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1.
Anticancer Res ; 39(8): 4227-4236, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31366510

RESUMO

BACKGROUND/AIM: Chest radiotherapy (RT) doubles late cardiac mortality. This study aimed to evaluate the evolution of cardiac changes in speckle tracking echocardiography during a three-year follow-up. MATERIALS AND METHODS: This prospective study included 81 chemotherapy-naïve early-stage breast cancer patients who were evaluated at baseline, immediately after RT and three years after RT. Sixty-one patients had left-sided (LSBC) and 20 right-sided breast cancer (RSBC). RESULTS: Global longitudinal strain (GLS) declined from baseline -18.0±3.3% to -17.0±3.0% (p=0.015) at the three-year follow-up examination. A decline over 15% (GLS15) was observed in 19 (27%) patients. GLS15 was independently associated with aromatase inhibitor use (ß=-1.977, p=0.001). In regional analysis, patients with LSBC had apical strain decline by 3.2±5.5% (p<0.001) and patients with RSBC showed basal rotation decline by 1.8° (-0.2°, 3.8°) (p=0.030). CONCLUSION: Even contemporary RT induced progressive global and regional decline in speckle tracking analysis. The regional changes complied with RT fields.


Assuntos
Neoplasias da Mama/radioterapia , Ventrículos do Coração/fisiopatologia , Radioterapia/efeitos adversos , Disfunção Ventricular Esquerda/fisiopatologia , Idoso , Neoplasias da Mama/complicações , Neoplasias da Mama/patologia , Ecocardiografia , Feminino , Coração/fisiopatologia , Coração/efeitos da radiação , Ventrículos do Coração/efeitos da radiação , Humanos , Pessoa de Meia-Idade
2.
Life Sci ; 234: 116734, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31394126

RESUMO

AIMS: Acute myocardial insulin resistance is an independent risk factor for patients who undergo cardiac surgery with cardiopulmonary bypass (CPB). However, the underlying mechanism of insulin resistance during CPB has not been fully investigated. MATERIALS AND METHODS: To explore the role of myocardial insulin resistance on the cardiac function and its underlying mechanism, CPB operation and pharmacological intervention were applied in mini pigs, and myocardial insulin signaling, glucose uptake, ATP production and cardiac function were examined. KEY FINDINGS: Our data showed that CPB elicited not only hyperglycemia and hyperinsulinemia, but also inactivated Akt, and impaired the transposition of membrane glucose transporter-4 (GLUT-4), reduced glucose uptake and ATP production in the myocardium as well, which in turn was accompanied with cardiac dysfunction. Meanwhile, linear correlations were established among reduced myocardial glucose uptake, ATP production, and depressed cardiac systolic or diastolic function. Reactivation of Akt by SC79, an Akt agonist, partially alleviated myocardial insulin resistance and restored post CPB cardiac function via augmenting myocardial glucose uptake and ATP production. SIGNIFICANCE: These findings revealed that acute myocardial insulin resistance due to inactivation of Akt played a key role in cardiac dysfunction post CPB via suppressing glucose metabolism related energy supply.


Assuntos
Ponte Cardiopulmonar/efeitos adversos , Resistência à Insulina , Insulina/metabolismo , Miocárdio/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Trifosfato de Adenosina/metabolismo , Animais , Glucose/metabolismo , Transportador de Glucose Tipo 4/metabolismo , Coração/fisiopatologia , Masculino , Miocárdio/patologia , Suínos , Porco Miniatura
3.
Expert Rev Med Devices ; 16(8): 675-682, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31306049

RESUMO

Introduction: Cardiovascular diseases are accompanied by autonomic nervous system (ANS) imbalance which is characterized by decreased vagal tone. Preclinical and clinical studies have revealed that increasing vagal activity via vagus nerve stimulation (VNS) could protect the heart. Based on these studies, VNS has emerged as a potential non-pharmaceutical treatment strategy. Although it's still difficult to find the optimal stimulus parameters, however, in arrhythmia model, it is reported that low-level VNS (LL-VNS) exacts paradoxical effects from the high-level VNS. Thus, the concept of LL-VNS is introduced. Areas covered: Animal and human studies have discussed the safety and efficacy of VNS and LL-VNS, and this review will discuss the research data in cardiovascular diseases, including atrial arrhythmia, ventricular arrhythmia, ischemia/reperfusion injury, heart failure, and hypertension. Expert opinion: In this regard, various clinical studies have been performed to verify the safety and efficacy of VNS. It is shown that VNS is well-tolerated and safe, but the results of its efficacy are conflicting, which may well block the translational process of VNS. The appearance of LL-VNS brings new idea and inspiration, suggesting an important role of subthreshold stimulation. A better understanding of the LL-VNS will contribute to translational research of VNS.


