Drug treatment of orthostatic hypotension and vasovagal syncope

Orthostatic hypotension is a common problem, estimated to occur in 5 out of every 1000 individuals and in as many as 7% to 17% of patients in an acute care setting. Moreover, orthostatic hypotension may be more prominent in elderly patients due to the increased intake of vasoactive medications and concomitant decrease in physiologic function, such as baroreceptor sensitivity, often seen with aging. Orthostatic hypotension is a fall in blood pressure on assuming an upright position. Absolute cutoffs for the drop in blood pressure are often difficult to determine because different patients exhibit varying degrees of tolerance to falls in blood pressure. Therefore, strict numerical criteria may lead to underdiagnosis and improper intervention. A thorough review of patient symptomatology combined with appropriate clinical tests should be employed to narrow the vast differential diagnosis and pinpoint the etiology. The fall in blood pressure seen in orthostatic hypotension results from the inability of the autonomic nervous system to adequately compensate for the 500 mL blood that is estimated to pool in the lower extremities on assuming an upright posture. The decrease in venous return results in a concomitant decrease in cardiac output and thus hypoperfusion of the cerebral circulation, possibly resulting in syncope or various other symptoms. A complete investigation should consider hypovolemia, removal of offending medications, primary autonomic disorders, secondary autonomic disorders and, of course, vasovagal syncope, the most common cause of syncope. Although further research is still necessary to rectify the disease process responsible for orthostatic hypotension, patients suffering from this disorder can effectively be treated through a combination of nonpharmacologic treatment, pharmacologic treatment and patient education. Agents such as fludrocortisone, midodrine and erythropoietin show promising results as therapeutic adjuncts. Treatment for recurrent vasovagal syncope includes increased salt intake, and various drug treatments, most of which are still under investigation.     

Role of impaired lower-limb venous innervation in the pathogenesis of the chronic fatigue syndrome

BACKGROUND: In patients with acute orthostatic hypotension, there is excessive pooling of blood in the legs, which may result from the strikingly subnormal compliance that is demonstrable in the pedal veins during norepinephrine infusion. The common occurrence of delayed orthostatic hypotension and/or tachycardia in the chronic fatigue syndrome (CFS) led to the present studies of foot vein compliance in CFS patients with a linear variable differential transformer. METHODS: Seven patients with CFS were compared with 7 age- and gender matched healthy control subjects in their blood pressure, heart-rate, and plasma norepinephrine responses to prolonged standing and in measurements of their foot vein contractile responses to intravenous norepinephrine infusions with the linear variable differential transformer. RESULTS: Excessive, delayed (usually after 10 min) orthostatic reductions in systolic and diastolic blood pressure (P < 0.01) and inconsistently excessive increases in heart rate were found in the CFS patients, in whom venous compliance in response to infused norepinephrine was significantly reduced (P < 0.05). CONCLUSIONS: In these patients with CFS, delayed orthostatic hypotension was clearly demonstrable, and, as in previously reported patients with orthostatic hypotension of acute onset, this was associated with reduced pedal vein compliance during norepinephrine infusion, implying impaired sympathetic innervation of foot veins. The rapid symptomatic improvement demonstrated in previous studies of CFS patients during correction of orthostatic venous pooling by inflation of military antishock trousers (MAST) to 35 mm Hg may suggest that excessive lower body venous pooling, perhaps by reducing cerebral perfusion, is involved in the orthostatic component of fatigue in these patients.     

Increased impedance to inspiration ameliorates hemodynamic changes associated with movement to upright posture in orthostatic hypotension: a randomized blinded pilot study.

