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2.
Zhongguo Zhong Yao Za Zhi ; 44(18): 3903-3907, 2019 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-31872723

RESUMO

Cream formula has been mostly used to treat deficiency syndrome. Currently,it has been used to recuperate the body,promote health against aging,and prevent and treat chronic disease. In modern medicine,there are only treatment concepts and methods of diseases,but lack of concepts of " deficiency syndrome" and " restoring deficiency". The concepts of " deficiency syndrome" and " restoring deficiency" could effectively supplement and improve the diagnosis and treatment scheme of some modern diseases. Refractory heart failure,dilated cardiomyopathy,ischemic cardiomyopathy,and valvular heart disease belong to the traditional category of " consumptive disease". The cream formula with the efficacy of restoring deficiency can not only alleviate symptoms and improve the quality of life,but also improve the structure and function of the heart,reduce the dosage of diuretics and the number of hospitalizations,and achieve the purpose of secondary prevention in the treatment of severe heart failure,dilated cardiomyopathy,ischemic cardiomyopathy and valvular heart disease. The cream formula for treating chronic heart failure include Shenqi Pills,Zhenwu Decoction,Yougui Pills,Wuling Powder,Linggui Zhugan Decoction,Danggui Shaoyao Powder,Lizhong Decoction,Buzhong Yiqi Decoction,Guipi Decoction,Yupingfeng Powder,Guizhi Decoction. Long-term administration of cream formula could not only resist aging,but also play an irreplaceable role in the secondary prevention of acute and critical diseases.


Assuntos
Cardiomiopatias/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Insuficiência Cardíaca/tratamento farmacológico , Doenças das Valvas Cardíacas/tratamento farmacológico , Humanos , Medicina Tradicional Chinesa , Pomadas
3.
Perm J ; 232019.
Artigo em Inglês | MEDLINE | ID: mdl-31496499

RESUMO

CONTEXT: Heart failure (HF) is rapidly increasing in incidence and is often present in patients receiving long-term statin therapy. OBJECTIVE: To test whether or not patients with HF on long-term statin therapy respond to discontinuation of statin therapy and initiation of coenzyme Q10 (CoQ10) supplementation. DESIGN: We prospectively identified patients receiving long-term statin therapy in whom HF developed in the absence of any identifiable cause. Treatment consisted of simultaneous statin therapy discontinuation and CoQ10 supplementation (average dosage = 300 mg/d). MAIN OUTCOME MEASURES: Baseline and follow-up physical examination findings, symptom scores, echocardiograms, and plasma CoQ10 and cholesterol levels. RESULTS: Of 142 identified patients with HF, 94% presented with preserved ejection fraction (EF) and 6% presented with reduced EF (< 50%). After a mean follow-up of 2.8 years, New York Heart Association class 1 increased from 8% to 79% (p < 0.0001). In patients with preserved EF, 34% had normalization of diastolic function and 25% showed improvement (p < 0.0001). In patients with reduced EF at baseline, the EF improved from a mean of 35% to 47% (p = 0.02). Statin-attributable symptoms including fatigue, muscle weakness, myalgias, memory loss, and peripheral neuropathy improved (p < 0.01). The 1-year mortality was 0%, and the 3-year mortality was 3%. CONCLUSION: In patients receiving long-term statin therapy, statin-associated cardiomyopathy may develop that responds safely to statin treatment discontinuation and CoQ10 supplementation. Statin-associated cardiomyopathy may be a contributing factor to the current increasing prevalence of HF with preserved EF.


Assuntos
Cardiomiopatias/induzido quimicamente , Inibidores de Hidroximetilglutaril-CoA Redutases/efeitos adversos , Ubiquinona/análogos & derivados , Idoso , Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/fisiopatologia , Colesterol/sangue , Feminino , Insuficiência Cardíaca/induzido quimicamente , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Volume Sistólico , Ubiquinona/sangue , Ubiquinona/uso terapêutico , Vitamina E/sangue
4.
Redox Biol ; 26: 101287, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31386965

