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At least 793 records · Page 44Linked to original sources
PubMed1992

Association of diabetic autonomic neuropathy with painless myocardial ischaemia induced by exercise.

Silent myocardial ischaemia is now well-recognised in patients with symptomatic coronary artery disease. Its pathogenesis remains speculative, though diminished sensitivity to pain is thought to be one of the mechanisms involved. Because cardiovascular autonomic dysfunction occurs frequently in diabetic patients, we postulate that it contributes towards painless myocardial ischaemia among them. Forty consecutive diabetic (type II) male patients and ten normal volunteers were studied. Using 5 previously-validated noninvasive tests for autonomic dysfunction, 14 of these diabetic men had definite autonomic neuropathy (at least 2 abnormal tests). All 50 subjects were then exercised on a motor-driven treadmill to either exhaustion or chest pains. Thirty-three diabetic subjects were tested positive, with significant (greater than 1 mm) ST segment depression over at least 2 contiguous leads. Of these, 18 were associated with typical angina but the other 15 stopped because of fatigue or exhaustion (ie painless). Thirteen subjects who had definite autonomic neuropathy (AN+) had positive exercise ECG tests-10 had painless ischaemia, and only 3 had angina. This contrasted with 15 patients who had painful ischaemia and 5 who had painless ischaemia among the group without (AN-)autonomic dysfunction (p = 0.0047, Fisher's exact test). There were no significant differences among the various groups for peak rate-pressure-product, all subjects attaining similar maximal oxygen consumption states during which ischaemic ST segment changes were noted (painful AN+: 21917 +/- 4753; painless AN+: 20117 +/- 6752; painful AN-: 16544 +/- 4063; painless AN-: 22220 +/- 4341, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Patients with diabetic neuropathy are at risk of a greater intraoperative reduction in core temperature.

BACKGROUND: Core hypothermia develops after the induction of general anesthesia, but intraoperative vasoconstriction usually prevents its progression. However, diabetes mellitus is often associated with autonomic neuropathy, which leads to abnormal peripheral neurovascular function. Accordingly, we tested the hypothesis that diabetic patients experience a greater reduction in core temperature during general anesthesia than nondiabetic patients. METHODS: We studied 36 nondiabetic patients (control group) and 27 diabetic patients (diabetic group) undergoing elective abdominal surgery. Both groups were divided into young (< 60 yr) and older age (>/= 60 yr) groups. Standard noninvasive autonomic tests (heart rate variation at deep periodical breathing, Valsalva maneuver, and head-up tilt) were carried out for each patient. The relation between the results of these tests of autonomic function and the tympanic membrane temperature during general anesthesia was assessed in relation to peripheral vasoconstriction. RESULTS: Thirteen patients in the diabetic group showed abnormal responses to two or more of the basal autonomic function tests (patients with autonomic dysfunction). Changes in core temperature among the groups were similar at 90 min after the induction of anesthesia. However, the core temperature of the diabetic patients with autonomic dysfunction was lower from 120 min (35.1 degrees C) onward compared with the young or older nondiabetic patients and the diabetic patients with normal autonomic function. Peripheral vasoconstriction, evaluated using the forearm-fingertip skin surface temperature gradient, was delayed in patients with autonomic dysfunction compared with the others. CONCLUSIONS: The current results indicate that diabetic autonomic neuropathy is associated with more severe intraoperative hypothermia. We postulate that diabetic patients become more hypothermic because their peripheral neuropathy delays the onset of thermoregulatory vasoconstriction and reduces its efficacy once triggered. These patients may therefore fail to develop a normal core temperature plateau.

Abdomen↗
PubMed1980

Autonomic neuropathy in non-insulin-dependent diabetes mellitus in the young.

