis were observed in the MHD 15 group at 6 months ( P<0.05), which occurred later than that in the MHD 25 group. Ejection fraction (EF) and fractional shortening (FS) were significantly decreased after 3 months in each irradiation group (all P<0.05), whereas the degree of decrease was similar among all groups (all P>0.05). The expression levels of myocardial enzymes and inflammatory cytokines did not significantly differ among different groups (all P>0.05). Conclusions:In the early stage, exposure to 15Gy/3f irradiation can cause cardiac function damage in SD rat hearts, such as the reduction of EF and FS, and even lead to myocardial fibrosis in the late stage, which is delayed and less severe than high-dose irradiation. Irradiation combined with Endostar has no significant effect on radiation myocardial injury in rats.
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OBJECTIVE@#To analyze the clinical manifestations of heart, liver and kidney damages in the early stage of COVID-19 to identify the indicators for these damages.@*METHODS@#We analyzed the clinical features, underlying diseases, and indicators of infection in 12 patients with COVID-19 on the second day after their admission to our hospital between January 20 and February 20, 2020.The data including CK-MB, aTnI, BNP, heart rate, changes in ECG, LVEF (%), left ventricular general longitudinal strain (GLS, measured by color Doppler ultrasound) were collected.The changes of liver function biochemical indicators were dynamically reviewed.BUN, UCR, eGFR, Ccr, and UACR and the levels of MA, A1M, IGU, and TRU were recorded.@*RESULTS@#The 12 patients included 2 severe cases, 8 common type cases, and 2 mild cases.Four of the patients presented with sinus tachycardia, ECG changes and abnormal GLS in spite of normal aTNI and LVEF; 1 patient had abnormal CKMB and BNP.On the first and third days following admission, the patients had normal ALT, AST and GGT levels.On day 7, hepatic function damage occurred in the severe cases, manifested by elevated ALT and AST levels.Abnormalities of eGFR, Ccr and UACR occurred in 8, 5 and 5 of the patients, respectively.Abnormal elevations of MA, A1M, IGU and TRU in urine protein were observed in 4, 4, 5, and 2 of the patients, respectively.@*CONCLUSIONS@#In patients with COVID-19, heart damage can be identified early by observing the GLS and new abnormalities on ECG in spite of normal aTNI and LVEF.Early liver injury is not obvious in these patients, but dynamic monitoring of the indicators of should be emplemented, especially in severe cases. In cases with normal CR and BUN, kidney damage can be detected early by calculating eGFR, Ccr and UACR and urine protein tests.
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Humans , Betacoronavirus , COVID-19 , Coronavirus Infections , Pandemics , Pneumonia, Viral , SARS-CoV-2ABSTRACT
Objective: To screen and optimize the modeling condition for radiation-induced heart damage (RIHD) models characterized by inflammatory-fibrosis pathological injury. Methods: The rats were irradiated with single whole-body X-ray to screen the maximal tolerated dose. Based on the screened whole-body dose, single local heart irradiation doses were used to screen the minimal X-ray dose which could induce the significant cardiac damage. And the RIHD rat model was established by exposure to the screened dose of X-ray. Tissue samples were harvested 1 day, 1 week, 2 weeks, 4 weeks and 6 weeks after irradiation. The cardiac pathological injury score, collagen volume fraction (CVF) in myocardial tissues by Masson staining, plasma myocardial enzyme level, and the expression of inflammatory and fibrosis factors in myocardial tissues were examined for evaluating the animal model. Results: The tolerance dose of whole-body irradiation was lower than 16 Gy for rats. Local irradiation dose at least 25 Gy could induce RIHD in rats. The pathological injury score of myocardial tissues, CVF in myocardial tissues and creatine kinase isoenzyme MB (CK-MB) and cardiac troponin (cTn) in plasma were increased in the RIHD model rats. Inflammatory factors including nuclear factor (NF)-κB p65, NF-κB p50 and tumor necrosis factor α (TNF-α) in myocardial tissues were increased 1 day after irradiation in the RIHD rats and maintained high to the fourth week. The expression levels of fibrotic molecules transforming growth factor β1 (TGF-β1), collagen type I (Col I) and Col III in myocardial tissues were increased gradually, and reached the peaks at week 4 after irradiation. Conclusion: Stable RIHD rat model can be established by irradiating the precardiac region with 25 Gy X-ray. Pathological observation and CVF can dynamically reflect the early inflammatory changes and the progression of fibrosis in RIHD rats. The sustained high expression of NF-κB p65, NF-κB p50 and TNF-α at early stage and the progressive increases of TGF-β1, Col I and Col III can be used to evaluate the acute inflammatory injury and delayed fibrosis in the RIHD inflammatory-fibrosis model.
