Effects of passive tilt and submaximal exercise on spectral heart rate variability in ventricular fibrillation patients without significant structural heart disease

It has been shown that tilt and exercise elicit significant changes in autonomic activity in normal subjects and that submaximal exercise causes a greater reduction in heart rate variability (HRV) in animals susceptible to ventricular fibrillation (VF). Whether there is an abnormal HRV response to tilt and exercise in patients at risk of sudden cardiac death (SCD) remains unknown. Short-term HRV before and during passive tilt and exercise was studied in 12 survivors of out-of-hospital cardiac arrest with documented VF and compared with 12 age- and sex-matched normal controls. No patient had significant structural heart disease or left ventricular dysfunction. HRV was computed as total-frequency (TF, 0.01 to 1.00 Hz), low-frequency (LF, 0.04 to 0.15 Hz) and high-frequency (HF, 0.15 to 0.40 Hz) components. There was no significant difference between normal controls and SCD survivors in HRV before or during tilt or submaximal exercise testing. The HF component was significantly decreased during tilt compared with that in the supine position in both normal controls (5.85 +/- 0.61 vs 5.08 +/- 0.95 In(msec2), p = 0.005) and patients (5.58 +/- 1.49 versus 4.74 +/- 1.18 In(msec2), p = 0.003). There was again no significant change in the TF or LF components during tilt in either patients or controls. All frequency components were significantly decreased during submaximal exercise testing in both patients and controls. However, there was no significant difference in any of these tilt- and exercise-induced changes in HRV between normal controls and SCD survivors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired heart rate variability in patients with symptomatic NYHA class II-III hypertrophic cardiomyopathy

Power spectral analysis of heart rate variability was performed to assess cardiac autonomic function using Holter monitoring in 19 hospitalized patients with symptomatic NYHA class II-III hypertrophic cardiomyopathy (sHCM), 20 ambulatory patients with asymptomatic NYHA class I hypertrophic cardiomyopathy (asHCM) and 20 normal control subjects. Power spectral analysis decomposed the heart rate variability into high-frequency power (HF: 0.15-0.40 Hz) and low-frequency power (LF: 0.04-0.15 Hz). HF was corrected by mean RR intervals (CCVHF). CCVHF values and LF/HF ratios were used as indices of vagal and sympathetic modulations, respectively. The sHCM group demonstrated no significant elevation in CCVHF during the nighttime as compared to the daytime, while asHCM and control groups showed significant CCVHF elevation during the nighttime (p < 0.05-0.01). The nighttime CCVHF, therefore, was significantly lower in the sHCM group than in the control or asHCM group (sHCM, 1.08 +/- 0.36%; control, 1.60 +/- 0.57%; asHCM 1.82 +/- 0.77%; sHCM vs. control or sHCM vs. asHCM, p < 0.01). All of these three groups showed significant reduction in LF/HF ratio during the nighttime as compared to the daytime (p < 0.01). However, the reduction in the sHCM group was not as great as that in the control group and there was a significant difference between the sHCM and control group (2.01 +/- 1.58 vs. 1.08 +/- 0.65, p < 0.05). Two patients in the sHCM group, who later died suddenly, demonstrated very low CCVHF throughout a 24-hour period (0.2-0.8%). Both vagal and sympathetic impairment with a predominance of vagal abnormalities is suggested in patients with symptomatic NYHA class II or III hypertrophic cardiomyopathy.     

Changes in psychological features in patients for anesthesia and operation during perioperative period