RESUMO

The basic pathophysiological mechanisms underlying septic cardiomyopathy have not yet been completely clarified. Disease-specific treatments are lacking, and care is still based on supportive modalities. The aim of our study was to assess the protective effects of melatonin on septic cardiomyopathy, with a focus on the interactions between receptor-interacting protein kinase 3 (Ripk3), the mitochondria, endoplasmic reticulum (ER) and cytoskeletal degradation in cardiomyocytes. Ripk3 expression was increased in heart samples challenged with LPS, followed by myocardial inflammation, cardiac dysfunction, myocardial breakdown and cardiomyocyte death. The melatonin treatment attenuated septic myocardial injury in a comparable manner to the genetic depletion of Ripk3. Molecular investigations revealed that Ripk3 intimately regulated mitochondrial function, ER stress, cytoskeletal homeostasis and cardioprotective signaling pathways. Melatonin-mediated inhibition of Ripk3 improved mitochondrial bioenergetics, reduced mitochondria-initiated oxidative damage, sustained mitochondrial dynamics, ameliorated ER stress, normalized calcium recycling, and activated cardioprotective signaling pathways (including AKT, ERK and AMPK) in cardiomyocytes. Interestingly, Ripk3 overexpression mediated resistance to melatonin therapy following the infection of LPS-treated hearts with an adenovirus expressing Ripk3. Altogether, our findings identify Ripk3 upregulation as a novel risk factor for the development of sepsis-related myocardial injury, and melatonin restores the physiological functions of the mitochondria, ER, contractile cytoskeleton and cardioprotective signaling pathways. Additionally, our data also reveal a new, potentially therapeutic mechanism by which melatonin protects the heart from sepsis-mediated dysfunction, possibly by targeting Ripk3.


Assuntos
Cardiomiopatias/etiologia , Cardiomiopatias/metabolismo , Retículo Endoplasmático/efeitos dos fármacos , Retículo Endoplasmático/metabolismo , Melatonina/farmacologia , Proteína Serina-Treonina Quinases de Interação com Receptores/genética , Sepse/complicações , Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/patologia , Cardiotônicos/farmacologia , Citoesqueleto/metabolismo , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Deleção de Genes , Humanos , Lipopolissacarídeos/imunologia , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos
5.
Int Immunopharmacol ; 75: 105782, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31376623

RESUMO

Sepsis-induced myocardial dysfunction (SIMD) is a manifestation of severe sepsis and is the main cause of increased mortality in sepsis patients. Naringin (Nar) has been reported to possess various biological activities and pharmacological properties. Therefore, the present study was undertaken to evaluate whether Nar can protect rats from the effects of LPS-induced SIMD. SD Rats were pre-treated with Nar (50 and 100 mg/kg) for 7 days before administration of a single dose of LPS (10 mg/kg, i.p.) on the seventh day. We found that Nar treatment markedly improved the global strain and strain rate of longitudinal, circumference, and radial direction (GLS/GLSr, GCS/GCSr, GRS/GRSr) compared to the LPS group. The layer-specific strain decreased gradually from the endocardial layer to epicardial layer, and the most serious damage occurred in the endocardial layer. Moreover, Nar significantly decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1ß, and IL-6) and myocardial enzymes (CK, LDH, and AST) induced by LPS and attenuated the inflammation response. Finally, Nar also inhibited NF-κB nuclear translocation and the activity of iNOS in H9c2 cardiomyocytes by activating PI3K/AKT signaling pathway. These results suggest that naringin may possess novel therapeutic potential for protection against LPS-induced myocardial dysfunction.


Assuntos
Cardiomiopatias/tratamento farmacológico , Cardiotônicos/uso terapêutico , Flavanonas/uso terapêutico , Sepse/tratamento farmacológico , Disfunção Ventricular Esquerda/tratamento farmacológico , Animais , Cardiomiopatias/etiologia , Cardiomiopatias/metabolismo , Cardiomiopatias/patologia , Cardiotônicos/farmacologia , Linhagem Celular , Citocinas/genética , Flavanonas/farmacologia , Lipopolissacarídeos , Masculino , Miocárdio/metabolismo , Miocárdio/patologia , NF-kappa B/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos Sprague-Dawley , Sepse/complicações , Sepse/metabolismo , Sepse/fisiopatologia , Disfunção Ventricular Esquerda/induzido quimicamente , Disfunção Ventricular Esquerda/metabolismo , Disfunção Ventricular Esquerda/fisiopatologia
6.
BMJ Case Rep ; 12(8)2019 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-31434668

RESUMO

We present the case of a 65-year-old woman who was referred urgently from primary care with worsening breathlessness for 3 weeks, associated with tachycardia and left bundle branch block (LBBB). She had a background of type 2 diabetes, asthma and hypertension. Initial ECG revealed atrial fibrillation with the fast ventricular rate on the background of LBBB. ECHO findings were consistent with systolic impairment. Initial testing including checking thyroid function test revealed hyperthyroidism. It became evident that this patient had thyrotoxic cardiomyopathy. Early advice from the endocrine team was sought and the patient was treated with a combination of carbimazole and ivabradine. After a hospital stay, she made a remarkable recovery.