Assuntos
Doenças Cardiovasculares/terapia , Estimulação do Nervo Vago/métodos , Animais , Encéfalo/fisiopatologia , Doenças Cardiovasculares/fisiopatologia , Coração/fisiopatologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Nervo Vago/fisiopatologia
4.
Bioelectrochemistry ; 129: 170-178, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31181439

RESUMO

Our aim was to investigate if the cardioplegic solution HTK can be improved by the addition of the ROS scavenger melatonin. 158 guinea pig hearts without (UI80) or with HTK protection (HTK80) were investigated in ischemia/reperfusion experiments. Ischemia lasted 80 min at 30 °C. Melatonin was given before ischemia (UI80 + M1, HTK80 + M1) or before and after ischemia (UI80 + M2, HTK80 + M2). We measured the left ventricular developed pressure (LVDP), diastolic pressure (LVPmin), cardiac rhythm (VC-RR), time of electrical cell uncoupling (t-in) and recovery (t-ret), intracellular Ca++ [Ca++], and postischemic ROS. After 45 min reperfusion, LVDP in UI80 was significantly higher than in HTK80 (p < .01). Compared to UI80, the postischemic ROS burst was slightly smaller in HTK80 and significantly smaller in HTK80 + M1 and HTK80 + M2 (p < .05). Melatonin had no effect on LVPmin, t-in, t-ret, [Ca++], and on LVDP in groups UI80 + M1 and HTK80 + M1, improved slightly VC-RR (n. s.) but significantly decreased LVDP in the groups UI80 + M2 and HTK80 + M2 (p < .01). With melatonin we were able to attenuate the postischemic ROS burst, but the tissue damage by ROS seemed to be less important for the chosen ischemia condition because melatonin was unable to improve the functional recovery during reperfusion of HTK protected hearts.


Assuntos
Soluções Cardioplégicas/uso terapêutico , Depuradores de Radicais Livres/uso terapêutico , Parada Cardíaca Induzida/métodos , Coração/efeitos dos fármacos , Melatonina/uso terapêutico , Traumatismo por Reperfusão Miocárdica/terapia , Animais , Feminino , Cobaias , Coração/fisiopatologia , Frequência Cardíaca/efeitos dos fármacos , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Traumatismo por Reperfusão Miocárdica/cirurgia
5.
Cell Physiol Biochem ; 53(1): 101-120, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31215778

RESUMO

In the recent decades, cardiovascular diseases emerged as the major leading cause of human mortality. However, current clinical approaches still do not encompass a thorough therapeutic solution for improving heart function of the patients who suffered an extensive myocardial injury. Based on this status quo, stem cells could become a novel option, as a natural source of the new myocardium lineage cells, being capable of paracrine factors secretion, protection or even regeneration of the damaged heart muscle. Efficient stem cell-based therapy of the heart should lead to repair or/and replacement of the degenerated tissue with functional myocardial and endothelial cells. Hereon, various types of pluripotent and multipotent stem cells have been already studied in the pre-clinical and clinical settings, demonstrating their cardiomyogenic and regenerative potential. In this context, as a type of male adult stem/ progenitors, spermatogonial stem cells feature a remarkable ability for a formation of cardiovascular lineages, based on our own observations. Presented data supports the presumption, that spermatogonial stem cells not only have a suitable capacity to generate functional heart cells but can also potentially improve the function of an injured myocardium. In this review article, we first describe the essential molecular and pathophysiological mechanisms involved in the heart tissue injury. Afterwards, based on our ongoing study, we review the impact of the stem cell technologies on the regeneration therapy in cardiovascular and myocardial diseases. Particular emphasis is being put on the usability of spermatogonial stem cells in cardiac therapy.


Assuntos
Células-Tronco Germinativas Adultas/citologia , Traumatismos Cardíacos/terapia , Coração/fisiologia , Regeneração , Transplante de Células-Tronco , Células-Tronco/citologia , Células-Tronco Germinativas Adultas/metabolismo , Células-Tronco Germinativas Adultas/transplante , Animais , Diferenciação Celular , Coração/fisiopatologia , Traumatismos Cardíacos/patologia , Traumatismos Cardíacos/fisiopatologia , Humanos , Miocárdio/citologia , Miocárdio/patologia , Miócitos Cardíacos/citologia , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Transplante de Células-Tronco/métodos , Células-Tronco/metabolismo
6.
Nat Commun ; 10(1): 2685, 2019 06 18.
Artigo em Inglês | MEDLINE | ID: mdl-31213605

RESUMO

Hypertrophic cardiomyopathy (HCM) affects 1 in 500 people and leads to hyper-contractility of the heart. Nearly 40 percent of HCM-causing mutations are found in human ß-cardiac myosin. Previous studies looking at the effect of HCM mutations on the force, velocity and ATPase activity of the catalytic domain of human ß-cardiac myosin have not shown clear trends leading to hypercontractility at the molecular scale. Here we present functional data showing that four separate HCM mutations located at the myosin head-tail (R249Q, H251N) and head-head (D382Y, R719W) interfaces of a folded-back sequestered state referred to as the interacting heads motif (IHM) lead to a significant increase in the number of heads functionally accessible for interaction with actin. These results provide evidence that HCM mutations can modulate myosin activity by disrupting intramolecular interactions within the proposed sequestered state, which could lead to hypercontractility at the molecular level.


