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PubMed2000

[Therapy of autonomic disorders by xanax (alprazolam)].

The paper presents an open noncomparative investigation of 36 patients with different manifestations of the syndrome of autonomic dystonia. 20 patients (group 1) had permanent autonomic disorder in context of generalyzed anxious disorders, 16 patients (group 2) had panic attacks. The examination was performed before and 4 weeks after monotherapy with xanax (1.5-2.5 mg/day). Clinical-neurologic study estimated both presence and a degree of manifestations of the syndrome of autonomic dysfunction, hyperventilatory syndrome and sleep disorders. Psychologic investigation included estimation of anxiety according to Spilberg's test, depression according to Beck's scale; SCL Scale was also used. Algesic syndrome was estimated by complex algesic questionnaire. Neurophysiologic study determined a contingent negative deviation and nociceptive flexory reflex. A positive therapeutic activity of xanax was established. The highest therapeutic effect was achieved in group 1 (83%) using lower doses (1.5 mg/day). In group 2 higher doses were needed (2.5 mg/day). In this case the effect was achieved in 83% of the cases, but full absence of panic attacks was observed only in 25% of the patients. Predictors of the drug's efficiency appeared to be short duration of the disease, slight manifestation of depression and absence of the algesic syndrome.

Adult↗

PubMed2006

Cardiac rehabilitation vs. home exercise after coronary artery bypass graft surgery: a comparison of heart rate recovery.

OBJECTIVE: The autonomic dysfunction is known to adversely affect clinical outcome in patients with cardiovascular disease, and exercise training has been shown to modify the sympathovagal control of heart rate. The purposes of this study were to investigate the effect of cardiac rehabilitation on heart rate recovery in patients who received coronary artery bypass grafting (CABG) and compare the effect with that of a home-based exercise program. DESIGN: Fifty-four male patients having undergone CABG were randomly assigned to a cardiac rehabilitation exercise program (n = 18), a home-based exercise program (n = 18), and a control group (n = 18) for 12 wks to evaluate the differences in heart rate recovery among groups. RESULTS: Patients in the cardiac rehabilitation group had significant increases in heart rate recovery (19.1 +/- 6.2 vs. 14.0 +/- 5.4 beats/min, P = 0.022) compared with those in the control group. There were no significant differences in heart rate recovery between cardiac rehabilitation and home-based exercise groups (16.2 +/- 4.8 beats/min) or between home-based exercise and control groups. All three groups had significantly improved heart rate recovery compared with their baseline data (P < 0.001, < 0.001, and 0.007). CONCLUSION: Our results point out that a cardiac rehabilitation exercise program has a positive effect on heart rate recovery in patients having undergone CABG and is consistent with the autonomic improvement. Although the home-based exercise group did not reveal statistical significances over those in the control group, it had comparable efficacy to that demonstrated in the cardiac rehabilitation group.

Coronary Artery Bypass↗

PubMed1988

Choledochal cysts. Oligoganglionosis in the narrow portion of the choledochus.

To investigate whether cystic dilation may be due to a reduction of postcholinergic cell bodies that leads to autonomic dysfunction, ganglion cell bodies were counted in five patients with choledochal cysts and five patients with normal choledochus. In the normal choledochus, the ganglion cell counts in the proximal and distal portions were 374.7 +/- 82.7/cm2 and 349.2 +/- 51.2/cm2, respectively. In cases of choledochal cysts, the ganglion cell counts in the dilated portion and narrow portions were 298.6 +/- 86.9/cm2 and 81.0 +/- 34.8/cm2, respectively. The cell ratio (narrow to dilated) was 0.271. Significant reductions of cell numbers were observed in all the choledochal cysts having various types of pancreatobiliary junctions. These findings indicate that the reduction in the number of ganglion cells in the narrow portion of the choledochal cysts supports the concept of oligoganglionosis in distal choledochus.

Adolescent↗

PubMedDate not supplied

[Neurovegetative symptoms in infants with sleep-related respiratory disorders].