BACKGROUND: Movement to upright posture may result in marked drop of blood pressure with susceptibility to injury from syncope and falls in patients with orthostatic hypotension. OBJECTIVE: The purpose of this study was to determine if increasing negative intrathoracic pressure by using an inspiratory impedance threshold device before change of posture diminishes blood pressure fall by enhancing venous return. METHODS: Eighteen healthy subjects and 22 orthostatic hypotension patients were randomized to either an active (impedance 7 cmH2O) or sham (no inspiratory impedance) impedance threshold device. Arterial blood pressure, heart rate, and estimated stroke volume and total peripheral resistance were recorded in the supine and upright postures using a noninvasive finger arterial blood pressure monitor. After a rest period, the alternate impedance threshold device (sham or active) was tested in each individual. RESULTS: Compared with the sham impedance threshold device test, the active impedance threshold device resulted in significant reduction in the magnitude of upright posture-induced fall in blood pressure and a greater increase of total peripheral resistance after standing in both healthy subjects and orthostatic hypotension patients. Stroke volume was not measurably altered. Among all subjects who exhibited a postural blood pressure drop >10 mmHg on the day of study, active impedance threshold device treatment consistently blunted blood pressure fall during the initial 100 seconds after standing (<0.04). Induced orthostatic symptoms were less severe with the active impedance threshold device both at onset of upright posture and during 30 seconds of standing. CONCLUSION: Enhancing impedance to inspiration may prove useful as adjunctive therapy for diminishing symptoms associated with movement to upright posture in individuals with orthostatic hypotension.     

Delayed orthostatic intolerance.

In seven patients who presented with lightheadedness, fatigue, "weakness," and sometimes syncope, blood pressure was found not to fall after standing for 3 to 4 minutes but to fall severely, frequently with syncope or presyncopal symptoms, after 13 to 30 minutes when measured every minute with an automatic device. This delayed orthostatic hypotension could be corrected with inflation of a pressure suit to 45 mm Hg. Its mechanism was further investigated with measurements of plasma catecholamines, plasma cortisol and aldosterone responses to corticotropin, and the effects of norepinephrine infusions on blood pressure and venous contractility. There was normal or excessive orthostatic norepinephrine release in all patients, evidence of impaired venous innervation in the legs in some, and various disorders in the other patients. Since therapeutic improvement in the orthostatic hypotension greatly reduced the symptoms, we concluded that orthostatic hypotension occurring after more than 10 minutes of standing is a potentially debilitating and often correctable disorder.     

Syncope and orthostatic hypotension

PURPOSE: The purpose of this study was to determine the postural blood pressure response over time, the prevalence of orthostatic hypotension in patients with syncope, and the relationship of orthostatic hypotension to recurrence of symptoms. PATIENTS AND METHODS: We prospectively evaluated 223 patients with syncope in a standardized manner. Orthostatic responses were measured in a standardized fashion at 0, 1, 2, 3, 5, and 10 minutes or until symptoms occurred. Follow-up was obtained at 3-month intervals. Causes of syncope were assigned by predetermined criteria. RESULTS: Orthostatic hypotension (20 mm Hg or greater systolic blood pressure decline) was found in 69 patients (31%). The median time to reach minimal standing systolic blood pressure was 1 minute for all subjects. In patients with orthostatic hypotension (20 mm Hg or greater), mean time to reach minimum blood pressure was 2.4 minutes. The vast majority of patients with significant orthostatic hypotension had this finding within 2 minutes of standing. Orthostatic hypotension was common in patients for whom other probable causes of syncope were assigned. The recurrence of syncope was not related to the degree of orthostatic hypotension; however, the recurrence of dizziness and syncope as end-points was lower in patients with 20 mm Hg or greater systolic blood pressure reductions as compared with patients with lesser degrees of orthostatic blood pressure declines. CONCLUSION: Orthostatic hypotension is common in patients with syncope and is detected in the vast majority of patients by 2 minutes. Although symptom recurrence on follow-up was lower in patients with more severe orthostatic hypotension, the clinical significance of this finding needs to be further defined by future studies.     