In patients with previous myocardial infarction (MI), depressed heart rate variability (HRV) may reflect a reduction in vagal activity and lead to cardiac electrical instability. Interventions designed to increase HRV may be of clinical interest. Data on the effects of calcium antagonists on HRV in post-MI patients are very limited. The aim of our study was to assess the effects of verapamil on HRV and on the sympathovagal balance after MI. Fifty consecutive patients with a first MI, stable sinus rhythm, and left ventricular ejection fraction >0.40 were studied. Each patient underwent two 24-hour Holter recordings, 1 at baseline and another after 4 days of treatment with verapamil retard (180 mg 2 times daily). Time and frequency domain parameters of HRV were analyzed. All time domain measurements increased significantly after verapamil: the standard deviation of all NN intervals (SDNN) from 87.1 +/- 31.4 to 98.1 +/- 30.3 ms (p <0.05) and the log-transformed percentage of pairs of adjacent NN intervals that differ >50 ms (pNN50) from 0.57 +/- 0.42 to 0.76 +/- 0.45 (p <0.01). The standard deviation of the averages of RR interevals (SDANN) (75.9 +/- 30.1 vs 86.3 +/- 29.4 ms, p <0.05), root-mean-square of successive differences between RR intervals (rMSSD) (23.0 +/- 11.7 and 28.1 +/- 13.1 ms, p <0.01), and the triangular HRV index (28.3 +/- 9.6 vs 23.4 +/- 8.6, p <0.001) also increased. A significant inverse correlation was found between improvement in HRV indexes induced by verapamil and baseline values. Spectral analysis showed a significant increase in high-frequency power of 58.5% without changes in low and very low components. With normalized units, significant reductions in low-frequency power and low- to high-frequency ratio were observed. Diabetic patients did not show any significant changes in HRV on administration of verapamil. These findings indicate that verapamil, administered during the subacute phase of MI, improves both global and short-period indexes of HRV and induces a shift in the sympathetic-parasympathetic interaction toward vagal predominance. This effect may contribute to an explanation of the beneficial effects of verapamil that have been reported in post-MI patients.     

Solitary plasmacytoma of the lung with light chain extracellular deposits: a case report and review of the literature

We studied a possible correlation between autonomic cardiac activity and the level of the red blood cell acetylcholinesterase (AChE) in patients with probable Alzheimer disease (AD). The influence of cholinesterase inhibitor treatment on this autonomic activity was evaluated. Twelve patients satisfying the NINCDS-ADRDA criteria of probable AD and 10 healthy controls were studied. Autonomic cardiac activity was evaluated by means of power spectral analysis (PSA) of heart rate variability (HRV) using an autoregressive algorithm on 250 consecutive electrocardiographic R-R intervals. All patients received oral eptastigmine, a new cholinesterase inhibitor, for 1 month. Before treatment, a simultaneous recording of the electrocardiographic and respiratory activities was performed at rest and subsequently during head-up tilt test at 700. Recording was repeated on the last day of treatment. The level of AChE activity during each recording was also evaluated. Spectrum power was calculated in three main frequency bands: high frequency (HF), 0.15-0.4 Hz; low frequency (LF), 0.04-0.15 Hz; very low frequency (VLF), <0.04 Hz. In addition, we calculated the total spectrum power (TSP) and the LF/HF ratio. The TSP and the absolute value of each spectral component were significantly lower in AD patients than in controls. In contrast with controls, AD patients did not show any significant change before treatment in either the LF and HF components or in the LF/HF ratio during the tilt test. However, the modification in the LF component, induced by tilting, showed a significant correlation with the level of AChE activity (p < 0.03). During the tilt test, the treatment caused changes in LF and HF components and in the LF/HF ratio similar to those observed in controls. These results suggest that the presence of autonomic cardiac dysfunction in AD patients might be due to a cholinergic deficit in the peripheral autonomic nervous system. Some aspects of this autonomic dysfunction can be normalized by cholinesterase inhibitor treatment.     

Left atrial "stunning" following radiofrequency catheter ablation of chronic atrial flutter

Patients with autonomic neuropathy are more susceptible to insulin-induced hypotension than normal subjects, but the mechanisms are unclear. We quantitated the hemodynamic and metabolic effects of two doses of i.v. insulin (1 and 5 mU/kg.min, 120 min each) and several aspects of autonomic function in 28 patients with insulin-dependent diabetes mellitus (IDDM) and in 7 matched normal subjects under standardized normoglycemic conditions. The autonomic function tests included those predominantly assessing the integrity of vagal heart rate control (the expiration inspiration ratio during deep breathing and high frequency power of heart rate variability) and tests measuring sympathetic nervous function (reflex vasoconstriction to cold and blood pressure responses to standing and handgrip). During hyperinsulinemia, heart rate increased less (2 +/- 1 vs. 6 +/- 2 beats/min; P < 0.04) and diastolic blood pressure fell more (-3.1 +/- 1.2 vs. 0.9 +/- 2.1; P = NS) in the patients with IDDM than in the normal subjects. Forearm vascular resistance decreased significantly in the patients with IDDM [by -7.1 +/- 1.4 mm Hg/(mL/dL.min); P < 0.001 for high vs. low dose insulin], but not in the normal subjects (-0.1 +/- 2.5 mm Hg/(mL/dL.min; P = NS). Reflex vasoconstriction to cold was inversely correlated with the decreases in diastolic (r = -0.51; P < 0.005) and systolic (r = -0.59; P < 0.001) blood pressure and forearm vascular resistance (r = -0.53; P < 0.005), but not with the change in heart rate. The expiration inspiration ratio was, however, directly correlated with the insulin-induced change in heart rate (r = 0.63; P < 0.001), but not with diastolic or systolic blood pressure or forearm vascular resistance. Whole body (48 +/- 2 vs. 67 +/- 5 mumol/kg.min; P < 0.005) and forearm (44 +/- 4 vs. 67 +/- 8 mumol/kg.min; P < 0.05) glucose uptake were significantly lower in the IDDM patients than in the normal subjects. The latter could be attributed to a defect in the forearm glucose arterio-venous difference (1.5 +/- 0.1 vs. 2.2 +/- 0.2 mmol/L, respectively; P < 0.01), but not in blood flow. We conclude that both impaired vagal heart rate control and sympathetic nervous dysfunction exaggerate the hemodynamic effects of insulin in patients with IDDM and could contribute to insulin-induced hypotension.     