A relationship between neurovegetative symptoms and an increased risk of sudden infant death (SID) has been frequently described. Such symptoms are vomiting because of gastroesophageal reflux, breathing disorders while nutritive sucking, excessive sweating during sleep, prolonged apneas and apneas with associated symptoms, further unexplained episodes of cyanosis, pallor and loss of muscle tone. An acute decompensation of the cardiorespiratory autonomic system during sleep is currently discussed to be one of the causes of SID. Polysomnographic investigations are used to diagnose sleep related cardiorespiratory autonomic dysfunction. In this study, infants up to the age of 5 months were examined using polysomnography throughout their entire nocturnal sleep. The findings from 79 infants with neurovegetative symptoms were compared with the results from 163 healthy control children. Indications of an impaired respiratory regulation during sleep were shown to be significantly more frequent in infants with neurovegetative symptoms. In particular the occurrence of periodic breathing with a high frequency of periodic apnea plus a large number of acute decreases in oxygen saturation could be shown in infants with neurovegetative symptoms. The findings were most pronounced during the first 1.5 months after birth. The results of this investigations lead to the conclusion that, in the case of young infants with breathing abnormalities, neurovegetative symptoms can frequently be observed. The occurrence of such symptoms should therefore be a reason for a polysomnographic examination.

Autonomic Nervous System↗

PubMed2005

Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice. IV. Characterization of acute and chronic effects of ambient air fine particulate matter exposures on heart-rate variability.

Long-term exposure to fine particulate air pollution (PM2.5) has been associated increased risk of death from cardiopulmonary diseases. Cardiac function parameters have also been affected by ambient particulate matter (PM) exposure, including heart-rate variability (HRV), a measure of autonomic function that has been recognized as a well-defined, quantitative indicator of autonomic dysfunction. However, the role of HRV in ambient PM-induced cardiovascular effect is not fully understood. In an accompanying article, we report significant decreasing patterns of heart rate (HR), body temperature, and physical activity for mice lacking apoliproprotein (ApoE-/-) over 5 mo of exposure to concentrated ambient PM (CAPs), with smaller and nonsignificant change for C57 mice. In this article, we report the effects of subchronic CAPs exposure on HRV parameters that are sensitive to cardiac sympathetic and parasympathetic nerve activity. The standard deviation of normal to normal beat intervals (SDNN) and the square root of the mean squared differences of successive RR intervals (RMSSD) in the late afternoon and overnight for the ApoE-/- mice showed a gradual increase for the first 6 wk, a decline for about 12 more wk, and a slight turn upward at the end of the study period. For C57 mice, there were no chronic effect changes of SDNN or RMSSD in the late afternoon, an a slight increase after 6 wk for the overnight period. The response patterns of ApoE-/- mice indicated a perturbation of the homeostatic function in the cardiovascular system (initial enhancement and late depression of the HRV parameters). Our results complement the findings in human panel and controlled CAPs exposure studies in demonstrating that increased levels of particle pollution are able to perturb cardiac autonomic function, which may lead to adverse cardiovascular outcomes.

Air Pollutants↗

PubMed1992

Heart rate variability during sleep in snorers with and without obstructive sleep apnea.

Changes in sympathetic and vagal tone may be the substrate for the development of cardiac arrhythmias in patients with obstructive sleep apnea (OSA). The cardiovascular responses in the traditional autonomic tests show great interindividual and intraindividual variations. During sleep there are repetitive modifications of heart rate (HR) that are not influenced by psychologic factors or the patient's cooperation. For this reason, we evaluated HR modifications in relation to spontaneous body movements (BM) and sleep apneas during nonrapid eye movement (NREM) and rapid eye movement (REM) sleep in habitual snorers with normal and pathologic respiratory disturbance index (RDI). From 132 consecutive patients referred to our sleep center for habitual snoring and/or daytime somnolence, we selected 35 male patients younger than 60 years without clinical evidence of autonomic dysfunction. They were divided into three groups: group A (RDI < 10); group B (RDI > 10 and < 20); and group C (RDI > 20). No significant difference was found among the three groups in the HR variability related to BM. In the evaluation of bradytachyarrhythmias related to apneic events of 20 to 30 s, we found a significant difference between group A and the other two groups. In patients with RDI > 10, a reduced HR variability related to a reduced sympathetic tone in the post-apnea phase was observed. Some authors suggested that an HR increase during the post-apnea period can be used as an index of "brainstem arousal." Our results seem to indicate a reduced apnea-related "arousability" in patients with RDI > 10. This finding might be one of the factors contributing to the worsening of OSA.

