RESUMO
The autonomic nervous system (ANS) plays an important role in the coordination of several physiological functions including sleep/wake process. Significant changes in ANS activity occur during wake-to-sleep transition maintaining the adequate cardiorespiratory regulation and brain activity. Since sleep is a complex homeostatic function, partly regulated by the ANS, it is not surprising that sleep disruption trigger and/or evidence symptoms of ANS impairment. Indeed, several studies suggest a bidirectional relationship between impaired ANS function (i.e. enhanced sympathetic drive), and the emergence/development of sleep disorders. Furthermore, several epidemiological studies described a strong association between sympathetic-mediated diseases and the development and maintenance of sleep disorders resulting in a vicious cycle with adverse outcomes and increased mortality risk. However, which and how the sleep/wake control and ANS circuitry becomes affected during the progression of ANS-related diseases remains poorly understood. Thus, understanding the physiological mechanisms underpinning sleep/wake-dependent sympathetic modulation could provide insights into diseases involving autonomic dysfunction. The purpose of this review is to explore potential neural mechanisms involved in both the onset/maintenance of sympathetic-mediated diseases (Rett syndrome, congenital central hypoventilation syndrome, obstructive sleep apnoea, type 2 diabetes, obesity, heart failure, hypertension, and neurodegenerative diseases) and their plausible contribution to the generation of sleep disorders in order to review evidence that may serve to establish a causal link between sleep disorders and heightened sympathetic activity.
Assuntos
Diabetes Mellitus Tipo 2 , Disautonomias Primárias , Transtornos do Sono-Vigília , Humanos , Sono/fisiologia , Transtornos do Sono-Vigília/complicações , Progressão da DoençaRESUMO
Abstract Background: Resting sympathetic hyperactivity and impaired parasympathetic reactivation after exercise have been described in patients with heart failure (HF). However, the association of these autonomic changes in patients with HF and sarcopenia is unknown. Objective: The aim of this study was to evaluate the impact of autonomic modulation on sarcopenia in male patients with HF. Methods: We enrolled 116 male patients with HF and left ventricular ejection fraction < 40%. All patients underwent a maximal cardiopulmonary exercise testing. Maximal heart rate was recorded and delta heart rate recovery (∆HRR) was assessed at 1st and 2nd minutes after exercise. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography. Dual-energy X-ray absorptiometry was used to measure body composition and sarcopenia was defined by the sum of appendicular lean muscle mass (ALM) divided by height in meters squared and handgrip strength. Results: Sarcopenia was identified in 33 patients (28%). Patients with sarcopenia had higher MSNA than those without (47 [41-52] vs. 40 [34-48] bursts/min, p = 0.028). Sarcopenic patients showed lower ∆HRR at 1st (15 [10-21] vs. 22 [16-30] beats/min, p < 0.001) and 2nd min (25 [19-39] vs. 35 [24-48] beats/min, p = 0.017) than non-sarcopenic. There was a positive correlation between ALM and ∆HRR at 1st (r = 0.26, p = 0.008) and 2nd min (r = 0.25, p = 0.012). We observed a negative correlation between ALM and MSNA (r = -0.29, p = 0.003). Conclusion: Sympatho-vagal imbalance seems to be associated with sarcopenia in male patients with HF. These results highlight the importance of a therapeutic approach in patients with muscle wasting and increased peripheral sympathetic outflow.
Resumo Fundamento: Hiperatividade simpática de repouso e uma reativação parassimpática diminuída pós-exercício têm sido descritas em pacientes com insuficiência cardíaca (IC). No entanto, a associação dessas alterações autonômicas em pacientes com IC sarcopênicos ainda não são conhecidas. Objetivo: O objetivo deste estudo foi avaliar o impacto da modulação autonômica sobre sarcopenia em pacientes com IC do sexo masculino. Métodos: Foram estudados 116 pacientes com IC e fração de ejeção ventricular esquerda inferior a 40%. Todos os pacientes foram submetidos ao teste de exercício cardiopulmonar máximo. A frequência cardíaca máxima foi registrada, e o delta de recuperação da frequência cardíaca (∆RFC) foi avaliado no primeiro e no segundo minuto após o exercício. A atividade nervosa simpática muscular (ANSM) foi registrada por microneurografia. A Absorciometria Radiológica de Dupla Energia foi usada para medir composição cpororal, e a sarcopenia definida como a soma da massa muscular apendicular (MMA) dividida pela altura em metros ao quadrado e força da mão. Resultados: A sarcopenia foi identificada em 33 pacientes (28%). Os pacientes com sarcopenia apresentaram maior ANSM que aqueles sem sarcopenia - 47 (41-52) vs. 40 (34-48) impulsos (bursts)/min, p = 0,028). Pacientes sarcopênicos apresentaram ∆RFC mais baixo no primeiro [15 (10-21) vs. 22 (16-30) batimentos/min, p < 0,001) e no segundo [25 (19-39) vs. 35 (24-48) batimentos/min, p = 0,017) minuto que pacientes não sarcopênicos. Observou-se uma correlação positiva entre a MMA e a ANSM (r = -0,29; p = 0,003). Conclusão: Um desequilíbrio simpático-vagal parece estar associado com sarcopenia em pacientes com IC do sexo masculino. Esses resultados destacam a importância de uma abordagem terapêutica em pacientes com perda muscular e fluxo simpático periférico aumentado.