Effects on hypoxaemia on foetal heart rate, variability and cardiac rhythm

1. Experiments were carried out in 30 chronically catheterized foetal sheep (128-144 days; term 150 days) and in seven of these foetuses before, during and after acute hypoxaemia. The extent to which changes in sympathoadrenal activity and cardiac vagal activity affected the foetal cardiac response to hypoxaemia was measured. Three measurements were used: foetal heart rate (FHR), heart rate variability (HRV; measured as the coefficient of variation in pulse interval) and power spectral density (PSD; measured over the frequency ranges of 0.04-1.3 Hz). Cardiac vagal activity was blocked by atropine, beta-adrenoceptor activity was blocked by propranolol. 2. Under normoxaemic conditions, cardiac vagal blockade caused a rise in mean arterial pressure (MAP; P < 0.001), an increase in FHR (P < 0.001), a decrease in HRV (P < 0.001) and a decrease in PSD (P < 0.001). beta-adrenoceptor blockade caused a rise in MAP (P < 0.001), a fall in FHR (P < 0.01), a decrease in HRV (P < 0.001) but no change in PSD. 3. During mild hypoxaemia (PO2 = 12-14.5 mmHg) and moderate hypoxaemia (PO2 = 10-11.9 mmHg), foetal MAP (P < 0.001, P< 0.001), HRV (P < 0.01, P < 0.001) and PSD in the frequency range 0.04-0.45 Hz increased (P < 0.05-P < 0.001). Foetal heart rate decreased when foetuses became moderately hypoxaemic (P < 0.001). 4. After cardiac vagal blockade, hypoxaemia was associated with an increase in FHR compared with non-blocked hypoxaemic foetuses (P < 0.01, P < 0.001). The increase in HRV was abolished (P < 0.001, P < 0.001) as was the increase in PSD (P < 0.01-P < 0.001). 5. After beta-adrenoceptor blockade, the bradycardia that occurred during hypoxaemia was enhanced (P < 0.01, P < 0.05), the increase in HRV was not affected and neither was the increase in PSD. 6. As FHR and HRV of normoxaemic foetal sheep were affected both by atropine and propranolol, it would seem that both cardiac vagal and sympathoadrenal activity modulate the foetal heart under resting conditions. The lack of any effect of beta-adrenoceptor blockade on PSD under these conditions suggests that power spectral analysis (PSA) is not as sensitive as the other two methods in detecting sympathetically mediated modulation of the heart. 7. Because the hypoxaemia induced bradycardia and increase in HRV and in PSD were abolished by atropine (P < 0.01-P < 0.001), it is concluded that during hypoxaemia foetal HRV is mainly modulated by changes in cardiac vagal tone. Propranolol had no effect on foetal HRV, although it reduced it under normoxaemic conditions; therefore, it is concluded that cardiac sympathetic neural activity was not increased in acute hypoxaemia uncomplicated by acidosis. However, there was strong evidence of increased sympathoadrenal tone on the foetal heart in hypoxaemia, that is, there was a rise in FHR in hypoxaemic atropinized foetuses and a greater fall in FHR in beta-adrenoceptor blocked hypoxaemic foetuses. Therefore, this increased sympathetic influence on the foetal heart during hypoxaemia must be predominantly the result of increased adrenomedullary secretion of catecholamines. 8. Maintenance of foetal cardiac output depends on the chronotropic and ionotropic effects of catecholamines. Therefore, this adrenomedullary influence on the foetal heart during hypoxaemia is important to offset the opposing effects of increased cardiac vagal tone.     