Treatment of chronic orthostatic hypotension with ergotamine

The acute and chronic effects of ergotamine were examined in four patients with chronic orthostatic hypotension. Chronic oral administration of ergotamine tartrate produced significant increases in standing blood pressure and marked clinical improvement, without appreciable recumbent hypertension. The blood pressure increases were not associated with significant changes in plasma norepinephrine or plasma renin activity. No major toxicity was observed at doses of 2-6 mg/day over treatment periods of 3-18 months. Hemodynamic studies on the effects of i.v. ergotamine tartrate (0.25-0.50 mg) revealed that the ergotamine-induced increase in blood pressure in the supine position was associated with an increase in total peripheral resistance (from 1616 +/- 165 to 2574 +/- 583 U) without a change in cardiac output. During 45-60 degrees upright tilt, ergotamine increased both total peripheral resistance (1801 +/- 296 to 3262 +/- 1107 U) and cardiac output (2.42 +/- 0.46 to 3.34 +/- 0.54 l/min). Forearm plethysmographic studies revealed decreased forearm blood flow and venous volume and increased vascular resistance with ergotamine. The orthostatic hypotensives had more platelet alpha-receptors (390 +/- 31 receptors/cell) than the control subjects (234 +/- 17 receptors/cell). The increased receptor level was associated with abnormally low circulating levels of norepinephrine and increased pressor responsiveness to infused norepinephrine in three of the four patients. Chronic ergotamine therapy appeared to reduce platelet alpha-receptor number to normal. The results indicate that ergotamine is of value in certain patients with chronic orthostatic hypotension and that the blood pressure effects are related to vasoconstriction in both arterial and venous beds.     

Orthostatic hypotension in the elderly: diagnosis and treatment

Orthostatic hypotension is a common problem among elderly patients, associated with significant morbidity and mortality. While acute orthostatic hypotension is usually secondary to medication, fluid or blood loss, or adrenal insufficiency, chronic orthostatic hypotension is frequently due to altered blood pressure regulatory mechanisms and autonomic dysfunction. The diagnostic evaluation requires a comprehensive history including symptoms of autonomic nervous system dysfunction, careful blood pressure measurement at various times of the day and after meals or medications, and laboratory studies. Laboratory investigation and imaging studies should be based upon the initial findings with emphasis on excluding diagnoses of neurodegenerative diseases, amyloidosis, diabetes, anemia, and vitamin deficiency as the cause. Whereas asymptomatic patients usually need no treatment, those with symptoms often benefit from a stepped approach with initial nonpharmacological interventions, including avoidance of potentially hypotensive medications and use of physical counter maneuvers. If these measures prove inadequate and the patient remains persistently symptomatic, various pharmacotherapeutic agents can be added, including fludrocortisone, midodrine, and nonsteroidal anti-inflammatory drugs. The goals of treatment are to improve symptoms and to make the patient as ambulatory as possible rather then trying to achieve arbitrary blood pressure goals. With proper evaluation and management, the occurrence of adverse events, including falls, fracture, functional decline, and myocardial ischemia, can be significantly reduced.     

Autonomic responses to glucose ingestion in elderly subjects with orthostatic hypotension

The cardiovascular and plasma catecholamine responses to oral glucose (50 g) ingestion were investigated in five elderly subjects with orthostatic hypotension and five elderly control subjects. All the orthostatic hypotension subjects showed blood pressure falls after glucose ingestion, as compared to only one of the control subjects. Significantly greater falls in the orthostatic hypotension as compared to control patients were observed for systolic blood pressure (P less than 0.01) at 60 and 90 min following glucose and mean blood pressure (P less than 0.05) at 60 min following glucose. The orthostatic hypotension subjects did not have evidence of reduced heart-rate or plasma catecholamine responses to the glucose ingestion. It is concluded that, in elderly patients with orthostatic hypotension, disorder of blood pressure control may also cause hypotension associated with eating.     