Assuntos
Bloqueio de Ramo/diagnóstico , Cardiomiopatias/diagnóstico , Anti-Hipertensivos/uso terapêutico , Bisoprolol/uso terapêutico , Bloqueio de Ramo/tratamento farmacológico , Bloqueio de Ramo/fisiopatologia , Carbimazol/uso terapêutico , Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/fisiopatologia , Diabetes Mellitus Tipo 2 , Dispneia , Eletrocardiografia , Feminino , Humanos , Pessoa de Meia-Idade , Taquicardia , Resultado do Tratamento
7.
Folia Biol (Praha) ; 65(2): 70-87, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31464183

RESUMO

We investigated the detrimental effects of diabetes on myocardium of pregestational streptozotocin (STZ)-diabetic mother rats and their neonates via evaluations of oxidative redox, inflammatory and apoptotic pathways, also aiming to characterize whether calcitriol and/or pomegranate peel extract confer myocardial protection in hyperglycaemic dams and their foetuses via modulation of the Raf/MEK/ERK cascade. Sixty Sprague-Dawley female rats were randomized into five groups (N = 12): control, diabetic, diabetic treated with calcitriol and/or pomegranate peel extract (PPE), and mated with non-diabetic healthy males. After confirmation of pregnancy, treatments were kept until gestational day (E-18). Serum and cardiac tissues of mothers and foetuses were collected and processed for biochemical, histopathological, and molecular assessments. We observed that, compared to the control, diabetic mothers showed dramatically increased hyperglycaemia and hyperlipidaemia associated with decreased myocardial functions and disrupted maternal performance. Also, diabetic mothers and their neonates exhibited elevated levels of myocardial injury (troponin I, endothelin 1, creatine kinase-MB, lactate dehydrogenase), with increased pro-inflammatory cytokines (interleukin 1, interleukin 1ß, transforming growth factor ß) and oxidative redox. Concurrently, the MAPK pathway was significantly down-regulated with increased myocardial apoptotic activity. Furthermore, mRNA expression of angiogenic and fibrotic markers was significantly increased. Paradoxically, calcitriol and/or pomegranate peel extract alleviated these diabetic myocardial insults and normalized the aforementioned assayed parameters. Our findings hypothesized that calcitriol and/or pomegranate peel extract exerted cardioameliorative impacts due to their unique anti-oxidative and anti-inflammatory properties, and thus may be a promising treatment that directly targets the secondary myocardial complications of diabetes in dams and their offspring.


Assuntos
Apoptose , Calcitriol/uso terapêutico , Cardiomiopatias/tratamento farmacológico , Diabetes Mellitus Experimental/tratamento farmacológico , Sistema de Sinalização das MAP Quinases , Extratos Vegetais/uso terapêutico , /química , Animais , Animais Recém-Nascidos , Apoptose/efeitos dos fármacos , Biomarcadores/metabolismo , Cardiomiopatias/complicações , Cardiomiopatias/patologia , Caspase 3/metabolismo , Citocinas/metabolismo , Dano ao DNA , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Experimental/patologia , Feminino , Feto/patologia , Fibrose , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Miocárdio/patologia , Neovascularização Fisiológica/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Fosforilação/efeitos dos fármacos , Ratos Sprague-Dawley , Reprodução , Espectroscopia de Infravermelho com Transformada de Fourier , Estreptozocina , Regulação para Cima/efeitos dos fármacos , Vitamina D/farmacologia , Vitamina D/uso terapêutico , Quinases raf/metabolismo
8.
Int J Mol Sci ; 20(15)2019 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-31382622

RESUMO

Cardiomyocytes from human induced pluripotent stem cells (hiPSC-CMs) are the most promising human source with preserved genetic background of healthy individuals or patients. This study aimed to establish a systematic procedure for exploring development of hiPSC-CM functional output to predict genetic cardiomyopathy outcomes and identify molecular targets for therapy. Biomimetic substrates with microtopography and physiological stiffness can overcome the immaturity of hiPSC-CM function. We have developed a custom-made apparatus for simultaneous optical measurements of hiPSC-CM action potential and calcium transients to correlate these parameters at specific time points (day 60, 75 and 90 post differentiation) and under inotropic interventions. In later-stages, single hiPSC-CMs revealed prolonged action potential duration, increased calcium transient amplitude and shorter duration that closely resembled those of human adult cardiomyocytes from fresh ventricular tissue of patients. Thus, the major contribution of sarcoplasmic reticulum and positive inotropic response to ß-adrenergic stimulation are time-dependent events underlying excitation contraction coupling (ECC) maturation of hiPSC-CM; biomimetic substrates can promote calcium-handling regulation towards adult-like kinetics. Simultaneous optical recordings of long-term cultured hiPSC-CMs on biomimetic substrates favor high-throughput electrophysiological analysis aimed at testing (mechanistic hypothesis on) disease progression and pharmacological interventions in patient-derived hiPSC-CMs.