Metaiodobenzylguanidine and heart rate variability in heart failure

It is assumed that the low-frequency power (LF) of heart rate variability (HRV) increases with progress of congestive heart failure (CHF), therefore positively correlating with cardiac 123I-metaiodobenzylguanidine (MIBG) washout. It is demonstrated here that HRV, including normalized LF, correlated inversely with MIBG washout and positively with the ratio of heart-to-mediastinum MIBG activity in controls and CHF patients, whereas these correlations were not observed within CHF patients. Thus MIBG washout may increase and HRV including normalized LF may decrease with CHF, although the HRV and MIBG measures may not similarly change in proportion to the severity of the cardiac autonomic dysfunction in CHF.     

Relationship between spectral components of cardiovascular variabilities and direct measures of muscle sympathetic nerve activity in humans

BACKGROUND: Spectral analysis of RR interval and systolic arterial pressure variabilities may provide indirect markers of the balance between sympathetic and vagal cardiovascular control. METHODS AND RESULTS: We examined the relationship between power spectral measurements of variabilities in RR interval, systolic arterial pressure, and muscle sympathetic nerve activity (MSNA) obtained by microneurography over a range of blood pressures. In eight healthy human volunteers, MSNA, RR interval, intra-arterial pressure, and respiration were measured during blood pressure reductions induced by nitroprusside and during blood pressure increases induced by phenylephrine. Both low-frequency (LF; 0.10 +/- 0.01 Hz) and high-frequency (HF; 0.23 +/- 0.01 Hz) components were detected in MSNA variability. Increasing levels of MSNA were associated with a shift of the spectral power toward its LF component. Decreasing levels of MSNA were associated with a shift of MSNA spectral power toward the HF component. Over the range of pressure changes, the LF component of MSNA variability was positively and tightly correlated with LF components of RR interval (in normalized units; P < 10(-6)) and of systolic arterial pressure variability (both in millimeters of mercury squared and normalized units; P < 5 x 10(-5) and P < 5 x 10(-6), respectively). The HF component of MSNA variability was positively and tightly correlated with the HF component (in normalized units) of RR-interval variability (P < 3 x 10(-4)) and of systolic arterial pressure variability (P < .01). CONCLUSIONS: During sympathetic activation in normal humans, there is a predominance in the LF oscillation of blood pressure, RR interval, and sympathetic nerve activity. During sympathetic inhibition, the HF component of cardiovascular variability predominates. This relationship is best seen when power spectral components are normalized for total power. Synchronous changes in the LF and HF rhythms of both RR interval and MSNA during different levels of sympathetic drive are suggestive of common central mechanisms governing both parasympathetic and sympathetic cardiovascular modulation.     

"Meta-analysis: statistical alchemy for the 21st century": discussion. A plea for a more balanced view of meta-analysis and systematic overviews of the effect of health care interventions

Ventricular arrhythmias and disturbed autonomic control, as reflected by abnormal heart rate variability (HRV), are related to hemodynamic impairment in chronic heart failure (CHF). We investigated the effects of orally (p.o.) administered isomazole, a new phosphodiesterase (PDE) inhibitor with calcium-sensitizing properties, on hemodynamics, ventricular arrhythmias, and HRV and examined a possible interaction between these parameters. Hemodynamic measurements and ambulatory ECG monitoring were performed in 12 patients with stable CHF class III-IV after single doses of isomazole 5-30 mg. Pulmonary wedge pressure decreased after 5, 10, 20, and 30 mg, but cardiac output, (CO) increased only after the higher doses [20 mg, + 20% (p = 0.031)] of isomazole. HR did not change. Mean arterial and pulmonary artery pressure, (MAP, PAP) decreased significantly in the 10- and 20-mg groups [10 mg, -6% (p = 0.035) and -14% (p < 0.001) respectively; 20 mg, -13% (p = 0.047) and -31% (p = 0.006), respectively]. Isomazole did not exert a significant effect on ventricular arrhythmias in the subsequent 24 h after acute dosing. Analysis of HRV showed that rMSSD and pNN50 (parameters of vagal tone) tended to increase after isomazole administration. Normalized high-frequency power during the day increased from 17.4 to 22.3 nu (p < 0.05), whereas low frequency tended to decrease from 52.7 to 48.2 nu (p = 0.06). Acute isomazole administration improves hemodynamics but has no effect on ventricular arrhythmias. The HRV variability data suggest development of an increase in vagal control of HR, parallel to the acute hemodynamic improvement after isomazole. Withdrawal of vagal control of HR in CHF may be a reversible process.     

