Testosterone deficiency increases hospital readmission and mortality rates in male patients with heart failure.

BackgroundTestosterone deficiency in patients with heart failure (HF) is associated with decreased exercise capacity and mortality; however, its impact on hospital readmission rate is uncertain. Furthermore, the relationship between testosterone deficiency and sympathetic activation is unknown.ObjectiveWe investigated the role of testosterone level on hospital readmission and mortality rates as well as sympathetic nerve activity in patients with HF.MethodsTotal testosterone (TT) and free testosterone (FT) were measured in 110 hospitalized male patients with a left ventricular ejection fraction < 45% and New York Heart Association classification IV. The patients were placed into low testosterone (LT; n = 66) and normal testosterone (NT; n = 44) groups. Hypogonadism was defined as TT < 300 ng/dL and FT < 131 pmol/L. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography in a subpopulation of 27 patients.ResultsLength of hospital stay was longer in the LT group compared to in the NT group (37 ± 4 vs. 25 ± 4 days; p = 0.008). Similarly, the cumulative hazard of readmission within 1 year was greater in the LT group compared to in the NT group (44% vs. 22%, p = 0.001). In the single-predictor analysis, TT (hazard ratio [HR], 2.77; 95% confidence interval [CI], 1.58-4.85; p = 0.02) predicted hospital readmission within 90 days. In addition, TT (HR, 4.65; 95% CI, 2.67-8.10; p = 0.009) and readmission within 90 days (HR, 3.27; 95% CI, 1.23-8.69; p = 0.02) predicted increased mortality. Neurohumoral activation, as estimated by MSNA, was significantly higher in the LT group compared to in the NT group (65 ± 3 vs. 51 ± 4 bursts/100 heart beats; p < 0.001).ConclusionThese results support the concept that LT is an independent risk factor for hospital readmission within 90 days and increased mortality in patients with HF. Furthermore, increased MSNA was observed in patients with LT

Effect of low-frequency electrical stimulation on sympathetic nerve activity and peripheral vasoconstriction in hospitalized advanced heart failure patients

Introdução. A insuficiência cardíaca (IC) é uma síndrome complexa que resulta em taxas elevadas de morbidade e mortalidade. Os pacientes em estágio avançado de IC podem ficar internados por um longo período para tratamento dessa síndrome. A restrição ao leito e a inatividade física prolongada geram complicações que resultam em piora na intolerância aos esforços, incluindo aqueles relacionados às atividades de vida diária. Por outro lado, existem evidências de que o tratamento com estimulação elétrica muscular de baixa frequência (EE) proporciona benefícios importantes para o paciente com IC. Neste estudo, nós testamos a hipótese de que o tratamento com EE melhora o controle neurovascular, a vasoconstrição periférica, a força muscular e a capacidade funcional em pacientes internados para tratamento da IC. Métodos. Trinta pacientes internados por IC descompensada, classe funcional IV da NYHA, fração de ejeção <= 30% foram consecutivamente randomizados em dois grupos: 1) EE funcional (n=15) e 2) controle, controle (n=15). A atividade nervosa simpática muscular (ANSM) foi avaliada diretamente no nervo fibular pela técnica de microneurografia, o fluxo sanguíneo muscular (FSM) do membro inferior e superior pela técnica de pletismografia de oclusão venosa, a frequência cardíaca e a pressão arterial pelo método indireto a cada batimento a batimento (Finometer), a força do músculo quadríceps femural por dinamometria, a capacidade funcional pelo teste de caminhada de seis minutos e a qualidade de vida pelo questionário Minnesota Living with Heart Failure. A EE funcional, iniciada após estabilização clínica, consistiu de estimulação dos membros inferiores, numa frequência de 10Hz, largura de pulso de 150ms, com ciclos de 20 segundos de estimulação e 20 segundos de repouso, durante 60 minutos, intensidade no limiar de desconforto do paciente até atingir um valor máximo de 70mA, por 10 dias consecutivos. O grupo controle seguiu o mesmo procedimento, exceto para a intensidade, que foi fixada em 20mA para não provocar contração muscular visível. Resultados. As características basais foram semelhantes entre os grupos estudados, apenas o grupo EE funcional tinha uma idade significativamente maior que o grupo controle. Após 10 dias de protocolo, a EE funcional reduziu a ANSM disparos/min e disparos/100 batimentos, aumentou o FSM e a condutância vascular na perna e no braço. Diferentemente, não houve alteração nestes parâmetros no grupo controle. Além disso, foi observado um aumento significativo da força do músculo quadríceps femural, na distância percorrida no teste de caminhada de seis minutos e na qualidade de vida em ambos os grupos. No entanto, a comparação entre os grupos mostrou que o aumento foi mais expressivo no grupo EE funcional em relação ao grupo controle. Conclusão. A EE muscular é uma intervenção segura que melhora o controle neurovascular, a vasoconstrição muscular, a capacidade funcional e a qualidade de vida em pacientes internados para tratamento da IC. Estes achados reforçam a importância da EE muscular em pacientes com IC na fase intra-hospitalar para compensação da síndromeIntroduction. Heart failure (HF) is a complex syndrome that results in elevated morbidity and mortality rate. Advanced HF patients may stay for a long period of time in the hospital for the treatment of HF. It is known that long-term bed rest and prolonged inactivity cause complications that result in worsening of exercise tolerance. On the other hand, there is evidence that treatment with low-frequency electrical stimulation (ES) provides important benefits for HF patients. Thus, we tested the hypothesis that treatment with ES improves neurovascular control, peripheral vasoconstriction, muscle strength and functional capacity in hospitalized advanced HF patients. Methods. Thirty hospitalized patients for treatment of decompensated HF, New York Heart Association class IV, left ventricular ejection fraction <= 30% were consecutively randomized into two groups: 1) Functional ES (n = 15) and 2) control (n = 15). Muscle sympathetic nerve activity (MSNA) was directly evaluated in the peroneal nerve by microneurography technique and lower and upper limb muscle blood flow by venous occlusion plethysmography. Heart rate and blood pressure were indirectly evaluated on beat-to-beat basis (Finometer). Quadriceps muscle strength was evaluated by dynamometer, functional capacity by six-minute walk test and quality of life by Minnesota Living with Heart Failure questionnaire. Functional ES, initiated after clinical stabilization, consisted of stimulation of lower limbs, at frequency of 10 Hz, pulse width of 150ms, with cycles of 20 seconds of stimulation and 20 seconds of rest for 60 minutes, according to the intensity threshold of patient discomfort until it reaches a maximum value of 70mA, 10 days. The control group followed the same procedure, except for the intensity, which was set at 20mA to not cause visible muscle contraction. Results. Baseline characteristics were similar between groups, except age that was higher in functional ES group. After 10 days of protocol, MSNA bursts/min and bursts/100 heart beats were significantly decreased in the patients submitted to ES. Functional ES increased lower and upper limb muscle blood flow and vascular conductance. In contrast, in the control group no changes in these parameters were found. Muscle strength, walk distance in six-minute walk test and quality of life were increased in both groups. However, the comparison between groups showed that these changes were greater in the functional ES group. Conclusion. ES is a safe intervention that significantly improves neurovascular control, vasoconstriction, functional capacity and quality of life in hospitalized advanced HF patients. These findings show the importance of the muscle ES in the treatment of hospitalized HF patient