Assuntos
Miosinas Cardíacas/metabolismo , Cardiomiopatia Hipertrófica/genética , Cardiomiopatia Hipertrófica/fisiopatologia , Contração Miocárdica/genética , Cadeias Pesadas de Miosina/metabolismo , Actinas/metabolismo , Animais , Miosinas Cardíacas/genética , Linhagem Celular , Movimento Celular/genética , Coração/fisiopatologia , Humanos , Camundongos , Mutação , Mioblastos , Cadeias Pesadas de Miosina/genética , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo
7.
Life Sci ; 232: 116526, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31170418

RESUMO

Tumors and heart disease are two of the leading causes of human death. With the development of anti-cancer therapy, the survival rate of cancer patients has been significantly improved. But at the same time, the incidence of cardiovascular adverse events caused by cancer treatment has also been considerably increased, such as arrhythmia, left ventricular (LV) systolic and diastolic dysfunction, and even heart failure (HF), etc., which seriously affects the quality of life of cancer patients. More importantly, the occurrence of adverse events may lead to the adjustment or the cessation of anti-cancer treatment, which affects the survival rate of patients. Understanding the mechanism of cardiotoxicity (CTX) induced by antineoplastic drugs is the basis of adequate protection of the heart without impairing the efficacy of antineoplastic therapy. Based on current research, a large amount of evidence has shown that oxidative stress (OS) plays an essential role in CTX induced by antineoplastic drugs and participates in its toxic reaction directly and indirectly. Here, we will review the mechanism of action of OS in cardiac toxicity of antineoplastic drugs, to provide new ideas for researchers, and provide further guidance for clinical prevention and treatment of cardiac toxicity of anti-tumor drugs in the future.


Assuntos
Antineoplásicos/metabolismo , Cardiotoxicidade/prevenção & controle , Estresse Oxidativo/fisiologia , Antineoplásicos/efeitos adversos , Arritmias Cardíacas/complicações , Arritmias Cardíacas/fisiopatologia , Cardiotoxicidade/metabolismo , Coração/fisiopatologia , Cardiopatias/tratamento farmacológico , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/fisiopatologia , Humanos , Neoplasias/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Qualidade de Vida
8.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 35(2): 173-177, 2019 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-31250612

RESUMO

OBJECTIVE: To investigate the effects of simulated hypobaric hypoxia environment at 7 000 m above sea level on cardiac structure and function in rats. METHODS: A total of 96 male SD rats were randomly divided into high-altitude hypobaric hypoxia group (hypoxia group) and normobaric normoxia group (control group). Rats of hypoxia group were placed in a large cabin simulated 7 000 m high-altitude hypobaric hypoxia environment. Operating time 23 h / d, the control circadian ratio of approximately 12 h:12 h. The rats in control group were bred under normobaric normoxia. The hypoxic group was divided into 3 d, 7 d, 14 d, 28 d groups according to hypoxic time, 12 rats in each group. Changes of structure and function of heart due to hypoxia were evaluated by echocardiography and electrocardiogram. Myocardial pathological changes were analyzed by hematoxylin-eosin staining(HE). RESULTS: Compared with the control group at the same time point ①With prolonged exposure to hypobaric hypoxia, the growth ratio of body mass in rats is slower. Arterial oxygen saturation was significantly lower in both 14 d and 28 d (P<0.05). ② Left ventricular end-diastolic anterior wall thickness (LVAWD) and left ventricular end-diastolic posterior wall thickness (LVPWD) of rats in 28 d were increased significantly (P<0.05). Left ventricular end-diastolic diameter (LVIDD) and left ventricular internal dimension systole (LVIDS) of rats in 28 d were decreased significantly (P<0.05, P<0.01). Left ventricular ejection fraction (EF), fractional shortening of left ventricle (FS), pulmonary vein (PV) peak velocity and PV peak gradient of rats in 7 d were decreased significantly (P<0.05, P<0.01). ③The QRS and QT interval period were significantly prolonged in 14 d and 28 d (P<0.05, P<0.01). The ST was significantly lower in 3 d and 7 d (P<0.05, P<0.01). The amplitude of R wave gradually shifted downward in 7 d, 14 d, 28 d (P<0.05, P<0.01). ④The red blood cell (RBC), hemoglobin (HGB), red blood cell distribution width (RDW) in hypoxic group were increased significantly (P<0.01). The platelet count (PLT) count was decreased significantly in 14 d and 28 d (P<0.01). The serum creatinine (CR) was increased significantly in 14 d and 28 d (P<0.05). ⑤Pathological changes such as myocardial edema, sarcolemma condensate, focal degeneration and necrosis with inflammatory cell infiltration could be found at early stage of hypoxia. Myocardial compensatory repair such as myocardial fibroblasts proliferation was significant at end stage of hypoxia. CONCLUSION: Left ventricular systolic functions of rats were decreased significantly after exposure to high altitude hypoxia hypobaric. The left ventricular systolic functions would recovery compensatory after one week exposed to high altitude hypoxia hypobaric.