Assuntos
Antagonistas Adrenérgicos beta/farmacologia , Cálcio/metabolismo , Cardiomiopatias/tratamento farmacológico , Células-Tronco Pluripotentes Induzidas/metabolismo , Potenciais de Ação/efeitos dos fármacos , Biomimética , Cardiomiopatias/genética , Cardiomiopatias/patologia , Diferenciação Celular/efeitos dos fármacos , Células Cultivadas , Acoplamento Excitação-Contração/efeitos dos fármacos , Humanos , Hidrogéis/farmacologia , Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Retículo Sarcoplasmático/efeitos dos fármacos , Retículo Sarcoplasmático/metabolismo , Especificidade por Substrato
9.
Environ Toxicol Pharmacol ; 71: 103221, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31365892

RESUMO

Our aim was to compare the protective efficacy of two different formulations of methylprednisolone in T-2 toxin-induced cardiomyopathy. Methylprednisolone (soluble form, Lemod-solu® and/or depot form, Lemod-depo®, a total single dose of 40 mg/kg im) was given immediately after T-2 toxin (1 LD50 0.23 mg/kg sc). The myocardial tissue samples were examinated by using histopathology, semiquantitative and imaging analyses on day 1, 7, 14, 21, 28 and 60 of the study. Therapeutic application of Lemod-solu® significantly decreased the intensity of myocardial degeneration and haemorrhages, distribution of glycogen granules in the endo- and perimysium, a total number of mast cells and the degree of their degranulation was in correlation with the reversible heart structural lesions (p <  0.01 vs. T-2 toxin). These changes were completely abolished by the therapeutic use of Lemod-solu® plus Lemod-depo® (p <  0.001 vs. T-2 toxin). Our results show that a significant cardioprotective efficacy of methylprednisolone is mediated by its anti-inflammatory activity.


Assuntos
Anti-Inflamatórios/uso terapêutico , Cardiomiopatias/tratamento farmacológico , Metilprednisolona/uso terapêutico , Miocárdio/patologia , Toxina T-2/toxicidade , Animais , Anti-Inflamatórios/administração & dosagem , Cardiomiopatias/induzido quimicamente , Preparações de Ação Retardada , Relação Dose-Resposta a Droga , Glicogênio/metabolismo , Masculino , Mastócitos/efeitos dos fármacos , Mastócitos/metabolismo , Mastócitos/patologia , Metilprednisolona/administração & dosagem , Miocárdio/metabolismo , Ratos Wistar
10.
Biomed Res Int ; 2019: 6595437, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31317035

RESUMO

Endothelial-to-mesenchymal transition (EndMT) is an essential mechanism in myocardial fibrosis (MF). Tongxinluo (TXL) has been confirmed to protect the endothelium against reperfusion injury after acute myocardial infarction (AMI). However, whether TXL can inhibit MF after AMI via inhibiting EndMT remained unknown. This study aims to identify the role of EndMT in MF after AMI as well as the protective effects and underlying mechanisms of TXL on MF. The AMI model was established in rats by ligating left anterior descending coronary artery. Then, rats were administered with high- (0.8 g·kg-1·d-1), mid- (0.4 g·kg-1·d-1), and low- (0.2 g·kg-1·d-1) dose Tongxinluo and benazepril for 4 weeks, respectively. Cardiac function, infarct size, MF, and related indicators of EndMT were measured. In vitro, human cardiac microvascular endothelial cells (HCMECs) were pretreated with TXL for 4 h and then incubated in hypoxia conditions for 3 days to induce EndMT. Under this hypoxic condition, neuregulin-1 (NRG-1) siRNA were further applied to silence NRG-1 expression. Immunofluorescence microscopy was used to assess expression of endothelial marker of vWF and fibrotic marker of Vimentin. Related factors of EndMT were determined by Western blot analysis. TXL treatment significantly improved cardiac function, ameliorated MF, reduced collagen of fibrosis area (types I and III collagen) and limited excessive extracellular matrix deposition (mmp2 and mmp9). In addition, TXL inhibited EndMT in cardiac tissue and hypoxia-induced HCMECs. In hypoxia-induced HCMECs, TXL increased the expression of endothelial markers, whereas decreasing the expression of fibrotic markers, partially through enhanced expressions of NRG-1, phosphorylation of ErbB2, ErbB4, AKT, and downregulated expressions of hypoxia inducible factor-1a and transcription factor snail. After NRG-1 knockdown, the protective effect of TXL on HCMEC was partially abolished. In conclusion, TXL attenuates MF after AMI by inhibiting EndMT and through activating the NRG-1/ErbB- PI3K/AKT signalling cascade.