Effects of amlodipine and nifedipine retard on autonomic nerve activity in hypertensive patients

1. The effects of 1,4-dihydropyridine calcium antagonists with different biological half-lives, amlodipine and nifedipine retard on 24 h blood pressure (BP), heart rate (HR) and autonomic nerve activity in patients with essential hypertension were compared. 2. Twenty patients (six men and 14 women; mean (+/- SEM) age 63 +/- 2 years) with essential hypertension were enrolled in the present study. Their ambulatory BP and electrocardiograms were monitored for 24 h at intervals of 30 min with a portable recorder after a 4 week drug-free period, after a 4 week treatment period with amlodipine (2.5 or 5 mg once daily) and after a 4 week treatment period with nifedipine retard (10 or 20 mg twice daily). The order of the three periods was randomized. Autonomic nerve activity was evaluated by power spectral analysis of HR variability, using the high frequency (HF) component as an index of parasympathetic activity and the ratio of the low frequency (LF) to the HF component as an index of sympathovagal balance. 3. Amlodipine and nifedipine retard significantly lowered the 24 h BP to a similar extent (amlodipine: -12.7 +/- 2.6/-5.6 +/- 1.4 mmHg, P < 0.01/P < 0.01; nifedipine retard: -15.1 +/- 2.1/-6.9 +/- 1.5 mmHg, P < 0.01/P < 0.01). Amlodipine did not change the 24 h average HR, while nifedipine retard significantly increased it (+3.3 +/- 1.2 b.p.m., P < 0.05). Amlodipine also did not change the HF component or the ratio of the LF to the HF component. However, nifedipine retard significantly decreased the HF component (P < 0.01) and increased the ratio of the LF to the HF component (P < 0.05). 4. These results suggest that nifedipine retard caused a decrease in parasympathetic activity and an increase in sympathetic activity with reflex tachycardia in these patients with essential hypertension, while amlodipine did not produce such effects on the autonomic nervous system.     

Protein and calorie effects on progression of induced chronic renal failure in cats

This study was designed to determine if there is a difference in autonomic regulation induced by posture change between postmenopausal and young women. To evaluate autonomic nervous system function, spectral analysis of heart rate variability (HRV) was done in postmenopausal women (n = 13, 46-59 years of age), age-matched men (n = 8, 45-55 years of age), and young women (n = 10, 20-37 years of age) for 3-min periods of controlled frequency breathing (15 breaths/min) in supine followed by sitting positions. In the supine position, the R-R interval variation in older persons decreased significantly compared with that during the follicular phase in young women. Furthermore, the high-frequency (HF) components of HRV, which reflect only parasympathetic activity, were lower in older subjects than in young women. Following a change of position from supine to sitting, the HF component did not change significantly in the postmenopausal women or the men, but the low/high frequency (LF/HF) component ratio, which reflects the balance of autonomic nerve activities, increased significantly in the men. These results suggest that cardiac parasympathetic tone may be reduced in older persons in comparison with young women. Furthermore, arterial baroreflex control of parasympathetic nerve activity caused by posture changes is impaired in the postmenopausal women and aged-matched men. The baroreflex control of the sympathetic component is maintained in the men but not in the postmenopausal women. These differences might result in part from changes in the level of female hormones.     

