Literatura académica sobre el tema "Cardioautonomic function"

The purpose of this study was to determine if the cardioautonomic responses to esophageal electric stimulation were mediated entirely through modulation of respiratory frequency or a direct vagal effect. We performed electric stimulation of the esophagus in 13 healthy male controls (24 +/- 6 yr) using a manometric catheter to which a stainless steel electrode was attached. Stimulation frequencies ranged from 0.1 to 1 Hz and were applied in random fashion. We computed the power spectra of the heart rate variability and respiratory frequency as measures of autonomic function. Electric stimulation of the esophagus produced significant increases in the high-frequency power of the heart rate autospectrum at all stimulation frequencies (maximal at 0.2 Hz). However, regardless of the frequency of esophageal stimulation, the respiratory rate was not changed from baseline. These studies indicate that enhancement of cardiac vagal modulation observed in response to esophageal electric stimulation is not primarily due to changes in respiratory frequency, but rather occurs through a direct, vagally mediated action through sensory neural pathways involving vagal esophageal afferents.

Objectives: Both polycystic ovarian syndrome (PCOS) and high body mass index (BMI) are associated with autonomic dysfunction. Most of the patients of PCOS have high BMI. Hence, BMI is likely to be a factor contributing to the autonomic dysfunction in PCOS. High-sensitivity C-reactive protein (hs-CRP) is a marker of inflammation and a predictor of future cardiovascular risk. PCOS patients have low-grade chronic inflammatory state. Coexistence of PCOS and obesity causes more increase in CRP, thereby further increasing the risk of cardiovascular morbidity. We have performed autonomic function tests and estimated hs-CRP in overweight patients of PCOS and compared our findings with the control group consisting of overweight normal subjects. Our aim is to find out whether the cardioautonomic and inflammatory changes seen in PCOS are due to the presence of increased weight or do the presence of increased weight add to the severity of these changes seen in PCOS. Materials and Methods: Cases consisted of 44 overweight patients of PCOS and controls included 44 healthy overweight subjects, all in the age group of 18–45 years. Autonomic function test consisted of three sympathetic and three parasympathetic reactivity tests. The following tests were done for parasympathetic reactivity: (a) Deep breathing test – expiration:inspiration ratio (E:I) was calculated. (b) Valsalva maneuver-Valsalva ratio was calculated. (c) Heart rate changes from lying to standing (LST) - 30:15 ratio was calculated. For assessing sympathetic reactivity, the following tests were used: (a) Isometric handgrip test – the difference between resting diastolic blood pressure (DBP) reading and the reading before release of hand grip is noted. (b) Cold pressor test (CPT) – The rise in DBP over the baseline DBP was noted. (c) Systolic BP (SBP) change in LST – the maximum fall in SBP was recorded. Measurement of serum hs-CRP was done using enzyme-linked immunosorbent assay. Results: We found that in the overweight PCOS group, there was a significant decrease in both sympathetic and parasympathetic reactivity than the overweight control group (p=0.000 for Valsalva ratio, 0.027 for 30:15 ratio, and 0.0005 for CPT). The difference between hs-CRP in controls and PCOS was also significant (P = 0.039). Conclusion: In our study, we concluded that the pathological changes due to PCOS could be attributed directly to the extent of inflammation measured by hs-CRP levels. These changes were not directly related to BMI as proven by comparing with controls (overweight non-PCOS subjects).