Autonomic Nervous System↗

PubMed1990

Circadian blood pressure variations under different pathophysiological conditions.

The daily variation in blood pressure (circadian blood pressure rhythm) is characterized by a nocturnal fall and a diurnal rise. The circadian blood pressure rhythm seems to be mediated mainly by the circadian rhythm of sympathetic tone, linked to changes in physical and mental activities, e.g. the waking-sleeping cycle. Statistically significant circadian blood pressure rhythms have been confirmed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, the normal pattern of circadian blood pressure rhythm is reversed in elderly people and in those with Cushing's syndrome, those undergoing glucocorticoid treatment, and those with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, tetraplegia, diabetic or uremic neuropathy, etc), chronic renal failure, renal or cardiac transplantation, congestive heart failure, eclampsia, sleep apnea syndrome, malignant hypertension, systemic atherosclerosis and accelerated hypertensive organ damage. However, in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, or those with cardiac pacing, a nocturnal blood pressure fall is ordinarily observed. It may be that a fall in cardiac output rather than in peripheral resistance may be mainly responsible for the nocturnal fall in blood pressure. It also seems that a nocturnal heart rate fall is not responsible for it, since the nocturnal blood pressure fall remained unchanged in patients undergoing cardiac pacing and was disturbed in patients with Cushing's syndrome or hyperthyroidism in whom the circadian heart rate rhythm remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System Diseases↗

PubMed2006

Nocturnal hypertension in mice consuming a high fructose diet.

OBJECTIVE: To investigate the effect of fructose consumption on the light/dark pattern of blood pressure, heart rate and autonomic neural function in mice. BACKGROUND: Insulin resistant diabetes is associated with hypertension and autonomic dysfunction. There is evidence that the increasing incidence of diabetes may be related to dietary changes, including consumption of high levels of fructose. DESIGN/METHODS: C57/BL mice, instrumented with radiotelemetric arterial catheters, were fed a control or high fructose diet (60%). Cardiovascular parameters measured were light/dark pattern of mean arterial pressure (MAP), heart rate (HR) and variability (time and frequency domain). We also measured plasma insulin, glucose, lipids and angiotensin II (Ang II) as well as glucose tolerance. In situ hybridization was used to measure brainstem expression of tyrosine hydroxylase (TH) and Ang AT1a mRNA. RESULTS: Fructose diet (8 weeks) produced an increase in MAP, variance and low frequency domain (14+/-3 vs. 33+/-4 mm Hg(2), variance and 10+/-2 vs. 26+/-4 mm Hg(2), LF, control vs. fructose, P<0.01). The changes occurred only at night, a period of activity for mice. Glucose tolerance was attenuated in the fructose group. Fructose also increased plasma cholesterol (80+/-1 vs. 126+/-2 mg/dl, control vs. fructose, P<0.05) and plasma Ang II (18+/-5 vs.65+/-12 pg/ml, control vs. fructose, P<0.05). Depressor responses to alpha(1)-adrenergic blockade with prasozin were augmented in fructose-fed mice. Using quantitative in situ hybridization, we found that Ang AT1a receptor and TH mRNA expression were significantly increased in the brainstem locus coeruleus. CONCLUSION: A high fructose diet in mice produced nocturnal hypertension and autonomic imbalance which may be related to activation of sympathetic and angiotensin systems.

Adrenergic alpha-Antagonists↗

PubMed1982

The neuroleptic malignant syndrome.