Assuntos
Humanos , Masculino , Adulto , Idoso , Adulto Jovem , Sistema Nervoso Autônomo/fisiopatologia , Sistema Nervoso Simpático/fisiopatologia , Sarcopenia/fisiopatologia , Insuficiência Cardíaca/fisiopatologia , Consumo de Oxigênio/fisiologia , Força da Mão/fisiologia , Teste de Esforço , Força Muscular/fisiologia , Frequência Cardíaca/fisiologia , Pessoa de Meia-IdadeRESUMO
Scorpionism is the clinical picture resulting from the inoculation of scorpion venom. It is considered a major public health problem, especially in countries with low resources and tropical or subtropical climate. Poisoning can be fatal especially in the first hours due to respiratory and / or cardiovascular collapse. The compromise of the central nervous system (CNS) is infrequent but varied and complex, being able to be triggered due to multiple and different neurotoxic properties of the toxin. We report here a severe case of poisoning with cardiovascular and neurological compromise in an endemic region of Argentina. After cardiorespiratory stabilization, neurological deterioration is detected secondary to intracerebral hemorrhage that required surgery and multimodal neuromonitoring. The outcome was fatal due to multiple neurological and systemic complications. Scorpion sting poisoning is a true neurologic and neurosurgical life-threatening emergency.
RESUMO
Fat embolism syndrome (FES) is a rare syndrome caused by embolization of fat particles into multiple organs including the brain. It typically manifests with petechial rash, deteriorating mental status, and progressive respiratory insufficiency, usually occurring within 24-48 h of trauma with long-bone fractures or an orthopedic surgery. The diagnosis of FES is based on clinical and imaging findings, but requires exclusion of alternative diagnoses. Although there is no specific treatment for FES, prompt recognition is important because it can avoid unnecessary interventions and clarify prognosis. Patients with severe FES can become critically ill, but even comatose patients with respiratory failure may recover favorably. Prophylactic measures, such as early stabilization of fractures and certain intraoperative techniques, may help decrease the incidence and severity of FES.
Assuntos
Embolia Gordurosa , Embolia Intracraniana , Adulto , Embolia Gordurosa/complicações , Embolia Gordurosa/diagnóstico , Embolia Gordurosa/etiologia , Embolia Gordurosa/terapia , Humanos , Embolia Intracraniana/complicações , Embolia Intracraniana/diagnóstico , Embolia Intracraniana/etiologia , Embolia Intracraniana/terapia , Masculino , Adulto JovemRESUMO
BACKGROUND: Atrial fibrillation (AF) commonly occurs in chronic kidney disease (CKD), occasioning adverse outcomes. Merging pulmonary vein isolation (PVI) and renal sympathetic denervation (RSD) may decrease the recurrence of AF in subjects with CKD and uncontrolled hypertension. We considered that RSD could reduce the recurrence of AF in patients with CKD by modulating sympathetic hyperactivity. We aimed to evaluate the impact of RSD or spironolactone 50 mg/day associated with PVI in reducing systolic blood pressure (BP), AF recurrence, and AF burden in patients with a history of paroxysmal AF and mild CKD. METHODS: This was a single-center, prospective, longitudinal, randomized, double-blind study. The individuals were randomly divided into two groups (PVI + spironolactone, n = 36, and PVI + RSD, n = 33). All of them were followed for exactly 1 year to assess maintenance of sinus rhythm and to monitor the other variables. RESULTS: Ambulatory BP measurements were reduced in both groups and at the 12th month also differed between groups. Significantly more patients in the PVI + RSD (61%) than in the PVI + spironolactone group (36%) were AF-free at the 12th month of follow-up, P = 0.0242. Toward the end of the study, the mean AF burden was lower in the PVI + RSD group as compared to PVI + spironolactone group, at the 9th month: ∆ = - 10% (P < 0.0001), and at the 12th month: ∆ = - 12% (P < 0.0001), respectively. CONCLUSIONS: PVI + RSD is safe and appears to be superior to PVI + spironolactone in BP reduction, augmentation of AF event-free rate, reduction of AF burden, and improvement of renal function.
