Juvenile fibromyalgia syndrome: Blunted heart rate response and cardiac autonomic dysfunction at diagnosis

2016 ◽  
Vol 46 (3) ◽  
pp. 338-343 ◽  
Author(s):  
Magda M. Maia ◽  
Bruno Gualano ◽  
Ana L. Sá-Pinto ◽  
Adriana M.E. Sallum ◽  
Rosa M.R. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Autonomic Dysfunction ◽  
Fibromyalgia Syndrome ◽  
Heart Rate Response ◽  
Juvenile Fibromyalgia ◽  
Cardiac Autonomic Dysfunction

Cardiac autonomic dysfunction in obese subjects

1989 ◽  
Vol 76 (6) ◽  
pp. 567-572 ◽  
Author(s):  
Marco ROSSI ◽  
Giuliano Marti ◽  
Luigi Ricordi ◽  
Gabriele Fornasari ◽  
Giorgio Finardi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Heart Rate ◽  
Autonomic Dysfunction ◽  
Cross Correlation ◽  
Heart Rate Response ◽  
Valsalva Manoeuvre ◽  
Deep Breathing ◽  
Cardiac Autonomic Dysfunction ◽  
Obese Subjects

1. The prevalence of cardiac autonomic alterations was evaluated in 23 obese subjects with body mass index 37.2 ± 3.03 kg/m2 (mean ± sd), compared with 78 controls with body mass index 22.5 ± 2.6 kg/m2 (P < 0.001). 2. Cardiac autonomic function was assessed by four standard tests (heart rate response to deep breathing and to the Valsalva manoeuvre, systolic blood pressure fall after standing and diastolic pressure rise during handgrip) and by the cross-correlation test, a new method of computerized analysis of respiratory sinus arrhythmia based on spectral analysis of electrocardiographic and respiratory signals. 3. Considering tests indicative of parasympathetic function, only the heart rate response to the deep breathing and the cross-correlation test were significantly lower in the obese than in the control group [deep breathing = 13.95 ± 8.65 beats/min (mean ± sd) vs 24.5 ± 7.65, P < 0.001; cross-correlation 4.28 ± 0.74 units vs 5.14 ± 0.63, P < 0.001]. Deep breathing and/or cross-correlation were abnormal in 10 (43.5%) obese subjects (deep breathing: seven subjects, cross-correlation: eight subjects). No significant difference between groups was found for the response to the Valsalva manoeuvre: the Valsalva ratio was 1.69 ± 0.45 in obese subjects and 1.88 ± 0.33 in controls (P = NS). The Valsalva ratio was abnormal in three obese subjects. 4. No significant differences were found between groups for tests indicative of sympathetic function. The rise in diastolic blood pressure after handgrip was 12.6 ± 6.2 mmHg (1.67 ± 0.82 kPa) in obese subjects and 18.2 ± 4.9 mmHg (2.42 ± 0.65 kPa) in controls (P = NS), and the fall in systolic blood pressure after standing was −6.8 ± 8.6 mmHg (−0.90 ± 1.14 kPa) in obese subjects and −6.9 ± 10.4 mmHg (−0.91 ± 1.38 kPa) in controls (P = NS). The handgrip test was abnormal in four obese subjects, while no obese subject had an abnormal blood pressure response to standing. 5. Our findings suggest a high incidence of cardiac autonomic dysfunction in obese subjects. Since cardiac autonomic alterations have been shown to be involved in the mechanisms of cardiac sudden death, our data suggest a possible role of autonomic dysfunction in the increased risk for sudden death in obesity.

Antidiuretic hormone response to volume depletion in diabetic patients with cardiac autonomic dysfunction

1985 ◽  
Vol 68 (5) ◽  
pp. 545-552 ◽  
Author(s):  
André Grimaldi ◽  
Wojciech Pruszczynski ◽  
Francis Thervet ◽  
Raymond Ardaillou
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Antidiuretic Hormone ◽  
Autonomic Dysfunction ◽  
Heart Rate Response ◽  
Plasma Aldosterone ◽  
Valsalva Manoeuvre ◽  
Diabetic Patients ◽  
Volume Depletion ◽  
Cardiac Autonomic Dysfunction

1. Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact’ patients) and 16 as with ('denervated’ patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied. 2. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection. 3. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in ‘denervated’ and ‘intact’ patients respectively) and heart rate response (+ 10.6 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the ‘intact’ patients whereas it fell in the ‘denervated’ patients (−13.5%). PRA (+ 161.5 and + 231.2% in ‘denervated’ and ‘intact’ patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in ‘intact’ patients (+ 55.3%). The failure of ADH to respond significantly to the volume stimulus in ‘denervated’ patients was confirmed by the results of the time-course study. Plasma ADH remained at the same levels in ‘denervated’ patients whereas it increased significantly (+ 82.4%) in ‘intact’ patients. There was no ADH response in the transplanted patient. 4. These results suggest that, in humans, cardiac receptors and vagal pathways play a role in ADH response to volume depletion.