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At present, heart has become an important organ at risk during radiotherapy for thoracic, mediastinal and breast carcinoma. Heart is relatively sensitive to radiation because of its anatomical location and structure. The incidence of radiation-induced cardiac adverse events can affect the long-term survival of patients. In this article, the recent progress on the basic research of radiation-induced heart damage was described as follows.
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At present,heart has become an important organ at risk during radiotherapy for thoracic,mediastinal and breast carcinoma.Heart is relatively sensitive to radiation because of its anatomical location and structure.The incidence of radiation-induced cardiac adverse events can affect the long-term survival of patients.In this article,the recent progress on the basic research of radiation-induced heart damage was described as follows.
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Objective To investigate whether pyrrolidine dithiocarbamate (PDTC) can attenuate the acute radiation-induced heart damage (RIHD) by inhibiting the activation of NF-κB and its downstream signaling pathways in rat models. Methods Twenty-one male adult Sprague-Dawley (SD) rats were randomly divided into the blank control, irradiation and PDTC plus irradiation groups (n=7 for each group). In the irradiation and PDTC+ irradiation groups,the rats received 6 MV X-ray at a single fraction of 20.0 Gy. In the PDTC+ irradiation group, intraperitonal injection of PDTC was administered at a dose of 120 mg/kg body weight,30 minutes prior to radiation, once daily for 1-14 days. On the 14thday,pathological changes of myocardial tissue were observed. Masson's trichrome staining was performed to calculate the collagen volume fraction (CVF) of myocardial cells. The expression levels of NF-κB family members including p50, p65,HIF-1α,connective tissue growth factor (CTGF) and collagen type 1(COL-1) proteins and mRNA were quantitatively measured by Western blot and quantitative real-time PCR (qPCR). Statistical analysis was conducted by using t-test. Results HE staining demonstrated that compared with the irradiation group, the severity of myocardial edema was alleviated,the infiltration of inflammatory cells was mitigated and the quantity of fibroblasts was reduced in the PDTC+irradiation group. Masson's trichrome staining revealed that PDCT intervention could decrease the deposition of collagen fiber in the interstitial tissues. Semi-quantitative analysis demonstrated that the CVF value in the PDTC+irradiation group was (9.99± 0.32)%, significantly lower compared with (22.05±0.21)% in the irradiation group (P<0.05). Western blot and qRT-PCR demonstrated that the expression levels of p50,p65,and HIF-1αproteins and mRNA in the PDTC+ irradiation group were significantly down-regulated compared with those in the irradiation group (all P<0.05). Compared with the irradiation group,the expression levels of CTGF protein and mRNA tended to decline (all P>0.05),and the expression levels of COL-1 protein and mRNA were equally inclined to decrease (P<0.05 and P>0.05). Conclusion PDTC can alleviate the acute RIHD by suppressing the activation of NF-κB and its downstream HIF-1α transcription.
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OBJECTIVE:To investigate the early changes of ECG,cTnⅠ,LDH,α-HBDH and CKMB in patients with anthra-cyclines chemotherapy-induced heart damage after breast cancer surgery,and to explore their significances in the diagnosis of early heart damage. METHODS:Medical information of 152 cases of anthracyclines chemotherapy after breast cancer surgery in our hos-pital during Jan. 2015-Jun. 2016 were analyzed retrospectively. According to diagnosis criteria of drug-induced cardiotoxicity,the occurrence of heart damage was evaluated during hospitalization and 1-year follow-up. According to evaluation results,those pa-tients were divided into heart damage group(50 cases)and control group(102 cases). The early changes of ECG,cTnⅠ,LDH, CKMB and α-HBDH were analyzed before chemotherapy(T0),24 h after first chemotherapy(T1),24 h after second chemothera-py(T2),24 h after forth chemotherapy. RESULTS:At T1,T2,T3,the proprotion of ECG abnormalities in heart damage group was significantly higher than control group;the serum levels of cTnⅠ,LDH,CKMB andα-HBDH in heart damage group were signifi-cantly higher than control group, with statistical significance (P<0.01). CONCLUSIONS:For anthracyclines chemotherapy drugs-induced heart damage after breast cancer surgery,early regular monitoring of ECG,cTnⅠ,LDH,CKMB and α-HBDH can improve the efficiency of early diagnosis of heart damage,and improve prognosis.