Orthostatic hypotension in elderly women with congestive heart failure

Orthostatic hypotension is common in the elderly and could be the cause of impaired vision, dizziness, fainting spells and falls. To date, studies on orthostatic hypotension have chiefly concentrated on elderly patients in nursing homes, outpatients or healthy subjects. Congestive heart failure (CHF) is one of the most common causes of hospitalization and pharmacotherapy in the elderly, but little is known about the orthostatic hypotension in patients with CHF. The aim of this study was to evaluate the prevalence of orthostatic hypotension and associated symptoms in elderly females hospitalized for CHF. The study group included 36 women aged 70-100 years (mean 82.2), admitted to hospital for congestive heart failure. The control group consisted of 15 women aged 71-95 years (mean 82.5) with no symptoms of heart failure or other diseases, who underwent earlier epidemiological studies on Cracow's elderly population. In all subjects a tilt test was performed (60 degree tilt for 10 minutes) under standardized conditions (fasting patients, 12 hours after the last administration of medications, between 8:00 and 10:00 a.m.). Orthostatic hypotension was defined as a decline of 20 mmHg or more in systolic blood pressure, or 10 mmHg or more in diastolic blood pressure on assumption of the upright position. Orthostatic hypotension was detected in 83.3% of CHF women, and 43.3% of them manifested clinical symptoms associated with it. In the control group, orthostatic hypotension was noted in 53.3% of women, but none was symptomatic. In particular, the CHF patients showed a decreased ability to develop compensatory tachycardia during hypotension. Moreover, reduction in systolic blood pressure was more pronounced in CHF patients, and diastolic blood pressure increase was less significant as compared with the control group.     

Comparative effects of clonidine and dihydroergotamine on venomotor tone and orthostatic tolerance in patients with severe hypoadrenergic orthostatic hypotension

PURPOSE: Clonidine, an alpha(2)-adrenergic agonist, raises blood pressure in patients with autonomic failure, in whom failure of reflex neurogenic venoconstriction leads to severe orthostatic hypotension. Because animal studies suggest that postjunctional alpha(2)-adrenoreceptors are located mainly on venous capacitance rather than arterial resistance vessels, we tested the hypothesis that venoconstriction is the main mechanism by which clonidine raises blood pressure in patients with autonomic failure. SUBJECTS AND METHODS: We measured forearm venous and arterial tone using plethysmography in 4 patients with autonomic failure before and after acute administration of clonidine (0.4 mg orally) or dihydroergotamine (0.15 mg intravenously), a known venoconstrictor agent. We also recorded supine intraarterial pressure at rest and during graded orthostatic stress with lower body negative pressure. RESULTS: Clonidine and dihydroergotamine caused similar increases in supine (mean +/- SD) arterial pressure (+23 +/- 11 mm Hg vs. and +27 +/- 5 mm Hg) and forearm vascular resistance (+36% +/- 13% vs. +28% +/- 9%). However, the drugs had different effects on forearm venous tone, which increased by 38% +/- 9% with dihydroergotamine (P = 0.01 vs. control) but was unaffected by clonidine (change = 0% +/- 14%). A single dose of clonidine was less effective than a single dose of dihydroergotamine in maintaining arterial pressure during graded orthostatic stress. CONCLUSION: In contrast with what has been hypothesized, clonidine appears to function mainly as an arterial constrictor in patients with hypoadrenergic orthostatic hypotension. Further studies are needed to determine if venoconstrictor agents are of greater therapeutic benefit in this condition than are pure arterial vasoconstrictors.     

Water drinking as a treatment for orthostatic syndromes

PURPOSE: Water drinking increases blood pressure in a substantial proportion of patients who have severe orthostatic hypotension due to autonomic failure. We tested the hypothesis that water drinking can be used as a practical treatment for patients with orthostatic and postprandial hypotension, as well as those with orthostatic tachycardia. SUBJECTS AND METHODS: We studied the effect of drinking water on seated and standing blood pressure and heart rate in 11 patients who had severe orthostatic hypotension due to autonomic failure and in 9 patients who had orthostatic tachycardia due to idiopathic orthostatic intolerance. We also tested the effect of water drinking on postprandial hypotension in 7 patients who had autonomic failure. Patients drank 480 mL of tap water at room temperature in less than 5 minutes. RESULTS: In patients with autonomic failure, mean (+/- SD) blood pressure after 1 minute of standing was 83 +/- 6/53 +/- 3.4 mm Hg at baseline, which increased to 114 +/- 30/66 +/- 18 mm Hg (P <0.01) 35 minutes after drinking. After a meal, blood pressure decreased by 43 +/- 36/20 +/- 13 mm Hg without water drinking, compared with 22 +/- 10/12 +/- 5 mm Hg with drinking (P <0.001). In patients with idiopathic orthostatic intolerance, water drinking attenuated orthostatic tachycardia (123 +/- 23 beats per minute) at baseline to 108 +/- 21 beats per minute after water drinking ( P <0.001). CONCLUSION: Water drinking elicits a rapid pressor response in patients with autonomic failure and can be used to treat orthostatic and postprandial hypotension. Water drinking moderately reduces orthostatic tachycardia in patients with idiopathic orthostatic intolerance. Thus, water drinking may serve as an adjunctive treatment in patients with impaired orthostatic tolerance.     