Assuntos
Altitude , Coração/fisiopatologia , Hipóxia , Animais , Masculino , Ratos , Ratos Sprague-Dawley
9.
Life Sci ; 231: 116542, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31176781

RESUMO

AIM: To compare the effect of 150 min vs. 300 min of weekly moderate intensity exercise training on the activation of the opioid system and apoptosis in the hearts of a diet-induced obesity model. METHODS: Male Wistar rats were fed with either control (CON) or high fat (HF) diet for 32 weeks. At the 20th week, HF group was subdivided into sedentary, low (LEV, 150 min·week-1) or high (HEV, 300 min·week-1) exercise volume. After 12 weeks of exercise, body mass gain, adiposity index, systolic blood pressure, cardiac morphometry, apoptosis biomarkers and opioid system expression were evaluated. RESULTS: Sedentary animals fed with HF presented pathological cardiac hypertrophy and higher body mass gain, systolic blood pressure and adiposity index than control group. Both exercise volumes induced physiological cardiac hypertrophy, restored systolic blood pressure and improved adiposity index, but only 300 min·week-1 reduced body mass gain. HF group exhibited lower proenkephalin, PI3K, ERK and GSK-3ß expression, and greater activated caspase-3 expression than control group. Compared to HF, no changes in the cardiac opioid system were observed in the 150 min·week-1 of exercise training, while 300 min·week-1 showed greater proenkephalin, DOR, KOR, MOR, Akt, ERK and GSK-3ß expression, and lower activated caspase-3 expression. CONCLUSION: 300 min·week-1 of exercise training triggered opioid system activation and provided greater cardioprotection against obesity than 150 min·week-1. Our findings provide translational aspect with clinical relevance about the critical dose of exercise training necessary to reduce cardiovascular risk factors caused by obesity.


Assuntos
Cardiomegalia/metabolismo , Condicionamento Físico Animal/fisiologia , Receptores Opioides/fisiologia , Adiposidade , Animais , Apoptose/fisiologia , Pressão Sanguínea , Peso Corporal , Dieta Hiperlipídica , Encefalinas/metabolismo , Glicogênio Sintase Quinase 3 beta/metabolismo , Coração/fisiopatologia , Sistema de Sinalização das MAP Quinases/fisiologia , Masculino , Obesidade/metabolismo , Obesidade/fisiopatologia , Fosfatidilinositol 3-Quinase/metabolismo , Condicionamento Físico Animal/métodos , Precursores de Proteínas/metabolismo , Ratos , Ratos Wistar
10.
Life Sci ; 231: 116554, 2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31194992

RESUMO

AIMS: Several adipokines have been proven to improve the therapeutic efficacy of mesenchymal stromal cells (MSCs) when used to treat ischemic heart disease. Asprosin (ASP) is a newly-discovered adipokine. ASP might also predict the severity of coronary pathology. We investigated the role of ASP on MSCs and the effects of ASP-pretreated MSCs on myocardial infarction (MI). MAIN METHODS: MSCs were labelled with a lentivirus carrying green fluorescent protein (GFP). For in vivo study, after pretreatment with vehicle or ASP, MSCs were injected into infarcted hearts. Cardiac function and fibrosis were then evaluated 4 weeks after the induction of MI and survival of MSCs evaluated after 1 week. MSCs proliferation and migration were investigated after ASP treatment in vitro. MSCs apoptosis induced by hydrogen peroxide (H2O2) was assessed using flow cytometry. KEY FINDINGS: Compared to vehicle-pretreated MSCs, ASP-pretreated MSCs significantly improved the left ventricular ejection fraction (LVEF), and inhibited myocardial fibrosis 4 weeks after MI. ASP pretreatment may have promoted homing of transplanted MSCs. In vitro results showed that ASP had no significant effect on MSC proliferation and migration, but protected these cells from H2O2-induced apoptosis. Among 21 molecules associated with antioxidation and cell death, the antioxidant enzyme SOD2 was significantly upregulated by ASP. Furthermore, ASP treatment inhibited H2O2-induced ROS generation and apoptosis via the activated ERK1/2-SOD2 pathway. SIGNIFICANCE: This is the first evidence that ASP can regulate MSCs function and enhance MSCs therapy for ischemic heart disease. Furthermore, we demonstrate that ASP protects MSCs from oxidative stress-induced apoptosis via the ERK1/2-SOD2 pathway.