Assuntos
Cardiomiopatias/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Fibrose/tratamento farmacológico , Infarto do Miocárdio/tratamento farmacológico , Animais , Cardiomiopatias/metabolismo , Cardiomiopatias/patologia , Hipóxia Celular/efeitos dos fármacos , Vasos Coronários/efeitos dos fármacos , Vasos Coronários/crescimento & desenvolvimento , Modelos Animais de Doenças , Células Endoteliais/efeitos dos fármacos , Endotélio/efeitos dos fármacos , Endotélio/metabolismo , Fibrose/metabolismo , Fibrose/patologia , Humanos , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/patologia , Miocárdio/metabolismo , Miocárdio/patologia , Fosfatidilinositol 3-Quinases/metabolismo , Fosforilação/efeitos dos fármacos , Ratos
11.
Biomed Res Int ; 2019: 6539050, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31309111

RESUMO

Objective: To determine whether the administration of intra-arrest cyclosporine (CCY) and methylprednisolone (MP) preserves left ventricular ejection fraction (LVEF) and cardiac output (CO) after return of spontaneous circulation (ROSC). Methods: Eleven, 25-30kg female swine were randomized to receive 10mg/kg CCY + 40mg MP or placebo, anesthetized and given a transthoracic shock to induce ventricular fibrillation. After 8 minutes, standard CPR was started. After two additional minutes, the experimental agent was administered. Animals with ROSC were supported for up to 12h with norepinephrine as needed. Echocardiography was performed at baseline, and 1, 2, 6 and 12h post-ROSC. Analysis was performed using generalized estimating equations (GEE) after downsampling continuously sampled data to 5 minute epochs. Results: Eight animals (64%) achieved ROSC after a median of 7 [IQR 5-13] min of CPR, 2 [ IQR 1-3] doses of epinephrine and 2 [IQR 1-5] defibrillation shocks. Animals receiving CCY+MP had higher post ROSC MAP (GEE coefficient -10.2, P = <0.01), but reduced cardiac output (GEE coefficient 0.8, P = <0.01) compared to placebo. There was no difference in LVEF or vasopressor use between arms. Conclusions: Intra-arrest cyclosporine and methylprednisolone decreased post-arrest cardiac output and increased mean arterial pressure without affecting left ventricular ejection fraction.


Assuntos
Cardiomiopatias/tratamento farmacológico , Ciclosporina/farmacologia , Parada Cardíaca/tratamento farmacológico , Metilprednisolona/farmacologia , Animais , Débito Cardíaco/efeitos dos fármacos , Reanimação Cardiopulmonar/métodos , Ecocardiografia/métodos , Cardioversão Elétrica/métodos , Epinefrina/farmacologia , Feminino , Ventrículos do Coração/efeitos dos fármacos , Suínos , Vasoconstritores/farmacologia , Fibrilação Ventricular/tratamento farmacológico
12.
Amyloid ; 26(3): 103-111, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31339362

RESUMO

Timely diagnosis of hereditary variant transthyretin (ATTRv) amyloidosis is critical for appropriate treatment and optimal outcomes. Significant differences are seen between patients receiving treatment and those who are not, though disease progression may continue despite treatment in some patients. Healthcare professionals caring for patients with ATTRv amyloidosis therefore need reliable ongoing assessments to understand the continuing course of disease and make appropriate treatment choices on an individual basis. Various signs and symptoms experienced by patients may be evaluated as indicators of disease progression, though there is currently no validated score that can be used for such ongoing assessment. Recognizing this situation, a group of clinicians highly experienced in ATTR amyloidosis developed an approach to understand and define disease progression in diagnosed and treated patients with ATTRv amyloidosis. The suggested approach is based on the recognition of distinct phenotypes which may usefully inform the particular tools, tests and investigations that are most likely to be appropriate for individual patients. It is aimed at implementing appropriate and ongoing assessment of patients being treated for ATTRv amyloidosis, such that the effectiveness of management can be usefully assessed throughout the course of disease and management can be tailored according to the patient's requirements.


Assuntos
Neuropatias Amiloides Familiares/diagnóstico , Cardiomiopatias/diagnóstico , Gerenciamento Clínico , Glaucoma/diagnóstico , Neuropatias Hereditárias Sensoriais e Autônomas/diagnóstico , Adulto , Idade de Início , Idoso , Neuropatias Amiloides Familiares/tratamento farmacológico , Neuropatias Amiloides Familiares/genética , Neuropatias Amiloides Familiares/fisiopatologia , Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/genética , Cardiomiopatias/fisiopatologia , Consenso , Progressão da Doença , Feminino , Glaucoma/tratamento farmacológico , Glaucoma/genética , Glaucoma/fisiopatologia , Testes de Função Cardíaca , Neuropatias Hereditárias Sensoriais e Autônomas/tratamento farmacológico , Neuropatias Hereditárias Sensoriais e Autônomas/genética , Neuropatias Hereditárias Sensoriais e Autônomas/fisiopatologia , Humanos , Testes de Função Renal , Masculino , Pessoa de Meia-Idade , Mutação , Fármacos Neuroprotetores/uso terapêutico , Pré-Albumina/deficiência , Pré-Albumina/genética
13.
Horm Mol Biol Clin Investig ; 39(2)2019 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-31301670