Testosterone Deficiency Increases Hospital Readmission and Mortality Rates in Male Patients with Heart Failure

Background: Testosterone deficiency in patients with heart failure (HF) is associated with decreased exercise capacity and mortality; however, its impact on hospital readmission rate is uncertain. Furthermore, the relationship between testosterone deficiency and sympathetic activation is unknown. Objective: We investigated the role of testosterone level on hospital readmission and mortality rates as well as sympathetic nerve activity in patients with HF. Methods: Total testosterone (TT) and free testosterone (FT) were measured in 110 hospitalized male patients with a left ventricular ejection fraction < 45% and New York Heart Association classification IV. The patients were placed into low testosterone (LT; n = 66) and normal testosterone (NT; n = 44) groups. Hypogonadism was defined as TT < 300 ng/dL and FT < 131 pmol/L. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography in a subpopulation of 27 patients. Results: Length of hospital stay was longer in the LT group compared to in the NT group (37 ± 4 vs. 25 ± 4 days; p = 0.008). Similarly, the cumulative hazard of readmission within 1 year was greater in the LT group compared to in the NT group (44% vs. 22%, p = 0.001). In the single-predictor analysis, TT (hazard ratio [HR], 2.77; 95% confidence interval [CI], 1.58–4.85; p = 0.02) predicted hospital readmission within 90 days. In addition, TT (HR, 4.65; 95% CI, 2.67–8.10; p = 0.009) and readmission within 90 days (HR, 3.27; 95% CI, 1.23–8.69; p = 0.02) predicted increased mortality. Neurohumoral activation, as estimated by MSNA, was significantly higher in the LT group compared to in the NT group (65 ± 3 vs. 51 ± 4 bursts/100 heart beats; p < 0.001). Conclusion: These results support the concept that LT is an independent risk factor for hospital readmission within 90 days and increased mortality in patients with HF. Furthermore, increased MSNA was observed in patients with LT

Testosterone Deficiency Increases Hospital Readmission and Mortality Rates in Male Patients with Heart Failure

Background: Testosterone deficiency in patients with heart failure (HF) is associated with decreased exercise capacity and mortality; however, its impact on hospital readmission rate is uncertain. Furthermore, the relationship between testosterone deficiency and sympathetic activation is unknown. Objective: We investigated the role of testosterone level on hospital readmission and mortality rates as well as sympathetic nerve activity in patients with HF. Methods: Total testosterone (TT) and free testosterone (FT) were measured in 110 hospitalized male patients with a left ventricular ejection fraction < 45% and New York Heart Association classification IV. The patients were placed into low testosterone (LT; n = 66) and normal testosterone (NT; n = 44) groups. Hypogonadism was defined as TT < 300 ng/dL and FT < 131 pmol/L. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography in a subpopulation of 27 patients. Results: Length of hospital stay was longer in the LT group compared to in the NT group (37 ± 4 vs. 25 ± 4 days; p = 0.008). Similarly, the cumulative hazard of readmission within 1 year was greater in the LT group compared to in the NT group (44% vs. 22%, p = 0.001). In the single-predictor analysis, TT (hazard ratio [HR], 2.77; 95% confidence interval [CI], 1.58–4.85; p = 0.02) predicted hospital readmission within 90 days. In addition, TT (HR, 4.65; 95% CI, 2.67–8.10; p = 0.009) and readmission within 90 days (HR, 3.27; 95% CI, 1.23–8.69; p = 0.02) predicted increased mortality. Neurohumoral activation, as estimated by MSNA, was significantly higher in the LT group compared to in the NT group (65 ± 3 vs. 51 ± 4 bursts/100 heart beats; p < 0.001). Conclusion: These results support the concept that LT is an independent risk factor for hospital readmission within 90 days and increased mortality in patients with HF. Furthermore, increased MSNA was observed in patients with LT