Abstract Background Sex differences characterize cardiovascular outcomes in patients with type 1 diabetes. Cardioautonomic neuropathy is a common complication of type 1 diabetes that associates increased morbi-mortality. Data regarding the interplay between sex and cardiovascular autonomic neuropathy are scarce and controversial in these patients. We aimed to address sex-related differences in the prevalence of seemingly asymptomatic cardioautonomic neuropathy in type 1 diabetes, and their associations with sex steroids. Methods We conducted a cross-sectional study including 322 consecutively recruited patients with type 1 diabetes. Cardioautonomic neuropathy was diagnosed using Ewing's score and power spectral heart rate data. We assessed sex hormones by liquid chromatography/tandem mass spectrometry. Results When considering all subjects as a whole, asymptomatic cardioautonomic neuropathy prevalence was not significantly different between women and men. When age was taken into account, the prevalence of cardioautonomic neuropathy was similar among young men and those > 50 years. However, in women > 50 years, the prevalence of cardioautonomic neuropathy doubled that of young women [45.8% (32.6; 59.7) vs. 20.4% (13.7; 29.2), respectively]. The OR of having cardioautonomic neuropathy was 3.3 higher in women > 50 years than in their younger counterparts. Furthermore, women presented more severe cardioautonomic neuropathy than men. These differences were even more marked when women were classified according their menopausal status instead of age. Peri- and menopausal women had an OR 3.5 (1.7; 7.2) of having CAN compared with their reproductive-aged counterparts [CAN prevalence: 51% (37; 65) vs. 23% (16; 32), respectively]. A binary logistic regression model (R2: 0.161; P = 0.001) displayed age > 50 years as a significant determinant of cardioautonomic neuropathy only in women. Androgens were positively associated with heart rate variability in men, and negatively in women. Accordingly, cardioautonomic neuropathy was associated with increased testosterone/estradiol ratio in women but to decreased testosterone concentrations in men. Conclusions Menopause in women with type 1 diabetes is accompanied by an increase in the prevalence of asymptomatic cardioautonomic neuropathy. This age-related excess risk of cardioautonomic neuropathy is not observed in men. Men and women with type 1 diabetes have opposite associations between circulating androgens and indexes of cardioautonomic function. Trial registration ClinicalTrials.gov Identifier: NCT04950634.

Introduction: Cardiac autonomic neuropathy, a risk factor of cardiovascular mortality, is a common manifestation of prediabetes. Evidence points to perivascular adipose tissue inflammation as a quintessential instigator of cardiovascular dysfunction in metabolic impairment. Interventions tailored to ameliorate such subtle cardiovascular involvement have not been forthcoming. Data emerging from our laboratory implicate alteration of adipocyte mitochondrial bioenergetics, particularly an upregulation of uncoupling protein 1 (UCP1) expression and subsequent augmentation of adipose tissue hypoxia, as a potential culprit driving localized adipose inflammation. Hypothesis: Inhibition of UCP1-mediated thermogenesis or activation of the alternative thermogenic pathway, futile creatine cycling, through supplementation with phosphate or creatine monohydrate, respectively, may ameliorate the inflammatory phenotype observed in non-obese prediabetic rats. Methods: A non-obese prediabetic rat model, developed in our laboratory was used. This phenotype is evoked by 12 weeks of hypercaloric feeding causing localized perivascular inflammation in absence of systemic markers of inflammation. Cardioautonomic function was assessed by invasive hemodynamics. Localized adipose tissue inflammation and macrophage polarization were examined. Results: UCP1 inhibition by phosphate supplementation reversed the blunted parasympathetic baroreflex sensitivity observed in prediabetic rats. This was associated with the alleviation of perivascular adipose tissue hypoxia, inflammation, and altered macrophage polarization. These changes were accompanied by normalization of metabolic efficiency that increased in prediabetic rats due to UCP1 upregulation. Similar functional effects were observed after creatine supplementation without changes in metabolic efficiency. Conclusions: Bypassing UCP1-mediated thermogenesis upregulated by increased caloric intake alleviates cardioautonomic deterioration triggered by perivascular inflammation. This is achieved by UCP1 inhibition with a potential risk of increased metabolic efficiency and weight gain, or by activation of the alternative thermogenic pathway of creatine cycling.

AbstractNormoferritinemic women with functional hyperandrogenism show a mild iron overload. Iron excess, hyperandrogenism, and cardioautonomic dysfunction contribute to blood pressure (BP) abnormalities in these patients. Furthermore, combined oral contraceptives (COC) prescribed for hyperandrogenic symptoms may worse BP recordings. Iron depletion by phlebotomy appears to lower BP in other acquired iron overload conditions. We aimed to determine the effect of iron depletion on the office BP, ambulatory BP monitoring, and frequency of hypertension in patients with functional hyperandrogenism submitted to standard therapy with COC. We conducted a phase 2 randomized, controlled, parallel, open-label clinical trial (NCT02460445) in adult women with functional hyperandrogenism including hyperandrogenic polycystic ovary syndrome and idiopathic hyperandrogenism. After a 3-month run-in period of treatment with 35 µg ethinylestradiol plus 2 mg cyproterone acetate, participants were randomized (1:1) to three scheduled bloodlettings or observation for another 9 months. Main outcome measures were the changes in office BP, 24-h-ambulatory BP, and frequency of hypertension in both study arms. From June 2015 to June 2019, 33 women were included in the intention-to-treat analyses. We observed an increase in mean office systolic BP [mean of the differences (MD): 2.5 (0.3–4.8) mmHg] and night-time ambulatory systolic BP [MD 4.1 (1.4–6.8) mmHg] after 3 months on COC. The percentage of nocturnal BP non-dippers also increased, from 28.1 to 92.3% (P < 0.001). Office and ambulatory BP did not change throughout the experimental period of the trial, both when considering all women as a whole or as a function of the study arm. The frequency of the non-dipping pattern in BP decreased during the experimental period [OR 0.694 (0.577–0.835), P < 0.001], regardless of the study arm. Decreasing iron stores by scheduled bloodletting does not override the BP abnormalities caused by COC in women with functional hyperandrogenism.