RESUMO

Beta-thalassemia major is a subtype component of hemoglobinopathies; autosomal recessive disorders complicated with anemia that affect at least 50,000 babies each year. It contributes to problems in reproductive entities such as infertility due to iron deposition in the endocrine organs, which leads to malfunction of the hypothalamus-pituitary axis. Due to this, there have been very few pregnancies discovered and reported with this type of condition as they usually required an ovulation-induction agent with assisted reproductive technique to achieved pregnancy. We report a successful spontaneous pregnancy in a woman with beta-thalassemia major who underwent splenectomy with lifelong transfusion-dependence complicated with myocardial siderosis and osteoporosis. The close monitoring and regular blood transfusion are a core of successful support to this type of pregnancy. The unintentional consumption of Fosamax, hydroxyurea and deferiprone (Ferriprox) up till 20 weeks of gestation did not show any adverse effects on fetal well-being. As expected, this pregnancy ended with the preterm delivery via cesarean section due to intrauterine growth restriction with oligohydramnios, and currently, this child is thriving. We concluded that pregnancy is not a contraindication in beta-thalassemia major; complex individual care is needed to achieve a safe outcome for the mother.


Assuntos
Cardiomiopatias/etiologia , Homozigoto , Osteoporose/etiologia , Siderose/etiologia , Globinas beta/genética , Talassemia beta/complicações , Transfusão de Sangue , Cardiomiopatias/diagnóstico , Cardiomiopatias/tratamento farmacológico , Deferiprona/administração & dosagem , Deferiprona/uso terapêutico , Feminino , Humanos , Quelantes de Ferro/administração & dosagem , Quelantes de Ferro/uso terapêutico , Osteoporose/tratamento farmacológico , Gravidez , Complicações na Gravidez , Resultado da Gravidez , Siderose/diagnóstico , Siderose/tratamento farmacológico , Esplenectomia/métodos , Adulto Jovem , Talassemia beta/diagnóstico , Talassemia beta/etiologia
14.
Rev Cardiovasc Med ; 20(2): 53-58, 2019 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-31344997

RESUMO

Peripartum cardiomyopathy is a type of non-ischemic cardiomyopathy with a high rate of thromboembolic events. Guiding strategies for anticoagulation in patients with peripartum cardiomyopathy and thromboembolic events are limited. Literature for all cases of peripartum cardiomyopathy with intracardiac thrombi were reviewed and summarized from twelve case reports. Based on the available literature, we conclude that patients with peripartum cardiomyopathy with ejection fraction of less than 30% should strongly consider anticoagulation therapy to avoid thromboembolic events. Future studies may be able to further elucidate the optimal indication and duration of anticoagulation.


Assuntos
Anticoagulantes/uso terapêutico , Coagulação Sanguínea/efeitos dos fármacos , Cardiomiopatias/tratamento farmacológico , Complicações Cardiovasculares na Gravidez/tratamento farmacológico , Trombose/tratamento farmacológico , Adulto , Anticoagulantes/efeitos adversos , Cardiomiopatias/sangue , Cardiomiopatias/diagnóstico , Cardiomiopatias/fisiopatologia , Feminino , Humanos , Período Periparto , Gravidez , Complicações Cardiovasculares na Gravidez/sangue , Complicações Cardiovasculares na Gravidez/diagnóstico , Complicações Cardiovasculares na Gravidez/fisiopatologia , Trombose/sangue , Trombose/diagnóstico , Trombose/fisiopatologia , Resultado do Tratamento , Adulto Jovem
15.
Rev Cardiovasc Med ; 20(2): 73-80, 2019 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-31344999

RESUMO

Currently, the percentage of non-specific myocardial lesions of non-inflammatory genesis has significantly increased in the structure of cardiovascular diseases in children and adolescents. Cardiomyopathies are a cluster of myocardial diseases that have become more of interest by cardiologists, morphologists, geneticists, and cardiac surgeons. Cardiomyopathies in children are regarded as a severe pathology characterized by a progressive course, resistance to therapy, and result in an unfavourable prognosis. The current article presents data from international publications dedicated to cardiomyopathy diagnostics in children. This article deals with terminology issues in compliance with international disease classification, primary diagnostic criteria of non-coronary myocardium pathology, and modern methods of diagnostics and pharmacotherapy.