The neuroleptic malignant syndrome (NMS) comprises hyperpyrexia, altered consciousness, muscular rigidity, and autonomic dysfunction. It is a rare idiosyncratic reaction to major tranquilizers, including the phenothiazines, butyrophenones, and thioxanthenes; haloperidol and fluphenazine enanthate or fluphenazine decanoate are the drugs most commonly incriminated. The syndrome occurs after therapeutic rather than toxic doses of neuroleptic drugs and is unrelated to the duration of therapy. The NMS is attributed to a disturbance of dopaminergic systems within the basal ganglia and hypothalamus. Associated laboratory abnormalities include leukocytosis, with elevated serum creatine phosphokinase (CPK) and liver enzyme concentrations. The NMS, which is known to some psychiatrists and neurologists but to few internists, probably is underdiagnosed; therefore, its true incidence is unknown. The NMS should be included in the differential diagnosis of any febrile patient with a history of neuroleptic treatment. Because the mortality of NMS is about 20%, early diagnosis and withdrawal of the neuroleptic drug therapy is crucial. Supportive treatment in a medical intensive care unit may be required.

Antipsychotic Agents↗

PubMed1990

Does ambulatory blood pressure monitoring improve the diagnosis of secondary hypertension?

Ambulatory blood pressure monitoring can determine the average blood pressure level and the short- and long-term blood pressure variability (circadian rhythm). The circadian blood pressure rhythm appears to be mediated mainly by the circadian rhythm of the sympathetic tone which is linked to changes in physical and mental activity, e.g. the waking-sleeping cycle. A statistically significant circadian blood pressure rhythm was observed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, in patients with Cushing's syndrome, under glucocorticoid treatment, or with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, spinal cord injury, brainstem lesions, diabetic neuropathy, uremic neuropathy, etc), chronic renal failure, eclampsia, malignant hypertension, sleep apnea syndrome or systemic atherosclerosis, the normal circadian blood pressure rhythm appears to be eliminated or reversed, while in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, diabetes insipidus, acromegaly, hyperparathyroidism or hyperprolactinemia, the nocturnal blood pressure fall has been observed as in normal subjects. The alteration in the circadian blood pressure rhythm was observed with different pathophysiological conditions, although no specific pattern was observed for any condition. A disturbance in any part of the hierarchy of factors that regulate the circadian rhythm of sympathetic neural tone seems to disturb the circadian blood pressure rhythm. We conclude that ambulatory blood pressure monitoring is not critically important in the diagnosis of secondary hypertension although it does help in screening for secondary hypertension.

Autonomic Nervous System Diseases↗

PubMed1997

[Cardiovascular risk factors in diabetic nephropathy].

BACKGROUND: Diabetic nephropathy is associated with increased cardiovascular mortality. This may be contributed to by changes in plasma lipids, fibrinogen and hemorheology. Cardiovascular autonomic dysfunction, which is related to an increased incidence of arrhythmic death, may also play a role. PATIENTS AND METHODS: Therefore, we investigated in 58 IDDM-patients with none (n = 28), incipient (albuminuria 30 to 300 mg/day, n = 11) and overt clinical nephropathy (albuminuria > 300 mg/day, n = 19) plasma concentrations of lipoproteins and fibrinogen, plasma viscosity, erythrocyte aggregation and erythrocyte rigidity. Assessments of neuropathy included tibial nerve motor conduction velocity, perception of vibration, beat-to-beat variation during rest and during forced respiration, heart-rate response to Valsalva maneuver and heart-rate response to standing (30:15). RESULTS: Patients with clinical overt nephropathy had, compared to those without nephropathy, significantly higher concentrations of LDL-cholesterol, triglycerides and fibrinogen, significantly lower concentrations of HDL-cholesterol and significantly higher plasma viscosity, erythrocyte aggregability and erythrocyte rigidity. Regarding the assessments of neuropathy we found in patients with nephropathy, compared to those without nephropathy, significantly reduced tibial nerve motor conduction velocity, reduced perception of vibration thresholds and reduced heart rate variability during rest, during forced respiration, in response to Valsalva maneuver and in response to standing. In diabetic patients with microalbuminuria erythrocyte aggregability and erythrocyte rigidity were significantly higher and heart rate variability during rest was significantly lower than in patients without nephropathy. CONCLUSION: In clinical overt nephropathy there is an aggregation of different cardiovascular risk factors, namely, disturbances in lipoprotein concentrations, increased fibrinogen concentration and disturbances in hemorheology. Furthermore marked deterioration in peripheral and autonomic cardial nerve function in these patients is evident accounting for a part of the greatly increased cardiovascular mortality of these patients.