Autonomic nervous system dysfunction in elderly hypertensive patients with abnormal diurnal blood pressure variation: relation to silent cerebrovascular disease

To investigate the relationships among diurnal blood pressure (BP) variations and autonomic nervous system dysfunction, we assessed heart rate variability (HRV) using power spectral analysis of the 24-hour RR interval in 51 asymptomatic elderly hypertensive patients with various patterns of nocturnal BP fall. The extreme-dippers with marked nocturnal BP fall (n=16) had lower asleep low-frequency power (LF)/high-frequency power (HF) ratios (a relative index of sympathetic nervous system activity), while the nondippers without nocturnal BP fall (n=18) had lower awake LF/HF ratios and asleep/awake ratio for HF (an index of parasympathetic nervous activity), when compared with dippers with appropriate nocturnal BP fall (n=17). The incidence of multiple lacunar infarction detected by brain magnetic resonance imaging was 56% in the extreme-dippers and 38% in the nondippers, and both were markedly higher than that (6.3%) in the dippers (both P<.01). There was no significant relationship between the BP level and any HRV parameter for either the daytime or nighttime period. The asleep/awake ratio for systolic BP was significantly correlated with the asleep/awake ratio for HF (r= -.363, P<.01) and with the asleep/awake ratio for the LF/HF ratio (r=.540, P<.001), regardless of whether multiple lacunar infarction was present. In conclusion, the autonomic nervous system activity is not related to high BP level per se, rather its diurnal variation is more important as a determinant of the diurnal BP patterns, regardless of the presence or absence of cerebrovascular disease.     

Clinical and haemodynamic correlates of heart rate variability in children with congenital heart disease

Heart rate variability (HRV) represents a noninvasive parameter for studying the autonomic control of the heart. Cardiac patients have a complex autonomic disturbance. The relation of HRV to this abnormality in children with congenital heart disease (CHD) has not yet been examined. The present study examined HRV indices from 24 h Holter recordings in 258 children with an operated or non-operated CHD, to determine their differences as an indicator of the severity of heart disease. The latter was defined clinically as New York Heart Association (NYHA) functional classes I to IV and haemodynamically by invasive parameters. Five time-domain measures (SDNN, SDNNi, SDANNi, rMSSD and pNN50) and three frequency-domain measures (LF, HF and balance LF/HF) were compared with normal ranges. HRV was reduced in children with CHD, except in patients of NYHA class I. The level of reduction depended on the NYHA functional class. None of the measures was significantly related to haemodynamic data. CONCLUSION: Heart rate variability is reduced in children with Congenital heart disease depending on the functional limitation but not on haemodynamic disturbances. Heart rate variability indices are sensitive markers of the clinical state.     

Polylactide macroporous biodegradable implants for cell transplantation. II. Preparation of polylactide foams by liquid-liquid phase separation

Good metabolic control may improve cardiac function in diabetic patients. It is not known, however, whether this functional improvement is associated with concomitant electrocardiographic changes. The aim of the present prospective study was to evaluate the quantitative electrocardiographic and vectorcardiographic correlates of metabolic control, left ventricular function and dimensions, and autonomic nervous function in patients with newly diagnosed Type 2 diabetes. We studied 35 patients (20 men, 15 women; age 52 +/- 6 years (mean +/- SD) with normal electrocardiograms at 1.5 and 15 months after the diagnosis of Type 2 (non-insulin-dependent) diabetes. During the follow-up, body weight decreased, and significant improvement was observed in metabolic control, cardiac function and autonomic nervous function. Concomitantly, maximal spatial vector of T wave increased from 238 +/- 122 to 284 +/- 141 microV (P < 0.01), and this increase was correlated with a decrease in glycosylated haemoglobin A1C (r = -0.45, P < 0.01) and plasma insulin (r = -0.46, P < 0.01). In addition, duration of QRS complex shortened from 94 +/- 9 to 92 +/- 8 ms (P < 0.05), and this shortening was correlated with an increase in heart rate variability (r = -0.34; P < 0.05) and a decrease in peak early to late left ventricular filling flow velocity (r = 0.35, P < 0.05). These changes were most prominent in patients with co-existing hypertension and coronary artery disease. In conclusion, improving metabolic control of diabetes is associated with changes in ventricular repolarization and shortening of QRS complex duration.     

Power spectral analysis of heart rate variability during graded head-up tilting in patients with vasodepressor syncope

1. Two groups of age- and sex-matched subjects, eight healthy controls and 10 patients, suffering from recurrent vasodepressor syncope, participated in a study to examine autonomic function and sequential changes in power distribution of heart rate (HR) variability during graded head-up tilt. 2. The following autonomic function tests were performed: valsalva ratio, HR responses to deep breathing and posture, BP responses to sustained handgrip and postural change. Each subject was tilted at 15 degrees, 30 degrees, 45 degrees, 60 degrees and 80 degrees head-up, each for 15 min, or until symptoms occurred. The eight control subjects completed the tilt study without any symptoms, while all 10 patients developed presyncope and/or syncope at various tilt angles. 3. Resting blood pressure (BP) was lower in the patient group, while resting HR, autonomic function tests and resting HR variability components were similar in the two groups. 4. The control group showed a progressive increase in low frequency power component (LF) from supine to end tilt (delta LF 20.06 +/- 14.50%) and a progressive fall in high frequency (HF) component (delta HF - 24.62 +/- 10.64%). In contrast, in the patient group, LF fell during tilt in the presyncope period (delta LF - 10.57 +/- 12.93%, P < 0.01 vs control group). HF and HF:LF ratio responses did not differ significantly in the two groups. 5. At end tilt, the increase in plasma noradrenaline was significantly greater in the control group than in the patient group (delta NA 0.83 +/- 0.27 vs 0.28 +/- 0.14 pmol/mL, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac autonomic patterns preceding occasional vasovagal reactions in healthy humans

BACKGROUND: The wide range of clinical presentation of orthostatic vasovagal syncope suggests different underlying changes in the cardiac autonomic modulation. METHODS AND RESULTS: To evaluate the beat-by-beat modifications in the neural control of heart period preceding a syncopal event, we studied RR interval variability in 22 healthy subjects who experienced fainting for the first time during a 90 degrees head-up tilt and in 22 control subjects by means of time-variant power spectral analysis. Sympathetic and vagal modulations to the sinoatrial node were assessed by the normalized power of the low-frequency (LF, approximately 0.1-Hz) and high-frequency (HF, approximately 0.25-Hz) oscillatory components of RR variability. When the patients were supine, no differences were observed in the hemodynamic and spectral parameters of the 2 groups. During the tilt procedure, RR, LFNU, and HFNU (NU=normalized units) values were relatively stable in control subjects. During early tilt (T1), subjects with syncope had reduced RR intervals compared with control subjects. In 13 subjects with syncope, RR decreased while LFNU and LF/HF increased in the last minute of tilt before syncope (T2). Conversely, in the remaining 9 fainters, LFNU and LF/HF decreased from T1 to T2 and HFNU increased slightly. CONCLUSIONS: Two different patterns may be recognized in the cardiac autonomic changes preceding an occasional vasovagal event, namely, one characterized by a progressive increase of the marker of cardiac sympathetic modulation up to the onset of syncope, the other by a sympathetic inhibition with an impending vagal predominance. The recognition of different pathophysiological mechanisms in fainters may have important therapeutic implications.     

Effects of mental state on heart rate and blood pressure variability in men and women

The effect of different mental states on autonomic modulation of the cardiovascular system was assessed in healthy, normotensive men (n = 18) and women (n = 12). Heart rate variability (HRV), systolic blood pressure variability (BPV) and arterial baroreflex function were assessed during 4 tests at rest ((10 min + 5 min recovery) x 4): (1) Control (spontaneous breathing, (SB) (2) Mental distraction (SB + word puzzle) (3) Conscious control of breathing (paced at SB rate) and (4) Mental stress (SB + computer quiz). There were no significant gender differences in the responses to the interventions in terms of arterial (spontaneous) baroreflex (SPBX) control of HR, and indices of time and frequency domains of HRV and BPV, with the exception of the sympathetic indicator of HRV (low frequency power/total power; P < 0.01) which was lower in women during control and mental stress tests. Conscious control of breathing at SB did not alter HRV, BPV or SPBX in either men or women. Mental distraction and mental stress led to decreases in indices of time and frequency domains of HRV and BPV in all subjects, as well as increases in HR during distraction and in systolic BP during stress. These findings suggest that in studies of cardiovascular control: (1) Paced breathing at SB can be used for individuals with irregular breathing patterns (2) The extent of mental stress achieved is intervention-specific and for the most part, independent of gender and (3) Resting assessment of HRV, BPV and SPBX can be made by having subjects sit quietly without interventions in a controlled laboratory setting.     

Heart rate and blood pressure variability in obese normotensive subjects

OBJECTIVE: To assess autonomic modulation of cardiovascular activity in massively obese subjects. DESIGN: Cross-sectional clinical study. SUBJECTS: 43 age-matched normotensive subjects: 15 moderately obese (body mass index (BMI) < 40); 14 massively obese (BMI > 40) and 14 nonobese controls (BMI < 26). MEASUREMENTS: Using power spectral analysis, heart rate and arterial pressure variability were determined at rest and after sympathetic stress (tilt). Two spectral components were analysed: a low-frequency (LF) component at around 0.1 Hz, predominantly reflecting sympathetic modulation and a high-frequency (HF) component at around 0.26 Hz, reflecting parasympathetic modulation. RESULTS: Spectral data for heart rate showed that the massively obese subjects had lower LF [mean +/- s.e.m.] normalized units (NUs) at rest (35.1 +/- 0.9) and after tilt (56.1 +/- 2.1), than the moderately obese subjects (LF NUs at rest 53.9 +/- 4.2, P < 0.001; LF NUs tilt: 66.8 +/- 5.6, P < 0.001) and nonobese control subjects (LF NUs at rest, 56.6 +/- 3.0, P < 0.001); (LF NUs tilt: 81.7 +/- 1.7, P < 0.001). Data for systolic arterial pressure variability measured at rest exhibited the inverse pattern, the massively obese group having higher mean LF values (LF mm Hg2 rest: 15.0 +/- 1.4; LF mm Hg2 tilt: 15.7 +/- 1.5) than the moderately obese group (LF mm Hg2 rest 3.2 +/- 0.7, P < 0.001; LF mm Hg2 tilt: 7.2 +/- 2.0, P < 0.001) and than the nonobese control subjects (LF mm Hg2 rest 3.5 +/- 0.5, LF mm Hg2 tilt 8.5 +/- 0.8, P < 0.001). Regression detected a significant association between BMI and LF of systolic pressure (beta = 0.364; P = 0.0007), In LF of heart rate (beta = -5.555; P = 0.00001) and very low frequency (VLF) of diastolic pressure (beta = -3.305; P = 0.0020). CONCLUSION: Obesity seems to increase sympathetic modulation of arterial pressure, but diminishes modulation of heart rate. Because our obese subjects had high plasma noradrenaline levels, their low LF power of heart rate could reflect diminished adrenoceptor responsiveness.     

Analysis of heart rate variability demonstrates effects of development on vagal modulation of heart rate in healthy children

OBJECTIVES: Analysis of heart rate variability (HRV) has been found to be a useful method of assessing cardiovascular autonomic control, but normal values for standard HRV measures in children have not been established. We analyzed HRV in 60 healthy children aged 3 to 15 years to determine normal values and to assess the effects of development on cardiac autonomic control with the use of ambulatory electrocardiographic monitoring. RESULTS: The high-frequency (HF) component, an index of cardiac autonomic tone, increased significantly with age from 3 to 6 years (p < 0.01) and decreased with age from 6 to 15 years (p < 0.01), and the magnitude of HF correlated significantly with the R-R intervals. Thus the changes in cardiac autonomic tone could be described as a simple equation using age and heart rate. CONCLUSIONS: We present normal values and changes in the cardiac autonomic system during childhood after HRV analysis, which could lead to a better understanding and treatment of cardiac disease in children.     

Hemorrhage exerts different effects on variabilities of heart rate and blood pressure in dogs

The aim of the present study was to evaluate the effects of hemorrhage on heart rate variability (HRV) and blood pressure variability (BPV) as indicators of autonomic nervous system (ANS) and hypovolemia. We induced hemorrhagic hypovolemia in 7 dogs by removing blood in graded stages (0%, 10%, 20%, 30%, 40% of the estimated blood volume; EBV). HR was unchanged during hemorrhage, while mean BP decreased significantly after 30% EBV hemorrhage. Low frequency component (LF: 0.04-0.15 Hz) of HRV significantly increased after 20% EBV hemorrhage but high frequency component (HF: 0.15-0.4 Hz) of HRV was not altered. LF of BPV increased significantly stepwise after 20% EBV hemorrhage and HF of BPV increased significantly after 30% EBV hemorrhage, showing that both LF and HF of BPV might indicate the degree of hypovolemia. During hemorrhage LF of HRV and BPV increased and HF of HRV was unchanged, indicating the shift of the autonomic balance toward sympathetic dominance. An excellent quantitative correlation between LF of BPV and the degree of hypovolemia was demonstrated during graded hemorrhage, while LF of HRV plateaued at its maximum value at 20% EBV hemorrhage. In conclusion, our study suggests that the spectral analysis of HRV and BPV during graded hemorrhage shows different characteristics in the quantitative evaluation of ANS and hypovolemia.