Assuntos
Cardiologia , Cardiomiopatias/metabolismo , Metabolismo Energético , Doenças Metabólicas/metabolismo , Miocárdio/metabolismo , Pediatria , Idade de Início , Animais , Cardiomiopatias/classificação , Cardiomiopatias/diagnóstico , Cardiomiopatias/tratamento farmacológico , Fármacos Cardiovasculares/uso terapêutico , Metabolismo Energético/efeitos dos fármacos , Humanos , Doenças Metabólicas/classificação , Doenças Metabólicas/diagnóstico , Doenças Metabólicas/tratamento farmacológico , Miocárdio/patologia , Valor Preditivo dos Testes , Fatores de Risco , Terminologia como Assunto , Resultado do Tratamento
17.
Eur J Pharmacol ; 859: 172490, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31229536

RESUMO

Doxorubicin (DOX) is a classic anti-tumor chemotherapeutic used to treat a wide range of tumors. One major downfall of DOX treatment is it can induce fatal cardiotoxicity. Astragaloside IV (AS-IV) is one of the primary active ingredients that can be isolated from the traditional Chinese herbal medicine, Astragalus membranaceus. This study uses both in vitro and in vivo tools to investigate whether AS-IV alleviates DOX induced cardiomyopathy. We found that AS-IV supplementation alleviates body weight loss, myocardial injury, apoptosis of cardiomyocytes, cardiac fibrosis and cardiac dysfunction in DOX-treated mice. Also, DOX-induced cardiomyocyte injury and apoptosis were effectively improved by AS-IV treatment in vitro. NADPH oxidase (NOX) plays an important role in the progress of the oxidative signal transduction and DOX-induced cardiomyopathy. In this study, we found that AS-IV treatment relieves DOX-induced NOX2 and NOX4 expression and oxidative stress in cardiomyocytes. In conclusion, AS-IV, an antioxidant, attenuates DOX-induced cardiomyopathy through the suppression of NOX2 and NOX4.


Assuntos
Cardiomiopatias/induzido quimicamente , Cardiomiopatias/tratamento farmacológico , Doxorrubicina/efeitos adversos , NADPH Oxidase 2/antagonistas & inibidores , NADPH Oxidase 4/antagonistas & inibidores , Estresse Oxidativo/efeitos dos fármacos , Saponinas/farmacologia , Triterpenos/farmacologia , Animais , Peso Corporal/efeitos dos fármacos , Cardiomiopatias/metabolismo , Cardiomiopatias/patologia , Cardiotoxicidade/tratamento farmacológico , Cardiotoxicidade/etiologia , Cardiotoxicidade/metabolismo , Cardiotoxicidade/patologia , Tamanho Celular , Regulação da Expressão Gênica/efeitos dos fármacos , Masculino , Camundongos , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , NADPH Oxidase 2/metabolismo , NADPH Oxidase 4/metabolismo , Tamanho do Órgão/efeitos dos fármacos , Ratos , Saponinas/uso terapêutico , Triterpenos/uso terapêutico
18.
J Vet Intern Med ; 33(4): 1585-1592, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31222803

RESUMO

BACKGROUND: Typical atrioventricular accessory pathways (APs) are composed of myocardial cells. They provide electrical connections between atria and ventricles separate from the normal conduction system. Accessory pathways can participate in a macroreentrant circuit resulting in orthodromic atrioventricular reciprocating tachycardia (OAVRT). HYPOTHESIS: Because of ultrastructural similarities of typical AP cells to ventricular myocardial cells, we hypothesized lidocaine would be effective in blocking AP conduction, thus terminating OAVRT. ANIMALS: Thirty-two consecutive client-owned dogs presenting with narrow complex tachyarrhythmias were confirmed to have OAVRT by electrophysiologic study (EPS). METHODS: Prospective, nonrandomized, single-arm study with lidocaine administered IV to dogs during OAVRT in 2 mg/kg boluses to a cumulative dose of 8 mg/kg or development of adverse effects. Electrocardiograms were monitored continuously. Subsequent EPS was performed to confirm OAVRT and the absence of other tachycardia mechanisms. RESULTS: Twenty-seven dogs experienced OAVRT cardioversion with lidocaine, before or at the time of adverse effects. Orthodromic atrioventricular reciprocating tachycardia in 5 dogs did not cardiovert before adverse effects, precluding additional dosing. Median total lidocaine dose for cardioversion was 2 mg/kg (interquartile range, 2-5.5 mg/kg). Dogs with right free wall APs had a significantly higher rate of cardioversion than did dogs with right posteroseptal APs. CONCLUSIONS AND CLINICAL IMPORTANCE: Lidocaine successfully cardioverted OAVRT in 84.4% of dogs in our study before adverse effects precluded additional dosing. In 5 dogs with dose limited by adverse effects, it is unknown whether cardioversion would have occurred at a higher cumulative dose.