Assuntos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Células-Tronco Mesenquimais/efeitos dos fármacos , Proteínas dos Microfilamentos/metabolismo , Infarto do Miocárdio/terapia , Fragmentos de Peptídeos/metabolismo , Hormônios Peptídicos/metabolismo , Superóxido Dismutase/metabolismo , Animais , Apoptose/fisiologia , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Coração/fisiopatologia , Peróxido de Hidrogênio/farmacologia , Masculino , Transplante de Células-Tronco Mesenquimais/métodos , Células-Tronco Mesenquimais/patologia , Camundongos , Camundongos Endogâmicos C57BL , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/patologia , Isquemia Miocárdica/metabolismo , Isquemia Miocárdica/patologia , Espécies Reativas de Oxigênio/metabolismo , Função Ventricular Esquerda
11.
Bone Joint J ; 101-B(5): 540-546, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-31039002

RESUMO

AIMS: Cardiac magnetic resonance (CMR) was used to assess whether cardiac function or tissue composition was affected in patients with well-functioning metal-on-metal hip resurfacing arthroplasties (MoMHRA) when compared with a group of controls, and to assess if metal ion levels correlated with any of the functional or structural parameters studied. PATIENTS AND METHODS: In all, 30 participants with no significant cardiac history were enrolled: 20 patients with well-functioning MoMHRA at mean follow-up of 8.3 years post-procedure (ten unilateral, ten bilateral; 17 men, three women) and a case-matched control group of ten non-MoM total hip arthroplasty patients (six men, four women). The mean age of the whole cohort (study group and controls) at the time of surgery was 50.6 years (41.0 to 64.0). Serum levels of cobalt and chromium were measured, and all patients underwent CMR imaging, including cine, T2* measurements, T1 and T2 mapping, late gadolinium enhancement, and strain measurements. RESULTS: None of the MoMHRA patients showed clinically significant cardiac functional abnormality. The MoMHRA patients had larger indexed right and left end diastolic volumes (left ventricular (LV): 74 ml/m2 vs 67 ml/m2, p = 0.045; right ventricular: 80 ml/m2 vs 71 ml/m2, p = 0.02). There was a small decrease in T2 time in the MoMHRA patients (median 49 ms vs 54 ms; p = 0.0003). Higher metal ion levels were associated with larger LV volumes and with shorter T2 time. CONCLUSION: Although cardiac function is not clinically adversely affected in patients with well-functioning MoMHRA, modern imaging is able to demonstrate subtle changes in structure and function of the heart. As these changes correlate with systemic ion measurements, they may be consequences of wear debris deposition. Longer, longitudinal studies are necessary to determine whether cardiac function will become affected. Cite this article: Bone Joint J 2019;101-B:540-546.


Assuntos
Artroplastia de Quadril/efeitos adversos , Coração/diagnóstico por imagem , Articulação do Quadril/cirurgia , Prótese de Quadril/efeitos adversos , Imagem Cinética por Ressonância Magnética/métodos , Próteses Articulares Metal-Metal/efeitos adversos , Adulto , Idoso , Estudos de Casos e Controles , Cromo/sangue , Cobalto/sangue , Feminino , Coração/fisiopatologia , Articulação do Quadril/diagnóstico por imagem , Humanos , Masculino , Pessoa de Meia-Idade , Complicações Pós-Operatórias/diagnóstico por imagem , Complicações Pós-Operatórias/etiologia
12.
J Med Food ; 22(5): 479-489, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31084538

RESUMO

Among the comorbidities of high body mass index, cardiovascular disease continued to be the leading cause of death and disability globally in 2015, while type 2 diabetes remained second. The primary objectives of this observational study were to confirm the safety, tolerability, and efficacy of our calorie-restricted Mediterranean diet with targeted dietary supplementation (PROG1) using globally recognized dietary supplementation. Fifty healthy overweight and obese subjects with cardiometabolic risk factors were assigned a modified Mediterranean diet, including protein shakes and targeted supplementation (PROG2), providing ∼68-76% of subject estimated calorie requirements. Salivary nitrite was assessed weekly and key cardiometabolic metrics were recorded at baseline and weeks 9 and 13. PROG2 was well tolerated with 86% compliance. The most common adverse effects were bloating, flatulence, and constipation, which were self-limiting. Subjects exhibited decreases (P < .01) from baseline of 12% in body weight, 18% in body fat, and 8.8% in waist circumference. Total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, and triglycerides (TG) were reduced (P < .01), respectively, 19%, 22%, and 40%. Lipid ratios of TC/high-density lipoprotein (HDL), TG/HDL, and oxidized LDL (oxLDL)/HDL were decreased 15% (P < .01), 35% (P < .01), and 13% (P < .05), respectively. Inflammation biomarkers, oxLDL and high-sensitivity C-reactive protein, were reduced 17% (P < .01) and 30% (P < .05), respectively. Reductions of 9.0% for systolic (P < .01) and 12% (P < .01) for diastolic blood pressure were noted. In concert, the nitrogen dioxide salivary biomarker for nitric oxide was increased relative to baseline. PROG2 produced a dramatic 50% reduction in subjects meeting cardiometabolic syndrome criteria and a 38% decrease in Framingham 10-year cardiovascular risk. These results confirmed our previous findings that the addition of targeted nutraceutical supplementation to a calorie-restricted Mediterranean diet with lifestyle modifications improves multiple longevity risk factors more effectively than diet and lifestyle modification alone.


Assuntos
Dieta Mediterrânea , Miocárdio/metabolismo , Sobrepeso/dietoterapia , Extratos Vegetais/administração & dosagem , Probióticos/administração & dosagem , Adulto , Biomarcadores/metabolismo , Peso Corporal/efeitos dos fármacos , Proteína C-Reativa/metabolismo , Estudos de Casos e Controles , Colesterol/metabolismo , Suplementos Nutricionais/análise , Feminino , Índice Glicêmico , Coração/efeitos dos fármacos , Coração/fisiopatologia , Humanos , Estilo de Vida , Longevidade/efeitos dos fármacos , Masculino , Pessoa de Meia-Idade , Sobrepeso/tratamento farmacológico , Sobrepeso/fisiopatologia , Sobrepeso/psicologia , Triglicerídeos/metabolismo
13.
Braz J Med Biol Res ; 52(6): e8085, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31141087

RESUMO

Obesity is often associated with changes in cardiac function; however, the mechanisms responsible for functional abnormalities have not yet been fully clarified. Considering the lack of information regarding high-saturated-fat diet-induced obesity, heart function, and the proteins involved in myocardial calcium (Ca2+) handling, the aim of this study was to test the hypothesis that this dietary model of obesity leads to cardiac dysfunction resulting from alterations in the regulatory proteins of intracellular Ca2+ homeostasis. Male Wistar rats were distributed into two groups: control (C, n=18; standard diet) and obese (Ob, n=19; high-saturated-fat diet), which were fed for 33 weeks. Cardiac structure and function were evaluated using echocardiographic and isolated papillary muscle analyses. Myocardial protein expressions of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), PLB serine-16 phosphorylation, PLB threonine-17 phosphorylation, ryanodine receptor, calsequestrin, Na+/Ca2+ exchanger, and L-type Ca2+ channel were assessed by western blot. Obese rats presented 104% increase in the adiposity index (C: 4.5±1.4 vs Ob: 9.2±1.5%) and obesity-related comorbidities compared to control rats. The left atrium diameter (C: 5.0±0.4 vs Ob: 5.5±0.5 mm) and posterior wall shortening velocity (C: 36.7±3.4 vs Ob: 41.8±3.8 mm/s) were higher in the obese group than in the control. The papillary muscle function was similar between the groups at baseline and after inotropic and lusitropic maneuvers. Obesity did not lead to changes in myocardial Ca2+ handling proteins expression. In conclusion, the hypothesis was not confirmed, since the high-saturated-fat diet-induced obese rats did not present cardiac dysfunction or impaired intracellular Ca2+ handling proteins.


Assuntos
Cálcio/fisiologia , Dieta Hiperlipídica/efeitos adversos , Coração/fisiopatologia , Obesidade/fisiopatologia , Trocador de Sódio e Cálcio/fisiologia , Animais , Pressão Sanguínea/fisiologia , Modelos Animais de Doenças , Ecocardiografia , Masculino , Ratos , Ratos Wistar
14.
Life Sci ; 228: 121-127, 2019 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-31039364

RESUMO

AIMS: B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. MAIN METHODS: Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1-/-) and B2-kinin (B2-/-) knockout mice. KEY FINDINGS: Impaired contractility in B1-/- and B2-/- hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1-/- and B2-/- hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1-/- and B2-/- hearts. SIGNIFICANCE: B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.


Assuntos
Cardiopatias/genética , Coração/fisiopatologia , Receptor B1 da Bradicinina/genética , Receptor B2 da Bradicinina/genética , Animais , Deleção de Genes , Cardiopatias/fisiopatologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Contração Miocárdica , NADPH Oxidases/metabolismo , Óxido Nítrico/metabolismo , Oxirredução , Espécies Reativas de Oxigênio/metabolismo , Receptor B1 da Bradicinina/metabolismo , Receptor B2 da Bradicinina/metabolismo
15.
Int J Mol Sci ; 20(9)2019 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-31071921