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Radiotherapy is an essential part of postoperative adjuvant therapy for breast cancer.However,postoperative radiotherapy for breast cancer poses a potential risk of heart damage.This article summarizes the general information and diagnosis and assessment indices of radiation-induced heart damage and its risk factors,as well as the influencing factors for radiotherapy and effective protective measures.
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Objective To investigate the incidence and clinical characteristics and look for assay or examination indexes or indicators with higher sensitivity and specificity of heart damage induced by exhaustive exercise in order to establish its preliminary clinical classification and diagnostic criteria. Methods In a military region for training staff,the clinical data of 88 soldiers who were admitted to the departments of cardiology in 6 general or central hospitals because of exhaustive exercise from January 2000 to December 2010 were analyzed. The myocardial enzyme, electrocardiogram(ECG),echocardiography and other related examination indexes or indicators were observed,and the changes of symptoms,signs and other relevant assay and examination indexes before and after treatment were recorded. Results Exhaustive exercise could cause the symptoms such as chest tightness,palpitations,chest pain, dizziness,shortness of breath,fatigue,syncope and other symptoms,as well as cardiac auscultation abnormalities. After treatment, aspartate aminotransferase〔AST(U/L):20.34±6.33 vs. 35.43±25.25〕,α-hydroxybutyrate dehydrogenase〔α-HBDH(U/L):130.47±9.04 vs. 168.93±62.69〕,lactate dehydrogenase〔LDH(μmol?s-1?L-1):2.48±0.62 vs. 3.58±1.34〕,creatine kinase〔CK(U/L):125.58±67.56 vs. 556.42±381.89〕,creatine kinase isoenzyme〔CK-MB(U/L):11.20±4.08 vs. 23.09±15.61〕were significantly lower than those before treatment(P<0.05 or P<0.01);cardiac troponin T(cTnT)was detected in 5 patients,its level after treatment was significantly lower than that before treatment(μg/L:0.07±0.05 vs. 1.26±0.78,P<0.05). The ECG abnormalities included primarily sinus bradycardia (16 cases),sinus arrhythmia (13 cases) and premature ventricular contractions (11 cases). Echocardiographic abnormalities appeared in 18 cases,they were chiefly as follows:valvular regurgitation, cardiac dysfunction,cardiac enlargement,etc,among which the most common one was valvular regurgitation(all the refluxes were of small amount). Based on the above clinical manifestations and examination results,the exhaustive cardiac injuries were preliminarily divided into common type(20 cases),arrhythmia type(56 cases),heart failure type(2 cases)and sudden death(10 cases). Conclusions The clinical manifestations of exhaustive heart damage may appear in different types. Abnormal changes of myocardial enzymes,ECG and echocardiography are the strong evidences for the damage. Clinicians should pay attention to its prevention and treatment.
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Background Chronic administration with inhibitor of nitric oxide synthase (N_?-nitro-L-arginine methyl ester,L-NAME) induces persistent hypertension,cardiovascular remodeling,surrounding vascular fibrosis, necrosis and hypertrophy of myocardium,and inflammation in cardiovascular system.Local RAS involves in hyper- tension and remodeling of cardiovascular system,via increasing production of oxygen free radicals (OFR).Objec- tive To elucidate the preventive and therapeutic effect of antioxidant Ebselen and/or VitE on hypertensive heart damage in NO~- deficient rats induced by L-NAME.Methods Thirty-two Wistar rats were administered with L- NAME 50 mg/(kg?d) by gavage for 8 weeks,and randomized to received a placebo(L),or Ebs(S,30 mg/kg?d), or VitE(V,40 mg/kg?d) or Ebs 30 mg/(kg?d)+VitE 40 mg/(kg?d),with 8 normal Wistar as control. Body mass and SBP were measured fortnightly.Plasma and homogenate of heart were collected for NO,Ang Ⅱ, GSH-PX,MDA and O_2~- determination.Results Eight weeks after L-NAME administration,SBP in experimental groups was obviously higher than that of control (P