Assuntos
Fibrilação Atrial/cirurgia , Ablação por Cateter/métodos , Hipertensão/tratamento farmacológico , Insuficiência Renal Crônica/complicações , Espironolactona/uso terapêutico , Simpatectomia/métodos , Idoso , Fibrilação Atrial/diagnóstico por imagem , Fibrilação Atrial/etiologia , Fibrilação Atrial/mortalidade , Terapia Combinada , Método Duplo-Cego , Ecocardiografia/métodos , Eletrocardiografia/métodos , Feminino , Humanos , Hipertensão/etiologia , Hipertensão/fisiopatologia , Estimativa de Kaplan-Meier , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Distribuição Normal , Marca-Passo Artificial , Projetos Piloto , Prognóstico , Estudos Prospectivos , Veias Pulmonares/cirurgia , Recidiva , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/terapia , Medição de Risco , Estatísticas não Paramétricas , Taxa de Sobrevida , Resultado do TratamentoRESUMO
BACKGROUND: Atrial fibrillation (AF) is highly common, and is most frequently observed in individuals with hypertension and structural cardiac disease. Sympathetic hyperactivity plays a fundamental role in the progression, maintenance and aggravation of arrhythmia. Endurance exercise training clearly lowers sympathetic activity in sympathoexcitatory disease states, and is well-tolerated by patients with chronic kidney disease (CKD). METHODS: We assessed 50 CKD patients with hypertension. Each patient provided a complete medical history and underwent a physical examination. We used an implantable cardiac monitor over a 3-year follow-up period to evaluate the effects of high-intensity interval training (HIIT) and moderate exercise (ModEx) physical activity protocols on AF occurrence, and determined the effectiveness of these protocols in improving renal function. Subjects were followed up every 6 months after the beginning of the intervention. RESULTS: During the 3-year follow-up, AF onset was higher in CKD patients who engaged in HIIT (72%) than in those who engaged in ModEx (24%) (hazard ratio, 3.847; 95% confidence interval, 1.694-8.740, P = 0.0013 by log-rank test). Both groups exhibited significant intra-group changes in the mean systolic 24-hour ambulatory blood pressure measurements (ABPM) between baseline and 12, 24, and 36 months. There were also significant differences in the mean systolic 24-hour ABPM between the groups at the same time points. CONCLUSION: In CKD patients with hypertension, improvements in AF onset, renal function and some echocardiographic parameters were more evident in subjects who engaged in ModEx than in those who engaged in HIIT during 3 years of follow-up.
RESUMO
BACKGROUND: Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Endurance exercise training clearly lowers sympathetic activity in sympatho-excitatory disease states and may be tolerated by patients with chronic kidney disease (CKD). METHODS: We assessed 40 CKD patients with hypertension with polymorphic PVCs. Patients underwent a complete medical history and physical examination. We evaluated the effectiveness of ß blocker only or ß blocker + exercise during 12 months of follow-up regarding the changes of the numbers of PVCs and mean heart rate (HR) by 24-hour-Holter. RESULTS: We observed in the ß blocker group a significant decrease in the number of polymorphic PVCs from baseline 36,515 ± 3,518 to 3, 6, 9 and 12 months of follow-up, 28,314 ± 2,938, 23,709 ± 1,846, 22,564 ± 1,673, and 22,725 ± 1,415, respectively (P < 0.001). In the ß blocker + exercise group a significant decrease in the number of polymorphic PVCs also occurred from baseline 36,091 ± 3,327 to 3, 6, 9 and 12 months of follow-up, 29,252 ± 3,211, 20,948 ± 2,386, 14,238 ± 3,338, and 6,225 ± 2,319, respectively (P < 0.001). Comparisons between the two groups at the same time point showed differences from the sixth month onwards: the 6th (Δ = -2,761, P = 0.045), 9th (Δ = -8,325, P < 0.001) and 12th (Δ = -16,500, P < 0.001) months. There was an improvement during the 12 months of follow-up vs. baseline, after the ß blocker or ß blocker + exercise in mean 24-hour HR Holter monitoring, creatinine values, eGFR, and ACR. CONCLUSION: Polymorphic PVCs may be modifiable by physical activity in CKD patients with hypertension without structural heart disease.