RESUMO

Activation of multiple pathways is associated with cardiac hypertrophy and heart failure. We previously published that CXCR4 negatively regulates ß-adrenergic receptor (ß-AR) signaling and ultimately limits ß-adrenergic diastolic (Ca2+) accumulation in cardiac myocytes. In isolated adult rat cardiac myocytes; CXCL12 treatment prevented isoproterenol-induced hypertrophy and interrupted the calcineurin/NFAT pathway. Moreover; cardiac specific CXCR4 knockout mice show significant hypertrophy and develop cardiac dysfunction in response to chronic catecholamine exposure in an isoproterenol-induced (ISO) heart failure model. We set this study to determine the structural and functional consequences of CXCR4 myocardial knockout in the absence of exogenous stress. Cardiac phenotype and function were examined using (1) gated cardiac magnetic resonance imaging (MRI); (2) terminal cardiac catheterization with in vivo hemodynamics; (3) histological analysis of left ventricular (LV) cardiomyocyte dimension; fibrosis; and; (4) transition electron microscopy at 2-; 6- and 12-months of age to determine the regulatory role of CXCR4 in cardiomyopathy. Cardiomyocyte specific-CXCR4 knockout (CXCR4 cKO) mice demonstrate a progressive cardiac dysfunction leading to cardiac failure by 12-months of age. Histological assessments of CXCR4 cKO at 6-months of age revealed significant tissue fibrosis in knockout mice versus wild-type. The expression of atrial naturietic factor (ANF); a marker of cardiac hypertrophy; was also increased with a subsequent increase in gross heart weights. Furthermore, there were derangements in both the number and the size of the mitochondria within CXCR4 cKO hearts. Moreover, CXCR4 cKO mice were more sensitive to catocholamines, their response to ß-AR agonist challenge via acute isoproterenol (ISO) infusion demonstrated a greater increase in ejection fraction, dp/dtmax, and contractility index. Interestingly, prior to ISO infusion, there were significant differences in baseline hemodynamics between the CXCR4 cKO compared to littermate controls. However, upon administering ISO, the CXCR4 cKO responded in a robust manner overcoming the baseline hemodynamic deficits reaching WT values supporting our previous data that CXCR4 negatively regulates ß-AR signaling. This further supports that, in the absence of the physiologic negative modulation, there is an overactivation of down-stream pathways, which contribute to the development and progression of contractile dysfunction. Our results demonstrated that CXCR4 plays a non-developmental role in regulating cardiac function and that CXCR4 cKO mice develop a progressive cardiomyopathy leading to clinical heart failure.


Assuntos
Cardiomiopatias/genética , Insuficiência Cardíaca/genética , Receptores CXCR4/genética , Animais , Fator Natriurético Atrial/genética , Cardiomiopatias/fisiopatologia , Quimiocina CXCL12/genética , Modelos Animais de Doenças , Regulação da Expressão Gênica/efeitos dos fármacos , Coração/efeitos dos fármacos , Coração/fisiopatologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Isoproterenol/administração & dosagem , Camundongos , Camundongos Knockout , Mitocôndrias Cardíacas/genética , Mitocôndrias Cardíacas/patologia , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Receptores Adrenérgicos beta/genética , Transdução de Sinais/genética
17.
Medicine (Baltimore) ; 98(15): e15151, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30985691

RESUMO

RATIONALE: Acute myocardial infarction is a rare complication of carbon monoxide poisoning. there is often no chest pain and other typical manifestations. We report a patient with mild carbon monoxide poisoning who had acute dyspnea as the earliest symptom and was later diagnosed with non-ST elevation myocardial infarction (NSTEMI) and acute left heart failure. PATIENT CONCERNS: A 73-year-old woman complained of dizziness and fatigue with shortness of breath after carbon monoxide intoxication. DIAGNOSES: This patient had a clear history of carbon monoxide poisoning, acute respiratory distress, bilateral lung dry and moist rale, chest X-ray showed bilateral pulmonary edema, Electrocardiograph indicated general depression of the ST segment of the leads in the chest, cardiac troponin I (CTNI) increased progressively, cardiac ultrasonography indicated abnormal ventricular wall movement, coronary angiography suggested left main trunk and 3-vessel lesions, suggesting diagnosis acute carbon monoxide poisoning, acute coronary syndrome, acute left heart failure. INTERVENTIONS: She was treated with a high concentration of oxygen, an inhibitor of platelet aggregation (aspirin plus clopidogrel), an anticoagulant (low molecular weight heparin), an antimicrobial (ceftizoxime), an expectorant (mucosolvan), diuresis (furosemide and spironolactone), and myocardial support (Metoprolol). Coronary angiography and stent placement were performed 8 days later. OUTCOME: On the 10th day after onset of the condition, echocardiography was performed, which showed that cardiac function was improved. Mild segmental wall motion abnormality was observed on echocardiography. After 14 days, the patient had recovered well and was discharged without chest tightness, chest pain, dizziness, headache, or unresponsiveness. LESSONS: This case suggests that the symptoms of carbon monoxide poisoning are complex and diverse. It can be manifested as a primary hypoxic symptom, or cause the exacerbation of underlying diseases due to hypoxia. Therefore, patients with carbon monoxide poisoning should actively seek comprehensive cardiac examination to ensure early diagnosis. Whenever necessary, coronary angiography and stent implantation should be performed to improve the likelihood of the patient's survival.