Adult↗

PubMed2002

Abnormalities of the electrocardiogram during hypoglycaemia: the cause of the dead in bed syndrome?

We have previously demonstrated that experimental hypoglycaemia in adults with type 1 diabetes causes an abnormal electrocardiogram (ECG), with increases in QT interval and dispersion. These abnormalities in cardiac repolarisation indicate a risk of ventricular tachycardia and sudden death in other conditions, including ischemic heart disease and congenital long QT syndrome. We have hypothesised that they could contribute to the dead in bed syndrome--the recently described sudden unexpected death in young people with type 1 diabetes--which occurs around three times more frequently than in those without diabetes. It is clearly impossible to explore the causes of a rare and fatal complication by direct observation. We have therefore explored the pathophysiology in a series of experimental studies involving non-diabetic subjects and surrogate endpoints. These have demonstrated that abnormal cardiac repolarisation occurs consistently during insulin-induced hypoglycaemia and that either potassium infusion or beta-blockade prevents increased QT dispersion but only partially prevents QT lengthening. The sympathoadrenal discharge induced by hypoglycaemia alters cardiac repolarisation by both direct and indirect (by reducing extracellular potassium) mechanisms. Other factors that might contribute to the clinical risk of cardiac arrhythmias during nocturnal hypoglycaemia include autonomic neuropathy. This is associated with prolonged QT interval in the non-hypoglycaemic state and has been proposed as a cause of sudden death in those affected. We have examined cardiac repolarisation during clamped hypoglycaemia in patients with type 1 diabetes, with and without autonomic neuropathy. Our data demonstrate lengthening of QTc (QT interval corrected for heart rate) during hypoglycaemia in all groups with no significant differences between the groups, suggesting that autonomic dysfunction does not contribute to hypoglycaemia-induced QTc lengthening in type 1 diabetes. Our hypothesis would be strengthened by demonstrating similar changes during clinical hypoglycaemia. We have recently completed studies in prepubescent children and adults that show modest but significant changes in QTc during nocturnal hypoglycaemia in both populations. We have also demonstrated that pre-treatment with beta-blocking agents prevents abnormal cardiac repolarisation during experimental hypoglycaemia. This has identified a possible treatment if we can identify patients at high risk. Further work is necessary to determine whether we can reliably identify patients who could be at special risk during hypoglycaemia and who might benefit from protection with agents such as beta-blockers. Sudden death in young people with diabetes is, thankfully, rare. However its consequences are so devastating that an excess risk of 3 to 4 times the non-diabetic population seems sufficient to warrant further investigation of the mechanisms that may cause it.

Adult↗

PubMed1970

Primary neurogenic orthostatic hypotension.

Eight further cases of neurogenic orthostatic hypotension are described together with a necropsy study on one case. Three cases showed evidence of autonomic dysfunction in isolation, while in five cases this was accompanied by evidence of more diffuse central nervous system degeneration. (Parkinsonism, cerebellar ataxia, dementia, pyramidal signs, bulbar weakness, and muscular wasting were all seen in varying proportions.)The various clinical presentations, investigations, pathology, treatment, and prognosis are discussed. In the experience of the authors, when assessed, an abnormal Valsalva response is invariable, confirming the breakdown of the circulatory reflex. A normal vasopressor response is likewise invariable, eliminating an abnormality of blood vessels themselves, and confirming the lesion as neurogenic. The demonstration of loss of sweating to indirect body heating, which also is usual suggests that the defect is central or on the efferent side of the reflex and a normal pilo-erector response to acetylcholine confirms this as preganglionic. Emphasis is laid on the non-specificity of many accepted physiological tests in this disorder and on the delay in diagnosis consequent upon the variable presentation.