Twenty-five cases of non-insulin-dependent diabetes mellitus in the young were investigated for autonomic dysfunction by simple electrophysiological tests to assess the integrity of the cardiovascular reflexes. The mean age of the group at the onset of symptomatic diabetes mellitus ws 27 +/- 0,7 years, and that at the time of investigation for autonomic dysfunction ws 34 +/- 1,3 years. Nine patients had clinical evidence of peripheral neuropathy, while only 3 of the 25 had symptoms of autonomic neuropathy. Fourteen patients showed an abnormality during one or more tests for autonomic function, and of this group 9 had unequivocal evidence of autonomic neuropathy. Only 3 patients displayed both sympathetic and parasympathetic impairment of autonomic function, being the only patients exhibiting symptoms of autonomic impairment. The remaining patients with autonomic dysfunction showed only parasympathetic dysfunction. This study demonstrates that subclinical autonomic neuropathy is not an uncommon occurrence in cases of non-insulin-dependent diabetes mellitus in the young and emphasizes the need for a greater awareness of this complication.

Adult↗
PubMed1997

Autonomic neuropathy in extra-hepatic portal vein thrombosis: evidence for impaired autonomic reflex arc.

BACKGROUND/AIMS: Autonomic dysfunction is common in cirrhosis, and may be associated with increased mortality and hyperdynamic circulatory changes. Our aim was to investigate whether autonomic disturbances occur in extrahepatic portal vein thrombosis and their correlation with hemodynamic abnormalities. PATIENTS AND METHODS: Heart rate variation in response to standing, deep breathing, and Valsalva maneuver, and blood pressure response to sustained handgrip and to standing, were studied in 16 subjects with portal vein thrombosis (10 males, 30.8+/-2.8 years: mean+/-SE), 12 with cirrhosis (7 males, 52+/-2.3 years), and 10 healthy controls (7 males, 30.8+/-3.0 years). Supine resting, and 10- and 30-min standing epinephrine and norepinephrine levels were measured and results correlated with cardiac output. RESULTS: Autonomic dysfunction occurred in 62% of portal vein thrombosis and 75% of cirrhosis subjects, but in no controls (p<0.02). Similarly, postural hypotension occurred in portal vein thrombosis (-10.25+/-0.65 mmHg, p=0.003) and cirrhosis (-7.42+/-0.82 mmHg, p=0.007) but not in controls. All groups had similar baseline epinephrine and norepinephrine concentrations. Epinephrine increased significantly in controls (45%, p<0.01 and 49%, p<0.02) after 10 of 30 min standing but not in the portal vein thrombosis or the cirrhotic group, and norepinephrine increased after 10 and 30 min standing in cirrhotics (128%, p<0.004 and 130%, p<0.008) and controls (129%, p<0.002 and 116%, p<0.004), but not portal vein thrombosis (34.5% and 39%, NS vs baseline). Portal vein thrombosis and cirrhosis groups had increased cardiac output (4441+/-509 and 3262+/-292) vs controls (1763+/-212 ml/min/m2, p<0.002), but there was no correlation with autonomic neuropathy or with catecholamine levels. CONCLUSIONS: Autonomic dysfunction and impaired catecholamine response to orthostatic stress occur commonly in portal vein thrombosis and suggest an impairment of the autonomic reflex arc, but changes do not correlate with hemodynamic abnormalities.

Adult↗
PubMed2002

Quantitative cardiovascular autonomic function study in Fisher syndrome.

Quantitative cardiovascular autonomic function tests were performed longitudinally in nine patients with Fisher syndrome (FS). Parasympathetic autonomic function was evaluated by the Valsalva ratio and RR interval variation during rest and deep breathing. Sympathetic autonomic function was evaluate by blood pressure responses to sustained handgrip and to active standing. None of the patients with FS had clinical signs of autonomic dysfunction during the course of their illness. However, autonomic function abnormalities were seen in up to 83% of patients with FS. Thus, bedside clinical signs of autonomic dysfunctions are inadequate for the assessment of autonomic abnormality compared with quantitative autonomic function examination. Most autonomic function tests tended to improve after 4-12 weeks. Although parasympathetic and sympathetic functions were both involved at the height of FS, parasympathetic fibres were less vulnerable than the sympathetic fibres.

Adolescent↗
PubMed1992

Noninvasive detection of cardiac sympathetic nervous dysfunction in diabetic patients using [123I]metaiodobenzylguanidine.

The association between clinical autonomic dysfunction and myocardial MIBG accumulation was investigated. The study groups comprised 6 male diabetic patients with autonomic neuropathy (ANP+ group), 6 male diabetic patients without autonomic neuropathy (ANP-group), and 6 male nondiabetic control subjects. The mean age was comparable in all groups, and the subjects had no evidence of coronary heart disease. Reduced heart-rate variation in a deep-breathing test was used as a criterion for autonomic neuropathy. Immediately after injection, the peak net influx rate of MIBG to myocardium was significantly (P less than 0.05) reduced in both diabetic groups. At 6 hr after MIBG injection, the MIBG uptake of the myocardium was significantly (P less than 0.05) smaller in the ANP+ group than in the control group. In the ANP- group, the MIBG uptake of the myocardium was between that of the ANP+ group and that of the control group. Our data show that reduced myocardial MIBG accumulation is associated with autonomic dysfunction in diabetic patients, but it can occur to a lesser extent also in diabetic patients without apparent autonomic neuropathy. The measurement of the myocardial MIBG accumulation is a promising new method to detect cardiac sympathetic nervous dysfunction in diabetic patients.

3-Iodobenzylguanidine↗
PubMed2002

Iodine-123 metaiodobenzylguanidine scintigraphic analysis of myocardial sympathetic innervation in patients with AL (primary) amyloidosis.

BACKGROUND: Although a high incidence of myocardial adrenergic denervation has been reported in patients with familial amyloid polyneuropathy, assessment of cardiac sympathetic nerve function has not been available in patients with AL (primary) amyloidosis. METHODS: To test the hypothesis that myocardial sympathetic nerve innervation might be impaired and variable according to the presence or absence of clinical autonomic abnormalities and congestive heart failure in AL amyloidosis, we examined 25 patients by use of iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy. RESULTS: Ten of the 16 patients without autonomic symptoms and 5 of the 9 patients with autonomic neuropathy showed congestive heart failure. The heart/mediastinal activity (H/M) ratio (1.53 +/- 0.06 vs 1.29 +/- 0.05 at 3 hours, P <.001) and myocardial washout ratio (41.5% +/- 4.8% vs 30.8% +/- 4.0%, P <.001) of MIBG were significantly increased in patients without autonomic symptoms compared with patients showing autonomic neuropathy. In patient groups with and without autonomic dysfunction, patients demonstrating congestive heart failure exhibited a significantly decreased H/M ratio and increased washout compared with patients with no heart failure, and left ventricular fractional shortening was positively correlated with the H/M ratio and inversely correlated with the washout ratio. There were significant correlations between the low-frequency component of the heart rate variability and the H/M ratio and washout ratio in the entire patient population. CONCLUSIONS: Patients with AL amyloidosis and no autonomic dysfunction showed variable degrees of enhanced cardiac adrenergic neuronal activity with presynaptic sympathetic dysfunction. In contrast, patients with AL amyloidosis and autonomic neuropathy exhibited prominent myocardial adrenergic denervation with normal or impaired sympathetic neural function of the heart. This study demonstrates that myocardial uptake and turnover of MIBG in patients with AL amyloidosis are heterogeneous and dependent on the presence or absence of congestive heart failure and cardiac autonomic dysfunction.

3-Iodobenzylguanidine↗
PubMed2006

Depression in patients with acute myocardial infarction: influence on autonomic nervous system and prognostic role. Results of a five-year follow-up study.

BACKGROUND: Although previous studies demonstrated an association between depressive symptoms and cardiac mortality after acute myocardial infarction (AMI) little is known about the possible mechanisms of this association. The aim of this study was to determine whether depressed patients present a cardiac autonomic dysfunction and whether this could represent the mediator of the influence of depression on their prognosis. METHODS: One hundred consecutive patients with AMI were recruited between January and December 1999. Major Depressive Disorder (MDD) was diagnosed by structured clinical interview and the presence of symptoms of depression was evaluated with self-administered Beck Depression Inventory (BDI). The influence of depression on autonomic nervous system was investigated measuring heart rate variability (HRV) and heart rate (HR) during 24-hour electrocardiographic monitoring. The end-points of the study were all-cause mortality, recurrent-AMI, revascularization and a composite end-point of all the previous. Potential confounders for depression status and events were entered into a multivariate regression model. RESULTS: Fifteen patients met the criteria for MDD and 35 patients showed mild-to-moderate symptoms of depression; women had a higher prevalence of depression than men (35% vs 9%; p<0.01). Depression was not related to the severity of ischaemic disease or to other clinical and demographic variables. Patients with MDD showed lower HRV (76+/-25 SD vs 99+/-33 SD ms; p<0.01) and higher HR (77+/-12 SD vs 68+/-9 SD bpm; p<0.01) than patients without MDD; moreover mild to moderate symptoms of depression (BDI score > or = 10) were associated with lower HRV (84+/-25 SD vs 102+/-35 SD ms; p=0.01) but not with significantly higher HR. After a mean follow-up of 60 months MDD was associated with an increase of all-cause mortality (OR 12; 95% CI 2.6-56; p<0.01) and of composite end-point (OR 2; 95% CI 1.2-3.6; p=0.01) but not with re-AMI and revascularization. In a simple regression model HRV values were predictors of mortality (p<0.01). However when added in the multiple regression model HRV did not have an independent correlation with the end-points considered and did not modify the correlation between depression and mortality. CONCLUSIONS: Patients with post-AMI depression have a cardiac autonomic dysfunction as reflected by decreased HRV and increased HR. This autonomic dysfunction seems not to be an independent mediator of the increased mortality observed in depressed patients during a 5-year follow-up.

Aged↗
PubMed2007

A pilot study of the efficacy of heart rate variability (HRV) biofeedback in patients with fibromyalgia.

UNLABELLED: Fibromyalgia (FM) is a non-inflammatory rheumatologic disorder characterized by musculoskeletal pain, fatigue, depression, cognitive dysfunction and sleep disturbance. Research suggests that autonomic dysfunction may account for some of the symptomatology of FM. An open label trial of biofeedback training was conducted to manipulate suboptimal heart rate variability (HRV), a key marker of autonomic dysfunction. METHODS: Twelve women ages 18-60 with FM completed 10 weekly sessions of HRV biofeedback. They were taught to breathe at their resonant frequency (RF) and asked to practice twice daily. At sessions 1, 10 and 3-month follow-up, physiological and questionnaire data were collected. RESULTS: There were clinically significant decreases in depression and pain and improvement in functioning from Session 1 to a 3-month follow-up. For depression, the improvement occurred by Session 10. HRV and blood pressure variability (BPV) increased during biofeedback tasks. HRV increased from Sessions 1-10, while BPV decreased from Session 1 to the 3 month follow-up. CONCLUSIONS: These data suggest that HRV biofeedback may be a useful treatment for FM, perhaps mediated by autonomic changes. While HRV effects were immediate, blood pressure, baroreflex, and therapeutic effects were delayed. This is consistent with data on the relationship among stress, HPA axis activity, and brain function.

Adolescent↗
PubMed1995

Effects of type 1 diabetes mellitus on cardiac function: a study of monozygotic twins.

OBJECTIVE: To investigate left ventricular size and function in type 1 diabetes and their relation with diabetes duration, glycaemic control, autonomic dysfunction, and complications of diabetes. DESIGN: Cross sectional study using a pulsed wave Doppler echocardiogram to assess left ventricular dimensions, wall thickness, and transmitral blood flow velocity signals. PATIENTS: 40 monozygotic twin pairs (23 male, mean age 26 years) discordant for type 1 diabetes and 40 non-diabetic singleton controls with no clinical evidence of cardiac ischaemia. RESULTS: For all Doppler echocardiographic measurements there were strong correlations between monozygotic twins but not between twins and control subjects. Left ventricular dimensions, wall thickness and systolic function, peak E velocity, and the velocity integrals of early left ventricular filling were similar in all three groups. Peak A velocity and the velocity integrals of late ventricular filling (mean (SD)) were greater in diabetic twins (45 (12) v 38 (8) cm/s, P = 0.002; and 32 (11) v 26 (6), P = 0.0002). Diabetic twins had lower E/A ratio (1.59 (0.39) v 1.83 (0.39), P < 0.001), greater atrial filling fraction to total diastolic filling (28 (6) v 25 (5)%, P = 0.002), and prolonged isovolumic relaxation time (72 (12) v 63 (9) ms, P < 0.001). The differences in Doppler findings between diabetic and non-diabetic twins were related to disease duration whereas the prolongation of the isovolumic relaxation time was related to cardiac autonomic dysfunction. CONCLUSIONS: These results show that twins with type 1 diabetes have left ventricular diastolic dysfunction related to diabetes duration and cardiac autonomic dysfunction but not to glycaemic control or microvascular complications. In addition, genetic factors contribute to left ventricular dimension and function.

Adolescent↗
PubMed1993

Prognostic significance of QT prolongation and autonomic nervous dysfunction in alcoholics with diabetes mellitus.

Rate-corrected QT interval (QTc) and the coefficient of variation of the RR interval (CVRR) were measured at rest on the 30th abstinent day in 58 diabetic alcoholics (DMAL) and 32 healthy controls. A ratio of CVRR to its standard predicted value (CVRR/CVp) of < 0.8 was judged to represent autonomic nervous dysfunction (AND). QTc correlated with CVRR/CVp (r = -0.55, p < 0.001) in DMAL, but not in normal controls. The incidence of prolongation (QTc > or = 440 msec) and mean value of QTc were higher in 39 DMAL with AND (72%, p < 0.005, 458 +/- 29 msec, p < 0.01) than in 19 DMAL without AND (26%, 425 +/- 24 msec) and normal controls (0%, 398 +/- 18 msec). The 2.5-year mortality in these DMAL was analysed. Eight out of 12 natural deaths were unexpected or sudden without prior hospitalization. CVRR/CVp in the expired patients was lower than that in the survived patients (0.52 +/- 0.19 vs 0.71 +/- 0.34, p < 0.05). QTc was longer in the former than in the latter (463 +/- 22 msec vs 442 +/- 32, p < 0.05). The 2.5-year survival rate of DMAL with AND was lower than that of DMAL without AND (71% vs 95, p < 0.05). DMAL with QTc prolongation had also a lower survival rate than DMAL without it (69% vs 92, p < 0.05). Stepwise logistic regression analysis showed that only two factors, alcohol abuse after discharge and QTc remained as significant predictors of outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Cardiovascular autonomic function, autoantibodies, and esophageal motor activity in patients with systemic sclerosis and mixed connective tissue disease.

OBJECTIVE: To study cardiovascular autonomic nerve function and presence of autoantibodies in relation to esophageal motor activity in patients with systemic sclerosis (SSc) and mixed connective tissue disease (MCTD). METHODS: Twenty-five patients with SSc (13 limited, 12 diffuse cutaneous disease; disease duration 1-19 yrs) and 6 patients with MCTD (disease duration 1-10 yrs) were studied. Cardiovascular autonomic function was assessed using 5 standard tests and autoantibody status determined. Esophageal motor activity and lower and upper esophageal sphincter pressures were recorded manometrically. RESULTS: Five patients with SSc had definite, 7 borderline, and 13 no autonomic dysfunction; 23 had antinuclear. 9 anti-Sc170, 4 anticentromere, and 1 U1snRNP antibodies. Contraction amplitudes in the smooth muscle as well as the striated muscle esophagus and lower esophageal sphincter pressures were significantly lower and autonomic dysfunction more frequent in patients with than in those without anti-Sc170 (6 of 9 vs 6 of 16 patients); upper esophageal sphincter pressures did not differ. All patients with MCTD had antinuclear antibodies, 5 had definite autonomic dysfunction; their lower esophageal sphincter pressures were significantly lower than in SSc patients without anti-Sc170 and anti-U1snRNP. CONCLUSION: Esophageal motor dysfunction may be associated with the presence of anti-Sc170 and anti-U1snRNP autoantibodies and prevail in patients with cardiovascular autonomic neuropathy.

Adult↗
PubMed2002

Pharmacotherapy of tetanus--a review.

With adequate immunization, tetanus caused by the gram-positive anaerobic cocci, clostridium tetani, is a preventable disease. In treating C. tetani infection, Metronidazole as an antibiotic is more effective than Penicillin G since it is a GABA antagonist. Agents used to control spasm and rigidity should have little effect on the level of consciousness, respiration and blood pressure. The drug of choice for treating spasm and rigidity is benzodiazepine, a GABA agonists. Large doses of benzodiazepines may be required to overcome the spasm and are safe. Baclofen is another GABA agonist, which has been tried as an alternative to benzodiazepine with moderate success. Clinical experience with dantrolene sodium is limited. Magnesium with its unique properties on the neuromuscular junction and sympathetic system has been used to treat both spasms and autonomic dysfunction with limited success. Neuromuscular blocking drugs are indicated depending on the severity of spasms. Neuromuscular blocking drugs with steroid molecule should be avoided in view of prolonged weakness. No drug has consistently proven to be effective in the treatment of autonomic dysfunction. Beta-blockers, variation of and beta blockers, opioids, clonidine, magnesium, spinal and epidural anaesthesia have been tried with varying success. Beta-blockers should be used with caution as they have been implicated in the deaths of some patients with autonomic dysfunction.

Anti-Bacterial Agents↗
PubMed1999

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↗
PubMed1992

Peripheral and cardiovascular autonomic impairment in chronic liver disease: prevalence and relation to hepatic function.

We have evaluated autonomic function using standard cardiovascular tests and a test of peripheral autonomic denervation, the acetylcholine sweatspot test, in 104 patients with biopsy proven chronic liver disease and 35 age- and sex-matched controls. Cardiovascular autonomic dysfunction was significantly more frequent in advanced liver disease compared with early liver disease (71.8% Child B or C vs. 39.7% Child A; p < 0.0006), and a strong correlation between the number of abnormal tests and Child-Pugh score could be demonstrated (Rs = 0.5; p < 0.0001). On multiple logistic regression analysis, cardiovascular autonomic dysfunction was related to age and to Child-Pugh score and occurred independently of the aetiology of liver disease. Peripheral autonomic denervation was found in 39% of patients, was significantly associated with cardiovascular abnormalities (p < 0.009) and correlated with the number of abnormal cardiovascular tests in each patient (Rs = 0.48; p < 0.0001). In chronic liver disease, the prevalence and severity of cardiovascular autonomic dysfunction is related to the severity of hepatic dysfunction and is independent of aetiology, suggesting a common pathogenetic basis related to hepatic damage; the association with peripheral autonomic denervation indicates that at least some of the abnormalities may be due to a true autonomic neuropathy. The possible significance of these findings to the complications of cirrhosis is discussed.

Acetylcholine↗
PubMed2004

Pacing does not improve hypotension in patients with severe orthostatic hypotension--a prospective randomized cross-over pilot study.

BACKGROUND: Tachypacing has been suggested to compensate for drop in blood pressure as a technique to improve symptoms in patients with severe orthostatic hypotension secondary to autonomic dysfunction. To date, however, no randomized controlled studies have been performed to validate the approach. METHODS AND RESULTS: Six patients with severe orthostatic hypotension and chronotropic incompetence secondary to autonomic dysfunction underwent a prospective randomized cross-over tilt table study with no pacing and with temporary DDD pacing at 90 and 110 bpm. Time to syncope or pre-syncopal symptoms, blood pressure changes, stroke volume and cardiac output were recorded using real time hemodynamic monitoring and echocardiography. All patients, except for one, had a drop in blood pressure and syncope or pre-syncopal symptoms during tilt regardless of whether they were paced or not. There was also no difference in any of the measured hemodynamic and vasomotor parameters with pacing. CONCLUSIONS: Pacing did not produce any benefits in terms of symptoms or in any of the measured hemodynamic variables during tilt for patients with severe orthostatic hypotension secondary to autonomic dysfunction in this limited pilot study.

Aged↗