Assuntos
Intoxicação por Monóxido de Carbono/complicações , Infarto do Miocárdio sem Supradesnível do Segmento ST/diagnóstico , Infarto do Miocárdio sem Supradesnível do Segmento ST/etiologia , Síndrome Coronariana Aguda/diagnóstico , Síndrome Coronariana Aguda/etiologia , Síndrome Coronariana Aguda/terapia , Idoso , Intoxicação por Monóxido de Carbono/diagnóstico , Intoxicação por Monóxido de Carbono/terapia , Diagnóstico Diferencial , Eletrocardiografia , Feminino , Coração/diagnóstico por imagem , Coração/fisiopatologia , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/terapia , Humanos , Infarto do Miocárdio sem Supradesnível do Segmento ST/terapia
18.
Bull Exp Biol Med ; 166(6): 726-730, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31020585

RESUMO

Autonomic regulation of the heart was examined in 5 groups of rats: intact, sham-operated, experimental chronic obstructive pulmonary disease, acute cerebral ischemia, and acute cerebral ischemia modeled against the background of chronic obstructive pulmonary disease. The latter was provoked by combination of inhaled papain and intraperitoneal bacterial LPS, whereas acute cerebral ischemia was modeled by single-stage bilateral occlusion of the common carotid arteries. Chronic obstructive pulmonary disease was verified by X-ray computed microtomography. The disturbances in autonomic control of the heart during comorbid pathologies were most prominent; they were manifested by overstrain and decompensation of the mechanisms implicated in the heart control and systolic-diastolic arterial hypotension. The correlations were established between blood oxygenation, respiration rate, and some parameters of autonomic cardiac regulation. The data attest to relevance and usefulness of the developed model of respiratory and cerebrovascular comorbidity in assessment of pathophysiological mechanisms underlying dysregulation of the heart and the development of personalized approaches for its pharmacological correction.


Assuntos
Vias Autônomas/fisiopatologia , Isquemia Encefálica/fisiopatologia , Coração/fisiopatologia , Pulmão/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Doença Aguda , Animais , Pressão Sanguínea/fisiologia , Isquemia Encefálica/diagnóstico por imagem , Isquemia Encefálica/cirurgia , Artérias Carótidas/cirurgia , Transtornos Cerebrovasculares/cirurgia , Modelos Animais de Doenças , Frequência Cardíaca/fisiologia , Lipopolissacarídeos/administração & dosagem , Masculino , Papaína/administração & dosagem , Doença Pulmonar Obstrutiva Crônica/induzido quimicamente , Doença Pulmonar Obstrutiva Crônica/diagnóstico por imagem , Ratos , Ratos Wistar , Taxa Respiratória/fisiologia , Tomografia Computadorizada por Raios X
19.
Sheng Li Xue Bao ; 71(2): 225-234, 2019 Apr 25.
Artigo em Chinês | MEDLINE | ID: mdl-31008482

RESUMO

The autonomic nervous system consists of the sympathetic nervous system and the parasympathetic nervous system. These two systems control the heart and work in a reciprocal fashion to modulate myocardial energy metabolism, heart rate as well as blood pressure. Multiple cardiac pathological conditions are accompanied by autonomic imbalance, characterized by sympathetic overactivation and parasympathetic inhibition. Studies have shown that overactive sympathetic nervous system leads to increased cardiac inflammatory reaction. Orchestrated inflammatory response serves to clear dead cardiac tissue and activate reparative process, whereas excessive inflammation may result in pathological cardiac remodeling. Since the discovery of the α7 nicotinic acetylcholine receptor (α7nAChR)-mediated cholinergic anti-inflammatory pathway (CAP), the protective effects of the parasympathetic nervous system in cardiac inflammation have attracted more attention recently. In this review, we summarized the role and underlying mechanisms of the sympathetic and parasympathetic nervous systems in cardiac inflammation, in order to provide new insight into cardiac inflammatory response in cardiovascular diseases.


Assuntos
Sistema Nervoso Autônomo/fisiologia , Coração/fisiopatologia , Inflamação/fisiopatologia , Sistema Nervoso Parassimpático/fisiologia , Humanos , Receptor Nicotínico de Acetilcolina alfa7/fisiologia
20.
Sensors (Basel) ; 19(8)2019 Apr 19.
Artigo em Inglês | MEDLINE | ID: mdl-31010113

RESUMO

The auscultation of heart sounds has been for decades a fundamental diagnostic tool in clinical practice. Higher effectiveness can be achieved by recording the corresponding biomedical signal, namely the phonocardiographic signal, and processing it by means of traditional signal processing techniques. An unavoidable processing step is the heart sound segmentation, which is still a challenging task from a technical viewpoint-a limitation of state-of-the-art approaches is the unavailability of trustworthy techniques for the detection of heart sound components. The aim of this work is to design a reliable algorithm for the identification and the classification of heart sounds' main components. The proposed methodology was tested on a sample population of 24 healthy subjects over 10-min-long simultaneous electrocardiographic and phonocardiographic recordings and it was found capable of correctly detecting and classifying an average of 99.2% of the heart sounds along with their components. Moreover, the delay of each component with respect to the corresponding R-wave peak and the delay among the components of the same heart sound were computed: the resulting experimental values are coherent with what is expected from the literature and what was obtained by other studies.


Assuntos
Ruídos Cardíacos , Coração/fisiopatologia , Fonocardiografia/métodos , Processamento de Sinais Assistido por Computador , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Algoritmos , Eletrocardiografia , Eletrodos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem
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