Adult↗

PubMed2005

Osmosensitive mechanisms contribute to the water drinking-induced pressor response in humans.

BACKGROUND: Water drinking elicits a sympathetically mediated pressor response in multiple-system atrophy patients through an unknown mechanism. We reasoned that gastrointestinal distention, hyposomotic stimulation, or both contribute to the water-induced pressor response. METHODS: We compared the response to normal saline and water on blood pressure in 10 patients with probable multiple-system atrophy. Patients featured moderate to severe autonomic dysfunction. EKG and finger arterial blood pressure were recorded continuously, and 500 mL normal saline and distilled water were each given in a single-blinded fashion. Fluids were applied through a previously inserted nasogastric tube within a 5-minute period. RESULTS: Blood pressure began to increase within 10 minutes after water administration and reached a maximum after 20 minutes. Blood pressure did not change after saline administration. The blood pressure change after 20 minutes was 8 +/- 9/2 +/- 5 mmHg with water and -1 +/- 11/-1 +/- 7 mmHg with normal saline administration (p = 0.02 between interventions). Heart rate did not change with either intervention. CONCLUSION: Ingestion of water elicits a greater pressor response than the ingestion of normal saline. Thus, gastric distention is probably not the crucial mechanisms for the water-induced pressor response. Instead, the response may be mediated through osmosensitive afferent structures in the gastrointestinal tract, portal vein, and liver.

Autonomic Nervous System Diseases↗

PubMed1971

Assessment of autonomic function in patients with a Parkinsonian syndrome.

The integrity of the autonomic nervous system was assessed in 11 Parkinsonian patients with symptoms suggestive of autonomic dysfunction. Three had the additional clinical features of the Shy-Drager variant of idiopathic orthostatic hypotension and were found to have a gross disturbance of vasomotor, sudomotor, pilomotor, and bladder function; assessment indicated that a lesion was present at sympathetic ganglionic level or beyond in two cases, though a more centrally placed lesion may well have been present also, as in the third case. In the remaining eight patients with paralysis agitans no unequivocal functional disturbance was found except in the bladder; nevertheless, the low resting blood pressure and the supersensitivity to intravenously infused L-noradrenaline in the three patients in whom it was tested is taken to imply defective regulation from higher centres, with a consequent reduction in impulse traffic at sympathetic nerve terminals. Such a concept is supported by experimental studies in animals and would account for the low renin and aldosterone secretion rates and reduced noradrenaline formation reported by others in patients with paralysis agitans.

Aged↗

PubMed1994

Relationship between diabetic autonomic neuropathy and gastric contents.

Delayed gastric emptying secondary to diabetic autonomic neuropathy (DAN) is a recognized risk factor for aspiration pneumonitis. The purpose of this study is to determine whether bedside autonomic function tests (AFTs) would predict gastric contents. Gastric volume and its pH were measured in 36 patients with diabetes mellitus (DM) and 15 nondiabetic patients at induction of general anesthesia for elective ambulatory surgery. Manifestations of autonomic dysfunction were assessed preoperatively in all 51 patients with five commonly used cardiovascular AFTs. According to the results of these five tests, 16 patients with DM met the criteria for the diagnosis and are called "DAN positive." The remaining 20 diabetics did not meet the criteria and are called "DAN negative." Fifteen patients without DM did not meet the criteria and are called "nondiabetics." Diabetic patients were significantly older and more obese than nondiabetics and those with DM more than 10 yr were more often DAN positive. Solid, undigested food particles were found more often in the gastric contents of DAN-positive patients compared to nondiabetics. Gastric liquid volume and pH were similar in diabetic patients (DAN positive and DAN negative) and nondiabetic controls. These results demonstrate that diagnosis of DAN by commonly used cardiovascular AFTs does not predict larger gastric liquid volume or lower pH, but does predict the presence of solid food particles.