Assuntos
Antiarrítmicos/farmacologia , Doenças do Cão/tratamento farmacológico , Lidocaína/farmacologia , Taquicardia Reciprocante/veterinária , Animais , Antiarrítmicos/administração & dosagem , Antiarrítmicos/efeitos adversos , Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/veterinária , Cães , Feminino , Lidocaína/administração & dosagem , Lidocaína/efeitos adversos , Masculino , Estudos Prospectivos , Taquicardia Reciprocante/tratamento farmacológico
19.
Life Sci ; 230: 19-27, 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31125563

RESUMO

AIMS: We investigated the effect of the selective sodium-dependent glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin on cardiac dysfunction and histopathology in a non-diabetic rat model of cardiomyopathy. MAIN METHODS: Ipragliflozin was mixed with chow (0.01%, w/w) and administered to male DahlS.Z-Leprfa/Leprfa (DS/obese) rats for 8 weeks. Male DahlS.Z-Lepr+/Lepr+ (DS/lean) rats of the same age were used as controls. Systolic blood pressure (SBP) and heart rate (HR) were measured every 4 weeks. After 8 weeks of treatment, echocardiography and histopathological examinations were performed. Further, the effect of ipragliflozin on blood and urine parameters were investigated. KEY FINDINGS: In the DS/obese rats, ipragliflozin delayed the age-related increase in SBP without affecting HR, reduced left ventricular (LV) mass and intraventricular septal thickness in echocardiography, and ameliorated hypertrophy of cardiomyocytes and LV fibrosis in histopathological examination. Although ipragliflozin significantly increased both urine volume and urinary glucose excretion in DS/obese rats, it did not alter plasma glucose levels. SIGNIFICANCE: Ipragliflozin prevented LV hypertrophy and fibrosis in non-diabetic DS/obese rats without affecting plasma glucose levels. These findings suggest that SGLT2 inhibitors have a cardio-protective effect in non-diabetic patients with cardiomyopathy.


Assuntos
Cardiomiopatias/tratamento farmacológico , Cardiomiopatias/patologia , Glucosídeos/farmacologia , Tiofenos/farmacologia , Animais , Pressão Sanguínea/efeitos dos fármacos , Modelos Animais de Doenças , Ecocardiografia , Fibrose/tratamento farmacológico , Fibrose/prevenção & controle , Glucosídeos/metabolismo , Coração/efeitos dos fármacos , Frequência Cardíaca/efeitos dos fármacos , Hipertrofia Ventricular Esquerda/tratamento farmacológico , Hipertrofia Ventricular Esquerda/prevenção & controle , Hipoglicemiantes/farmacologia , Masculino , Síndrome Metabólica/fisiopatologia , Obesidade , Ratos , Ratos Endogâmicos Dahl , Transportador 2 de Glucose-Sódio/efeitos dos fármacos , Transportador 2 de Glucose-Sódio/metabolismo , Inibidores do Transportador 2 de Sódio-Glicose/metabolismo , Inibidores do Transportador 2 de Sódio-Glicose/farmacologia , Sístole/efeitos dos fármacos , Tiofenos/metabolismo
20.
J Biomed Sci ; 26(1): 32, 2019 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-31064352

RESUMO

BACKGROUND: Our previous studies have demonstrated that Ca2+ desensitizing catechin could correct diastolic dysfunction in experimental animals with restrictive cardiomyopathy. In this study, it is aimed to assess the effects of green tea extract catechin on cardiac function and other clinical features in pediatric patients with cardiomyopathies. METHODS: Twelve pediatric cardiomyopathy patients with diastolic dysfunction were enrolled for the study. Echocardiography, ECG, and laboratory tests were performed before and after the catechin administration for 12 months. Comparison has been made in these patients before and after the treatment with catechin. Next Generation Sequencing was conducted to find out the potential causative gene variants in all patients. RESULTS: A significant decrease of isovolumetric relaxation time (115 ± 46 vs 100 ± 42 ms, P = 0.047 at 6 months; 115 ± 46 vs 94 ± 30 ms, P = 0.033 at 12 months), an increase of left ventricle end diastolic volume (40 ± 28 vs 53 ± 28 ml, P = 0.028 at 6 months; 40 ± 28 vs 48 ± 33 ml, P = 0.011 at 12 months) and stroke volume (25 ± 16 vs 32 ± 17 ml, P = 0.022 at 6 months; 25 ± 16 vs 30 ± 17 ml, P = 0.021 at 12 months) were observed with echocardiography in these patients 6-month after the treatment with catechin. Ejection fraction, left ventricular wall thickness, biatrial dimension remained unchanged. No significant side effects were observed in the patients tested. CONCLUSIONS: This study indicates that Ca2+ desensitizing green tea extract catechin, is helpful in correcting the impaired relaxation in pediatric cardiomyopathy patients with diastolic dysfunction.


Assuntos
Camellia sinensis/química , Cardiomiopatias/tratamento farmacológico , Catequina/farmacologia , Extratos Vegetais/farmacologia , Adolescente , Criança , Pré-Escolar , Ecocardiografia , Eletrocardiografia , Feminino , Humanos , Lactente , Masculino
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