Pulmonary hypertension in systemic sclerosis determines cardiac autonomic dysfunction assessed by heart rate turbulence

2010 ◽  
Vol 141 (3) ◽  
pp. 322-325 ◽  
Author(s):  
Piotr Bienias ◽  
Michał Ciurzyński ◽  
Dariusz Korczak ◽  
Krzysztof Jankowski ◽  
Maria Glińska-Wielochowska ◽  
...  
Keyword(s):  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Systemic Sclerosis ◽  
Autonomic Dysfunction ◽  
Heart Rate Turbulence ◽  
Cardiac Autonomic Dysfunction

scholarly journals Chemical Sympathectomy Restores Baroreceptor-Heart Rate Reflex and Heart Rate Variability in Rats With Chronic Nitric Oxide Deficiency

2015 ◽  
pp. 459-466 ◽  
Author(s):  
M. CHASWAL ◽  
S. DAS ◽  
J. PRASAD ◽  
A. KATYAL ◽  
M. FAHIM
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Frequency Domain ◽  
Autonomic Dysfunction ◽  
Sympathetic Innervation ◽  
Chemical Sympathectomy ◽  
Principal Mechanism ◽  
Cardiac Autonomic Dysfunction

Nitric oxide (NO) plays a crucial role not only in regulation of blood pressure but also in maintenance of cardiac autonomic tone and its deficiency induced hypertension is accompanied by cardiac autonomic dysfunction. However, underlying mechanisms are not clearly defined. We hypothesized that sympathetic activation mediates hemodynamic and cardiac autonomic changes consequent to deficient NO synthesis. We used chemical sympathectomy by 6-hydroxydopamine to examine the influence of sympathetic innervation on baroreflex sensitivity (BRS) and heart rate variability (HRV) of chronic NG-nitro-L-arginine methyl ester (L-NAME) treated adult Wistar rats. BRS was determined from heart rate responses to changes in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. Time and frequency domain measures of HRV were calculated from 5-min electrocardiogram recordings. Chronic L-NAME administration (50 mg/kg per day for 7 days orally through gavage) in control rats produced significant elevation of blood pressure, tachycardia, attenuation of BRS for bradycardia and tachycardia reflex and fall in time as well as frequency domain parameters of HRV. Sympathectomy completely abolished the pressor as well as tachycardic effect of chronic L-NAME. In addition, BRS and HRV improved after removal of sympathetic influence in chronic L-NAME treated rats. These results support the concept that an exaggerated sympathetic activity is the principal mechanism of chronic L NAME hypertension and associated autonomic dysfunction.

Abstract 19072: Cardiac Autonomic Dysfunction in Mice Lacking Methyl CpG Binding Protein 2

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jose A Herrera ◽  
Christopher S Ward ◽  
Jeffrey L Neul
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Heart Rate Response ◽  
Binding Protein ◽  
Neurodevelopmental Disorder ◽  
Av Block ◽  
Cardiac Phenotype ◽  
Cardiac Autonomic Dysfunction ◽  
Chemical Denervation ◽  
Deficient Mice

Background: Rett Syndrome (RTT) is an X-linked dominant neurodevelopmental disorder primarily caused by mutations in Methyl-CpG-binding protein ( MECP2 ), a transcriptional regulator. Twenty-five percent of all deaths in RTT are sudden and unexpected, and autonomic nervous system (ANS) dysfunction is hypothesized to be the cause of sudden deaths in RTT. However, the role of MeCP2 in cardiac autonomic function has not been investigated in depth. Design/Methods: Male (2 months) and female (9 months) Mecp2 deficient and wildtype mice were implanted with ETA-F10 telemeters and 24h recordings were taken to calculate heart rate, heart rate variability, and incidence of arrhythmic events. Effects of pharmacological stimulants or inhibitors on heart rate were normalized to saline injection response. Results: Male Mecp2 deficient mice (NULL) have a decreased heart rate (WT = 634 ±3, NULL = 518 ±8, p<0.001), while female deficient mice (NULL/+) do not present with a decreased heart rate. Interestingly, NULL and NULL/+ mice both have a high incidence of sinus pauses and AV block (WT 1/5, NULL 6/6, NULL /+ 4/4, p<0.05). Additionally, both NULL and NULL/+ mice have increased bradycardia events defined as a heart rate below 200 bpm, (WT = 17 ±6, NULL = 307 ±94, NULL/+ = 198 ±67, p<0.05) and an increased heart rate variability. The normalized heart rate response to atropine, a parasympathetic blocker, of NULL mice was above wildtype levels (p<0.05) Chemical denervation by combined antagonism of parasympathetic (atropine) and sympathetic (propranolol) resulted in NULL mice having an increased normalized heart rate response compared to wildtype (p<0.05). Finally, the incidence of AVB/sinus pauses counts per 30 minutes post-acute treatment with atropine and chemical denervation (NULL saline 49 ±10, NULL atropine 8 ±5, NULL atropine/propranolol 0.5 ±0.5 p<0.05) decreased the severity of the cardiac phenotype in NULL mice. Conclusions: In summary, Mecp2 is required for a normal heart rhythm. Loss of Mecp2 causes bradycardia, sinus pauses, AV block, and increased heart rate variability that may be attributed by aberrant innervation. Acute atropine and chemical denervation was therapeutic and ameliorated the cardiac phenotype observed in Mecp2 deficient mice.

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