Adult↗

PubMed2004

Worsening of depressive symptoms 6 months after an acute coronary event in older adults is associated with impairment of cardiac autonomic function.

BACKGROUND: Depression increases mortality of coronary patients, and autonomic dysfunction has been proposed as an explanation for this association. METHODS: In a sample of 38 adults > or = 60 years with myocardial infarction or unstable angina, we studied depression (presence of a major depressive episode and 21-item Hamilton depression score) and heart rate variability (HRV) of 550 normal beats shortly after admission to the coronary care unit (CCU). Thirty patients were alive at 6 months and were studied at that time as well. Spectral HRV measurements included power in the high-frequency range (HF, 0.15-0.55 Hz, a measure of parasympathetic activity) and low-frequency range (LF, 0.03-0.15 Hz). Nonspectral HRV measurements included standard deviation of normal beats (SDNN) and two measures of vagal activity: percentage of adjacent cycles differing by >50 ms (pNN50) and the root-mean-square of differences in successive beats (rMSNN). RESULTS: Patients who died within 6 months (n=8) had a higher Hamilton-D score than survivors (13.9+/-6.5 vs. 18.4+/-5.6, P=0.039) and were more likely to have an episode of major depression upon admission to the CCU (71 vs. 27%, P=0.027). An increase in Hamilton-D score at 6 months correlated with a decrease in total (r=-0.48, P=0.014), high-frequency (r=-0.49, P=0.007), and low-frequency HRV (r=-0.46, P=0.014). LIMITATIONS: Patients belonged to a single institution and there was a small proportion of men. CONCLUSIONS: Progression of mood symptoms 6 months after an acute coronary event is associated with an impairment of autonomic control of the heart in elderly individuals.

Acute Disease↗

PubMed2001

Effect of beta-blockade on autonomic modulation of heart rate and neurohormonal profile in decompensated heart failure.

BACKGROUND: One of the putative mechanisms for the salutary effects of beta-blockers in patients with congestive heart failure (CHF) is their ability to improve autonomic dysfunction. However, patients with profound neurohumoral abnormalities derive little survival benefit from beta-blockers. The purpose of the current study was to evaluate the effect of beta-blockers on heart rate variability (HRV) in decompensated CHF. METHODS: Time and frequency domain HRV indices were obtained from 24-hour Holter recordings and compared to assess the role of beta-blockade in 199 patients (mean age 60 +/- 14 years) with decompensated CHF. Neurohormonal differences were assessed by measuring norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6 in a subset of 64 patients. RESULTS: All HRV indices were markedly suppressed but were substantially higher in patients who were on beta-blockers. Time domain measures of parasympathetic cardiac activity, the percentage of R-R intervals with > 50 ms variation (4.9 +/- 0.6 vs 7.7 +/- 1.2%, P = 0.006) and the square root of mean squared differences of successive R-R intervals (22.7 +/- 2.0 vs 31.6 +/- 4.1 ms, P = 0.004), were higher in the beta-blocker group. Spectral analysis revealed that the total power and the ultra-low frequency power were significantly higher in patients on beta-blockers (82% and 59%, respectively). The high frequency power, a spectral index of parasympathetic modulation, was 41% higher in the beta-blocker group (121 +/- 25 vs 171 +/- 27 ms(2), P = 0.02). Norepinephrine and interleukin-6 levels were substantially lower in patients on beta-blockers (28% and 61%, respectively). However, these differences did not reach statistical significance. CONCLUSIONS: Beta-blockers improve the impaired cardiac autonomic regulation during high sympathetic stress of decompensated CHF. This effect may play an important role in protecting the myocardium and preventing arrhythmias during transient increases in sympathetic activity.

Adrenergic beta-Antagonists↗