Background: type 2 diabetes is determined by a reduction of β cell mass and function besides a defect in insulin sensitivity. It was demonstrated that pancreatic islets are innervated by sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) fibers and autonomic function contributes to the regulation of glucose homeostasis. An alteration in neuronal control of β cell function could be involved in the pathogenesis of the type 2 diabetes. Aim: we focused on finding a possible association between autonomic function and the different parameters that describe β cell function in The Maastricht Study, a population-based cohort. We sought this association also in the population of Verona Newly Diagnosed Type 2 Diabetes Study (VNDS), a study of patients with newly diagnosed type 2 diabetes. Research design and Methods: in the Maastricht study population from 24-h electrocardiogram we derived Heart Rate Variability (HRV) time and frequency domains (individual z-scores, based upon seven and six variables, respectively). From a standard 2-hour 75 g OGTT we estimated different aspects of β cell function, i.e. C-peptidogenic index t0-30, overall insulin secretion, β cell glucose sensitivity, β cell potentiation factor, and β cell rate sensitivity, using formula-based methods and mathematical modeling. In the VNDS study cardiovascular autonomic function was assessed by a computerized system which analyzed heart rate and blood pressure variations during lying to standing (LS), deep breathing (DB), and Valsalva maneuver (VM), following the criteria presented by Ewing and Clarke. From a 5-hour 75g OGTT we estimated through mathematical modelling two main parameters of beta cell glucose sensitivity: derivative (first phase) and proportional control (second phase) of insulin secretion. Results: in the Maastricht study we analyzed 2007 individuals with a mean  standard deviation (SD) age of 59.8  8.2 years, of whom 52% were men and 24% with type 2 diabetes (oversampled by design). After adjustment for age, sex, educational level and Matsuda index, time and frequency domain HRV were significantly and directly associated with C-peptidogenic index, β cell glucose sensitivity and β cell potentiation factor, but not with overall insulin secretion. Then, further adjustment for cardiovascular risk factors (model 4) did not materially alter these associations, though only the association of HRV with C-peptidogenic remained statistically significant (standardized β [95%CI] per 1-SD increment in HRV TIME domain, for respectively C-peptidogenic index, overall insulin secretion, β cell glucose sensitivity, and β cell potentiation, 0.05 [0.00; 0.09]; 0.04 [-0.00; 0.08]; 0.04 [0.00; 0.08] ; and 0.04 [-0.00; 0.08]; standardized β [95%CI] per 1-SD increment in HRV FREQUENCY domain, for respectively C-peptidogenic index, overall insulin secretion, β cell glucose sensitivity, and β cell potentiation, 0.05 [0.00; 0.09]; 0.04 [-0.00; 0.08]; 0.04 [0.00; 0.08] ; and 0.04 [-0.00; 0.08]). HRV time and frequency domain weren’t significantly associated with rate sensitivity. Furthermore, we evaluated data of 537 patients with newly diagnosed type 2 diabetes with a mean ± SD age of 58.3 ± 9.6 of whom 66.3% were male. 91 subjects (16.9%) showed at least one abnormal test used to evaluate cardiovascular autonomic function (CAN). We found a worse derivative control of beta cell function in people with signs of cardio autonomic neuropathy as compared to the other group. This difference however did not reach statistical significance (p=0.063). Conclusion: In summary, in the present research we analyzed a possible association between autonomic function and β cell secretion, estimated from OGTT. We found that autonomic dysregulation could contribute to β-cell dysfunction, in particular affecting the first phase of insulin secretion. This mechanism could add to the other factors that lead to the impairment of glucose homeostasis.