RESUMO
BACKGROUND OR PURPOSE: Polymorphic premature ventricular complexes (PVCs) are very common, appearing most frequently in patients with hypertension, obesity, sleep apnea, and structural heart disease. Sympathetic hyperactivity plays a critical role in the development, maintenance, and aggravation of ventricular arrhythmias. Recently, the relevance of sympathetic activation in patients with ventricular arrhythmias was reported, and this finding suggested a potential role for catheter-based renal sympathetic denervation in reducing the arrhythmic burden. METHODS: We evaluated the effectiveness of the renal sympathetic denervation (RSD) in comparison to antiarrhythmic pharmacologic therapy in reducing polymorphic PVCs refractory to medication therapy and cardiac parameters assessed by 24-h Holter monitoring and cardiac magnetic resonance (CRM), respectively, in patients with structurally normal heart. RESULTS: Thirty-four patients were included in this study, 14 served as control, and 20 were treated with an ablation cardiac catheter with open irrigated tip. RSD was performed by a single operator following the standard technique. All the patients included had polymorphic PVCs and structurally normal heart. Data were obtained at baseline at the 12th month of follow-up (sixth month after RSD or adjustment of antiarrhythmic dosage). In RSD group, we observed a significant decrease in the number of polymorphic PVCs from baseline 36,091 ± 3327 to 3, 6, 7 (first month after RSD, without drugs), and 12 months (sixth month after RSD, without drugs) of follow-up, 31,009 ± 3251, 20,411 ± 3820, 7701 ± 1549, and 1274 ± 749, respectively, in all patients, P < 0.0001 to all the comparisons between the mean of each time point with the mean of every other time point. No changes in mean 24-h ABPM and renal function in both groups were observed at 12th month of follow-up. However, 24-h Holter mean heart rate decreased in control group at 12th month of follow-up, which did not happen with the RSD group. At the sixth month post-RSD in comparison to baseline, a significant reduction in the number of polymorphic PVCs (∆ = -34,817 ± 3590, P < 0.0001) was observed, as well as, in CRM parameters such as left ventricular mass/body surface area (∆ = -5.4 ± 2.1 g/m2, P < 0.0001) and left ventricular ejection fraction (∆ = +3.0 ± 1.8 %, P < 0.0001). In comparison to control group at the same time point, these findings were statistically superior in RSD group (P > 0.05). A significant correlation was found between the Δ number of polymorphic PVCs at the sixth month (r = -0.6723, P = 0.0012) after the RSD and the total number of RSD ablated spots. CONCLUSIONS: Polymorphic PVCs refractory to medication therapy may be modifiable by RSD in patients without structural heart disease. Although encouraging, our data are preliminary and need to be validated in a large population and in long term.
Assuntos
Antiarrítmicos/uso terapêutico , Rim/inervação , Rim/cirurgia , Simpatectomia/métodos , Complexos Ventriculares Prematuros/diagnóstico , Complexos Ventriculares Prematuros/terapia , Estudos de Viabilidade , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Resultado do TratamentoRESUMO
Heart failure is a common endpoint for many forms of cardiovascular disease and a significant cause of morbidity and mortality. Chronic neurohumoral excitation (i.e., sympathetic hyperactivity) has been considered to be a hallmark of heart failure and is associated with a poor prognosis, cardiac dysfunction and remodeling, and skeletal myopathy. Aerobic exercise training is efficient in counteracting sympathetic hyperactivity and its toxic effects on cardiac and skeletal muscles. In this review, we describe the effects of aerobic exercise training on sympathetic hyperactivity, skeletal myopathy, as well as cardiac function and remodeling in human and animal heart failure. We also discuss the mechanisms underlying the effects of aerobic exercise training.
Assuntos
Animais , Humanos , Camundongos , Exercício Físico/fisiologia , Insuficiência Cardíaca/prevenção & controle , Coração/fisiopatologia , Músculo Esquelético/fisiopatologia , Condicionamento Físico Animal/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Tolerância ao Exercício/fisiologia , Insuficiência Cardíaca/fisiopatologia , Função Ventricular/fisiologia , Remodelação Ventricular/fisiologiaRESUMO
The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium-derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation ofβ-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations.