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Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

BACKGROUND: Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. METHODS AND RESULTS: General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

Adult↗

Effects of a residential exercise training on baroreflex sensitivity and heart rate variability in patients with coronary artery disease: A randomized, controlled study.

BACKGROUND: Myocardial ischemia and infarction impair baroreflex sensitivity (BRS), which when depressed is predictive of future cardiac events after myocardial infarction (MI). The main objective of this study was to determine whether exercise training improves BRS in patients with coronary artery disease. METHODS AND RESULTS: Ninety-seven male patients with and without a previous MI were recruited after myocardial revascularization surgery and randomized into trained (TR) or untrained (UTR) groups. TR patients underwent a residential exercise program at 85% of maximum heart rate (HRmax) consisting of 2 daily sessions 6 times a week for 2 weeks. Eighty-six patients (45 TR and 41 UTR) completed the study. BRS was assessed at baseline and at the end of the protocol by the spontaneous baroreflex method. The standard deviation of mean R-R interval (RRSD) was also assessed as a measure of heart rate variability. At baseline, there were no significant differences between TR and UTR patients in any variable. In TR patients, BRS increased from 3.0+/-0.3 to 5.3+/-0.7 ms/mm Hg (P:<0.001), RRSD from 18.7+/-1.4 to 23.6+/-1.6 ms (P:<0.01), and R-R interval from 792. 0+/-15.5 to 851.3+/-20.5 ms (P:<0.001). No significant changes occurred in UTR patients. Increases in BRS and RRSD were significant in patients either with or without a previous MI. CONCLUSIONS: Exercise training increases BRS and heart rate variability in patients with coronary artery disease. Improved cardiac autonomic function might add to the other benefits of exercise training in secondary prevention of ischemic heart disease.

Baroreflex↗

Circadian rhythms of frequency domain measures of heart rate variability in healthy subjects and patients with coronary artery disease. Effects of arousal and upright posture.

BACKGROUND: Altered neural regulation of the cardiovascular system may be an important factor for various manifestations of ischemic heart disease. This research was designed to compare the circadian rhythm of cardiac neural regulation and autonomic responses to arousal and upright posture between patients with uncomplicated coronary artery disease (CAD) and age-matched subjects with no evidence of heart disease. METHODS AND RESULTS: Twenty-four-hour heart rate variability (HRV) in the frequency domain was analyzed in 20 male patients (mean age, 52 +/- 7 years) with angiographic evidence of CAD without prior myocardial infarction and in 20 healthy men (mean age, 51 +/- 8 years) with no clinical, echocardiographic, or exercise ECG evidence of heart disease. None of the 24-hour average frequency-domain components of HRV differed significantly between the two groups. Healthy subjects had a significant circadian rhythm of normalized units of high-frequency (HF) power of HRV with higher values during sleep. Normalized units of low-frequency (LF) power and the LF/HF ratio also showed a significant circadian rhythm in healthy subjects, with higher values during the daytime. No significant circadian rhythms in any of the normalized spectral components of HRV were observed in patients with CAD, and the night-day difference in LF/HF ratio was smaller in the patients with CAD than in the healthy subjects (0.5 +/- 1.4 versus 1.8 +/- 0.7, P < .001). Awakening when in the supine position resulted in a significant increase in the LF/HF ratio (P < .01) in the healthy subjects, but no significant changes in HRV were observed after awakening in patients with CAD. Assumption of upright position resulted in a comparable decrease in the components of HRV between the groups. CONCLUSIONS: The circadian rhythm of cardiac neural regulation is altered in patients with uncomplicated CAD. Reduced autonomic responses to sleep-wake rhythm suggest that the modulation of cardiac autonomic function by stimuli from the central nervous system is impaired in CAD.

Arousal↗

Dispersion of the QT interval and autonomic modulation of heart rate in hypertensive men with and without left ventricular hypertrophy.

Left ventricular hypertrophy is an independent risk factor for sudden cardiac death in hypertension, but the mechanisms of electrical instability associated with hypertrophy are not well known. We studied dispersion of the QT interval, an index of inhomogeneity of repolarization, and heart rate variability, a measure of cardiac autonomic modulation, in a randomly selected population of 162 men with systemic hypertension and made comparisons between the patients with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index > or = 131 g/m2, n = 44) and those without hypertrophy (left ventricular mass index < 131 g/m2, n = 118). The heart rate-corrected QT dispersion (67 +/- 37 versus 53 +/- 21 milliseconds, P < .05) and QT apex dispersion (55 +/- 22 versus 44 +/- 16 milliseconds, P < .01) were significantly longer in the patients with left ventricular hypertrophy than in those without hypertrophy. Thirteen of the 44 patients (30%) with hypertrophy versus 7 of the 118 patients (6%) without hypertrophy had an abnormally long QT apex dispersion ( > 70 milliseconds) (P < .001). The time and frequency domain measures of heart rate variability did not differ significantly between the patient groups with and without left ventricular hypertrophy. The measures of heart rate variability were not related to QT dispersion or left ventricular mass index but had a negative correlation with blood pressure values (eg, r = -.30 between the low-frequency component of heart rate variability and systolic pressure, P < .001). Age, body mass index, antihypertensive medication, and the other demographic variables were similar between the groups, but the patients with left ventricular hypertrophy had higher systolic (P < .01) and diastolic (P < .01) pressures compared with the patients without hypertrophy. Left ventricular hypertrophy in hypertensive men is associated with inhomogeneity of the early phase of ventricular repolarization, favoring susceptibility to reentrant ventricular tachyarrhythmias. Abnormalities in cardiac autonomic function, which may trigger a spontaneous onset of arrhythmias, are related to elevated blood pressure but not specifically to left ventricular hypertrophy.

Adult↗

Reduced heart rate variability and new-onset hypertension: insights into pathogenesis of hypertension: the Framingham Heart Study.

Heart rate variability (HRV) is a useful noninvasive tool to assess cardiac autonomic function. The purpose of this study was to (1) compare measures of HRV between hypertensive and normotensive subjects and (2) examine the role of HRV as a predictor of new-onset hypertension. The first 2 hours of ambulatory ECG recordings obtained from 931 men and 1111 women attending a routine examination at the Framingham Heart Study were processed for HRV. Three time-domain and 5 frequency-domain variables were studied: standard deviation of normal RR intervals (SDNN), percentage of differences between adjacent normal RR intervals exceeding 50 milliseconds, square root of the mean of squared differences between adjacent normal RR intervals, total power (0.01 to 0.40 Hz), high frequency power (HF, 0.15 to 0.40 Hz), low frequency power (LF, 0.04 to 0.15 Hz), very low frequency power (0.01 to 0.04 Hz), and LF/HF ratio. On cross-sectional analysis, HRV was significantly lower in hypertensive men and women. Among 633 men and 801 women who were normotensive at baseline (systolic blood pressure <140 mm Hg and diastolic blood pressure <90 mm Hg and not receiving antihypertensive treatment), 119 men and 125 women were newly hypertensive at follow-up 4 years later. After adjustment for factors associated with hypertension, multiple logistic regression analysis revealed that LF was associated with incident hypertension in men (odds ratio per SD decrement [OR], 1.38; 95% confidence interval [CI], 1.04 to 1.83) but not in women (OR, 1.12; 95% CI, 0.86 to 1.46). SDNN, HF, and LF/HF were not associated with hypertension in either sex. HRV is reduced in men and women with systemic hypertension. Among normotensive men, lower HRV was associated with greater risk for developing hypertension. These findings are consistent with the hypothesis that autonomic dysregulation is present in the early stage of hypertension.

Adult↗

Cardiac autonomic control in obstructive sleep apnea: effects of long-term CPAP therapy.

To determine how long-term treatment with continuous positive airway pressure (CPAP) affects cardiac autonomic function, we measured R-R interval (RRI), respiration, and blood pressure in 13 awake patients with moderate-to-severe obstructive sleep apnea (OSA) in both supine and standing postures, before and after 3 to 9 mo of home therapy. Using visual feedback, the subjects controlled their respiration to track a randomized breathing pattern. From the RRI spectrum, we computed high-frequency power and the ratio of low-frequency to high-frequency power (LHR). To correct for differences in breathing, the average transfer gain relating respiration to RRI changes (G(RSA)) and the modified low-frequency to high-frequency ratio (MLHR) were also derived. CPAP therapy did not change the conventional spectral indices of heart rate variability (HRV). However, G(RSA) increased with average nightly CPAP use in supine (p < 0.01) and standing (p < 0.03) postures, whereas MLHR decreased with CPAP compliance during standing (p < 0.03). Supine mean heart rate decreased with compliance (p < 0.03). None of the estimated parameters was correlated with duration of therapy when actual CPAP use was not taken into account. These results suggest that CPAP treatment improves vagal heart rate control in patients with OSA and that the degree of improvement varies directly with compliance level.

Adult↗

Effects of reboxetine on sleep and nocturnal cardiac autonomic activity in patients with dysthymia.

Antidepressants may have sleep and autonomic side-effects. The acute and long-term effect of reboxetine (2 mg b.i.d.) on sleep and cardiac autonomic activity was compared with that of placebo in a single-blind study. Twelve patients affected by dysthymia underwent four polysomnographic studies at baseline (placebo); at night 3 (reboxetine; acute effect); at night 9 (reboxetine; intermediate-term effect); and at night 122 (reboxetine; chronic effect). After the first administration, reboxetine increased time awake after sleep onset, number of awakenings, percentage of stages 1 and 2 non-rapid eye movement (REM), and reduced the amount of stages 3-4 non-REM, but all these effects disappeared by continuing treatment. However, reboxetine caused a persistent suppression of REM sleep, which was accompanied by an increase of REM sleep latency. The spectral analysis of heart rate variability showed a trend towards an increase in sympathetic activity with both acute and intermediate reboxetine use. Long-term treatment with 4 mg reboxetine does not cause significant changes in cardiac autonomic function.

Adrenergic Uptake Inhibitors↗

Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.

Air Pollution↗

Effects of intravenous lidocaine on QTd and HRV changes due to tracheal intubation during sevoflurane induction.

The aim of the present study was to evaluate the effects of IV lidocaine on autonomic cardiac function changes in tracheal intubation (TI) during sevoflurane anaesthesia by using more reliable parameters, namely, the analysis of QT dispersion and heart rate variability (HRV) from Holter monitoring. In this prospective, double-blind study, 44 American Society of Anaesthesiologists class I-II patients scheduled for hysterectomy were randomly and equally divided into 2 groups; a control sevoflurane group (group S, n = 22) and a lidocaine sevoflurane group (group LS, n = 22). Before the induction of anaesthesia, the electrocardiograms (ECG) of all patients were recorded for 3 minutes as baseline parameters. In both groups, the anaesthesia was induced with 7% sevoflurane in O(2 )at 6L min(-1) via a facemask for 2 minutes. However, before the induction of sevoflurane anaesthesia in group LS, 1 mg kg(-1) of lidocaine was given intravenously (IV). For muscle relaxation during TI, vecuronium was given to all participants. Three minutes after administration of vecuronium, TI was performed and an ECG was recorded synchronously for another 3 minutes. The results from the later records were used as postintubation parameters. Baseline and postintubation data were analysed. When compared to baseline values, postintubation LF/HF and SDNN values were increased in group S (P = 0.005, P = 0.001, respectively), whereas postintubation LF and HF values were decreased in group LS (P = 0.014, P = 0.041, respectively). Under the influence of sevoflurane anaesthesia, TI resulted in sympathetic activation. However, this activation was attenuated by the administration of IV 1 mg kg(-1) lidocaine 5 minutes prior to TI.

Administration, Inhalation↗

Diabetic gastroparesis in association with autonomic neuropathy and microvasculopathy.

Gastroparesis is a frequent and sometimes life-threatening complication of diabetes mellitus. Autonomic neuropathy seems to be one of the most important mechanisms underlying this entity, together with the other probable pathologies. The present study was performed in order to identify an alternative to gastric scintigraphy as a screening test. The gastric emptying times of 60 subjects (Group 1: 20 insulin-dependent patients, Group 2: 20 non-insulin-dependent diabetes mellitus patients, and Group 3: 20 healthy volunteers) were monitored by gastric scintigraphy. Perception thresholds for cold, heat, and vibration were tested by a quantitative sensory test, and QTc dispersions were calculated from standard electrocardiography recordings. In addition, fasting blood glucose, hemoglobin A1c and urine beta2-microglobulin and microalbumin concentrations were determined for the patient groups. Funduscopic examination was performed by an independent ophthalmologist. Gastroparesis was determined in both patient groups, regardless of fasting blood glucose and hemoglobin A1c concentrations. A strong correlation was observed between nephropathy, retinopathy, and cardiac autonomic denervation (QTc) and gastroparesis. In conclusion, retinal and renal microvasculopathy parameters and cardiac autonomic function tests may be useful for screening diabetic patients for gastroparesis.

Adult↗

Do antiepileptic drugs play a role in sudden unexpected death in epilepsy?

Sudden unexpected death in epilepsy (SUDEP) accounts for approximately 2% of deaths in population-based cohorts of epilepsy, and up to 25% of deaths in cohorts of more severe epilepsy. When it occurs, SUDEP usually follows a generalised tonic-clonic seizure. Unresponsiveness, apnoea, and cardiac arrest occur in SUDEP, rather than the typical gradual recovery. The great majority of tonic-clonic seizures occur without difficulty and how the rare seizure associated with SUDEP differs from others is unknown.Three mechanisms have been proposed for SUDEP: cardiac arrhythmia, neurogenic pulmonary oedema, and postictal suppression of brainstem respiratory centres leading to central apnoea. Recent studies have found that the incidence of SUDEP increases with the severity of epilepsy in the population studied. The duration of epilepsy, number of tonic-clonic seizures, mental retardation, and simultaneous treatment with more than two antiepileptic drugs are independent risk factors for SUDEP. Some studies have reported that carbamazepine use, carbamazepine toxicity, and frequent, rapid changes in carbamazepine levels, may be associated with SUDEP. Other evidence indicates that carbamazepine could potentially increase the risk for SUDEP by causing arrhythmia or by altering cardiac autonomic function. However, this evidence is tenuous and most studies have not found an association between the use of carbamazepine or any other individual antiepileptic drug and SUDEP. There is little information regarding antiepileptic drugs other than phenytoin and carbamazepine. The incidence of SUDEP with gabapentin, tiagabine, and lamotrigine clinical development programmes is in the range found in other populations with refractory epilepsy. This suggests that these individual antiepileptic drugs are no more likely to cause SUDEP than antiepileptic drugs in general. Best current evidence indicates that the risk of SUDEP can be decreased by aggressive treatment of tonic-clonic seizures with as few antiepileptic drugs as necessary to achieve complete control. At present there is no strong reason to avoid any particular antiepileptic drug. Further studies are needed to elucidate the potential role of individual antiepileptic drugs in SUDEP and establish clinical relevance, if any. These studies may be challenging to conduct and interpret because SUDEP is relatively uncommon and large numbers will be necessary to narrow confidence intervals to determine the clinical relevance. Also adjustments will be needed to account for the potent risks associated with other independent factors.

Anticonvulsants↗

Autonomic neuropathy in nondiabetic offspring of type 2 diabetic subjects is associated with urinary albumin excretion rate and 24-h ambulatory blood pressure: the Fredericia Study.

The aim of this study was to examine the impact of parental type 2 diabetes on the autonomic nervous system and to determine whether autonomic neuropathy is present and associated with changes in 24-h ambulatory blood pressure (AMBP) and urinary albumin excretion rate (UAER) in nondiabetic subjects with parental type 2 diabetes. We examined 223 nondiabetic offspring of type 2 diabetic subjects and a control group of 258 offspring of nondiabetic subjects. The autonomic nervous system was assessed by three cardiovascular reflex tests, 24-h AMBP was measured with an oscillometric recorder (90207; Spacelabs, Redmond, WA), and UAER was determined through three overnight urine samples. The subjects with parental type 2 diabetes had significantly lower heart rate variation in all three bedside tests (P < 0.01) than subjects without parental diabetes. The prevalence of autonomic neuropathy in the nondiabetic offspring with parental type 2 diabetes (6.7%) was significantly (P < 0.01) higher compared with the control group (1.6%). Autonomic neuropathy was associated with a higher fasting insulin level (P < 0.05), higher UAER (P < 0.001), higher 24-h mean AMBP (P < 0.01), and reduced diurnal blood pressure variation (P < 0.001) after adjustment for age, sex, and BMI. In conclusion, parental type 2 diabetes was found to be associated with alterations in the autonomic nervous system in nondiabetic subjects. The presence of autonomic neuropathy in subjects with parental type 2 diabetes was associated with higher UAER, fasting insulin level, and 24-h AMBP and a reduced diurnal blood pressure variation. This study indicates that parental type 2 diabetes has an impact on the cardiac autonomic function in nondiabetic subjects.

Aged↗

Corrected Q-T interval prolongation as diagnostic tool for assessment of cardiac autonomic neuropathy in diabetes mellitus.

A simple method for evaluating alterations in cardiac sympathetic innervation may be measurement of the Q-T interval. Seventy-three diabetic patients (46 insulin dependent and 27 non-insulin dependent) were separated into four groups based on the presence and degree of cardiac autonomic neuropathy (CAN) with noninvasive cardiovascular reflexes and blood pressure responses. None of the patients had evidence of ischemic heart disease, kidney disease, or the idiopathic long Q-T-interval syndrome. The corrected Q-T interval (Q-Tc) was determined at rest with Bazett's formula. As a group, diabetic patients with greater than or equal to 2 abnormalities of cardiac autonomic function had a longer Q-Tc interval than those with no evidence of CAN. Diabetic patients with greater than or equal to 1 abnormality had a prolonged Q-Tc interval compared with a control group of 96 healthy nondiabetic subjects (mean +/- SD 397 +/- 18). The frequency of prolonged (greater than 433 ms, normal mean + 2SD) resting Q-Tc intervals increased with the increasing number of abnormalities (0, 1, 2, greater than or equal to 3): 11, 25, 41, and 75%, respectively. Twenty-three of 25 (92%) patients with a Q-Tc greater than 433 ms had evidence of CAN. However, 57% (31 of 54) of the patients with CAN had a normal Q-Tc interval. These data provide further evidence of a relationship between the presence and severity of CAN and degree of Q-Tc interval prolongation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cardiovascular autonomic neuropathy in non-diabetic Nigerian patients with chronic renal failure.

AIMS: To determine the frequency of cardiovascular autonomic neuropathy (CAN), its pattern and clinical predictors in Nigerians with non-diabetic chronic renal failure (CRF). METHODS: A total of 120 subjects comprising 60 pre-dialysis CRF patients and an equal number of age- and sex-matched healthy controls were studied. Five standard cardiovascular reflex (CVR) tests namely: heart rate response to deep breathing, Valsalva manoevre and posture, as well as blood pressure response to hand grip and posture were used to evaluate the cardiac autonomic functions. A pre-tested questionnaire was administered, with neurological examination and serum biochemical investigations also included in the evaluation. RESULTS: The frequency of CAN in non-diabetic CRF was 65%. Dysfunction of both the parasympathetic and sympathetic divisions of the ANS occurred in CRF patients. Significant impairment in all the heart rate reflex tests (39%) and blood pressure response to the handgrip tests (28%) occurred in patients with CAN. Symptoms of autonomic neuropathy with clinical correlation with CAN included: constipation (60%), hyposialism (51%) and hypohidrosis (33%), whilst those of peripheral neuropathy were: loss of sensation (50%) and numbness (40%). Of the biochemical parameters, serum creatinine and urea had significant correlation with autonomic neuropathy. CONCLUSION: Autonomic neuropathy is common in Nigerian patients with non-diabetic CRF, especially in those with symptoms of constipation, hypohidrosis, numbness and prickly sensations.

Adolescent↗

Heart rate variability in severe aortic stenosis.

BACKGROUND AND AIM OF THE STUDY: Autonomic dysfunction may be a risk factor for the generation of arrhythmias and sudden death in patients with severe aortic stenosis; thus, patients with this condition were studied to assess cardiac autonomic function. METHODS: Twelve patients (five males, seven females; mean age 63 +/- 13 years) with severe symptomatic aortic stenosis before and after aortic valve replacement, were compared with a control group matched by age and sex. In the study group, mean fractional shortening was 36.5 +/- 5% and maximal aortic gradient 94.7 +/- 12 mmHg, assessed echocardiographically. Autonomic dysfunction was evaluated by following heart rate variability in both time and frequency domains. Spectral analysis was assessed at very low frequency (VLF: 0.017-0.05 Hz), low frequency (LF: 0.05-0.15 Hz) and high frequency (HF: 0.15-0.50 Hz). Heart rate variability was analyzed during three intervals, between 6:00-8:00 am (morning), 14:00-16:00 (afternoon) and 02:00-04:00 (night), and re-evaluated at 8-10 months after aortic valve replacement. RESULTS: Compared with controls, patients with aortic stenosis presented a significantly lower heart rate variability in the morning and afternoon, analyzed either by time or frequency domain: 50 +/- 22 versus 132 +/- 52 ms (p < 0.05); VLF 5.0 +/- 1.5 versus 7.9 +/- 1.4 ln (ms)2 (p < 0.05); LF 4.9 +/- 1.7 versus 7.5 +/- 1.8 ln (ms)2 (p < 0.05); HF 5.3 +/- 1.4 versus 7.5 +/- 1.8 ln (ms)2 (p < 0.05). Results at night showed a similar tendency, but were not statistically significantly different. At 8-10 months after aortic valve replacement, heart rate variability was increased significantly during the morning, from 50 +/- 22 to 79.5 +/- 22 ms (p < 0.05); VLF from 5.0 +/- 1.5 to 6.7 +/- 0.8 ln (ms)2 (p < 0.05); LF from 4.9 +/- 1.7 to 6.2 +/- 1.3 ln (ms)2 (p < 0.05). HF values tended to increase, though not significantly so. During the remainder of the day there was also a non-statistically significant increment in all values of heart rate variability. CONCLUSIONS: The study results suggest that patients with severe symptomatic aortic stenosis present with autonomic dysfunction that tends to normalize within the first year of valve replacement.

Aortic Valve Stenosis↗

Effects of relaxing music on cardiac autonomic balance and anxiety after acute myocardial infarction.

BACKGROUND: Acute myocardial infarction places additional demands on an already compromised myocardium. Relaxing music can induce a relaxation response, thereby reversing the deleterious effects of the stress response. OBJECTIVES: To compare the effects of relaxing music; quiet, uninterrupted rest; and "treatment as usual" on anxiety levels and physiological indicators of cardiac autonomic function. METHODS: A 3-group repeated measures experimental design was used. Forty-five patients, 15 per group, with acute myocardial infarction were assigned randomly to 20 minutes of (1) music in a quiet, restful environment (experimental group); (2) quiet, restful environment without music (attention); or (3) treatment as usual (control). Anxiety levels and physiological indicators were measured. RESULTS: Immediately after the intervention, reductions in heart rate, respiratory rate, and myocardial oxygen demand were significantly greater in the experimental group than in the control group. The reductions in heart rate and respiratory rate remained significantly greater 1 hour later. Changes in heart rate, respiratory rate, and myocardial oxygen demand in the attention group did not differ significantly from changes in the other 2 groups. The 3 groups did not differ with respect to systolic blood pressure. Increases in high-frequency heart rate variability were significantly greater in the experimental and attention groups than in the control group immediately after the intervention. State anxiety was reduced in the experimental group only; the reduction was significant immediately and 1 hour after the intervention. CONCLUSIONS: Patients recovering from acute myocardial infarction may benefit from music therapy in a quiet, restful environment.

Analysis of Variance↗

Early detection of sympathetic myocardial denervation in patients with familial amyloid polyneuropathy type I.

INTRODUCTION: Type I familial amyloid polyneuropathy (FAP I) is an autosomal dominant inherited disorder due to a genetic defect in transthyretin and is characterized by deposition of amyloid in various organs and tissues. The principal manifestations are related to polyneuropathy and dysautonomia. The aim of this study was to assess cardiac involvement and to correlate the findings with neurological status. METHODS: 34 patients with FAP (15 male and 19 female; mean age 43 +/- 15 years) underwent I123-labeled metaiodobenzylguanidine (MIBG) myocardial scintigraphy in order to evaluate cardiac sympathetic innervation. In addition they underwent ambulatory blood pressure monitoring (ABPM) and two-dimensional and Doppler echocardiography. Neurological involvement was quantified according to a neurophysiologic score (EMG; 0 = no abnormality and 100% = maximal disability). RESULTS: The mean value of cardiac MIBG uptake was 1.75 +/- 0.5 (normal = 2.6 +/- 0.3) and correlated inversely with the EMG score (r = -0.67; p = 0.001). In 27 (79%) of the 34 patients there was a decrease in MIBG accumulation, in 18 (53%) an alteration in the circadian BP pattern and/or an increase in systolic and/or diastolic BP loads at night, and in 17 (50%) left ventricular hypertrophy and/or diastolic dysfunction. Twenty-two patients were symptomatic and had a mean EMG score of 37.7 +/- 25% (group I). The remaining 12 were asymptomatic and without neurological involvement (group II). Group I was characterized by older age (48 +/- 15 vs. 33 +/- 10.2 years, p = 0.01), lower MIBG uptake (1.5 +/- 0.4 vs. 2.2 +/- 0.5, p = 0.001), higher systolic (129 +/- 16 vs. 119 +/- 6 mmHg, p = 0.01) and diastolic daytime BP (82 +/- 10 vs. 76 +/- 6 mmHg, p = 0.05), and higher systolic (119 +/- 17 vs. 105 +/- 7 mmHg, p = 0.01) and diastolic nocturnal BP (71 +/- 11 vs. 62 +/- 9 mmHg, p = 0.01) than patients in group II. In 21/22 patients in group I and in 6/12 in group II there was a decrease in cardiac MIBG activity. Sixteen patients in group I and 2 in group II had abnormal circadian BP pattern. Left ventricular hypertrophy was only seen in group I. CONCLUSIONS: Patients with FAP have a high incidence of cardiac denervation and an abnormal circadian BP pattern. These alterations in cardiac autonomic function precede the development of clinical manifestations and may be an important factor in determining the optimal timing for liver transplantation, which is currently the only way to control the progression of the disease.

Adult↗

The influence of autonomic neuropathy on mortality in insulin-dependent diabetes.

Five-year survival was investigated in 506 randomly selected patients with insulin-dependent diabetes mellitus screened for autonomic neuropathy with a series of cardiac autonomic function tests. Of the 484 diabetics traced, 44 (9 per cent) had died. The cumulative 5-year mortality rate was increased more than five-fold in those with autonomic neuropathy: 27 per cent vs. 5 per cent in those with normal autonomic function. Discriminant analysis of survivors and non-survivors showed that autonomic neuropathy was the most important independent predictor of death. Among those who died, autonomic neuropathy was associated with an increased frequency of retinopathy and peripheral neuropathy and a slightly lower frequency of macrovascular disease. Autonomic neuropathy was associated with an increased mortality rate from renal failure, but not from any other causes.

Adolescent↗