Orthostatic hypotension

A common problem among elderly people, orthostatic hypotension is associated with significant morbidity and mortality, which may be caused by medications, the cumulative effects of age- and hypertension-related alterations in blood pressure regulation, or age-associated diseases that impair autonomic function. Evaluation requires multiple blood pressure measurements taken at different times of the day and after meals or medications. Central and peripheral nervous system disorders should be sought, and the laboratory evaluation should concentrate on ruling out diabetes mellitus, amyloidosis, occult malignancy, and vitamin deficiencies. If orthostatic hypotension is detected, it should be considered a risk factor for adverse outcomes and treated first with nonpharmacologic interventions, including the withdrawal of potentially hypotensive medications. In patients with hypertension and orthostatic hypotension, the judicious treatment of hypertension may be helpful. For persistent, symptomatic orthostatic hypotension caused by autonomic failure, pharmacologic interventions include fludrocortisone, midodrine, and a variety of other agents. The careful evaluation and management of orthostatic hypotension will hopefully result in a significant reduction in falls, syncope, and fractures, and an attenuation of functional decline in elderly patients.     

体位性低血压的两种分型

体位性低血压是老年人中常见的体征,也是心脑血管疾病和跌倒的独立危险因素,并增加全因死亡率。目前在研究体位性低血压时,越来越多采用连续无创血压测量设备,且常结合直立倾斜试验,并根据血流动力学参数进行分型。本综述将重点介绍公认的两种分型,即形态学分型及生理学分型。     

Head-up tilt and hemodynamic changes during orthostatic hypotension in patients with supine hypertension

Objectives. This study assessed the mechanism(s) of the decrease in upright blood pressure in patients with supine hypertension by using the tilt test and a hemodynamic approach.Background. Orthostatic hypotension in patients with supine hypertension creates a pathophysiologic and therapeutic dilemma.Methods. We studied 28 consecutive patients with history of orthostatic intolerance amounting to recurrent syncope in 13 of them (15 men, 13 women; mean [SD] age 65 ± 11 years). They all had supine hypertension (systolic blood pressure >160 mm Hg) and orthostatic hypotension (found to be a decrease in systolic blood pressure >30 mm Hg during tilt test). Cardiac output, and orthostatic hypotension (found to be a decrease in systolic radionuclide first-pass technique (technetium-99m red blood cell tagging). Total blood volume was determined by radioiodinated serum albumin, and the ratio of cardiopulmonary to total blood volume was used as an index of venous capacitance.Results. Twenty-one patients had accentuated venous pooling defined as a tilt-induced decrease in cardiopulmonary volume/ total blood volume ratio >15% from baseline or a supine ratio < 14% (normal 16% to 18%), or both. Seven of the 28 patients had autonomic insufficiency; 6 of the 7 also had venous pooling; 1 patient had autonomic insufficiency only. Neither clinical history nor changes during tilt differentiated the subgroups. Plasma catecholamine levels increased during head-up tilt in all subgroups, and differences in their increase were not significant between patients with venous pooling and those with autonomic insufficiency. However, radionuclide hemodynamic variables revealed that patients with venous pooling compensated for the decrease in stroke volume by increasing peripheral resistance, whereas patients with autonomic dysfunction did not.Conclusions. Orthostatic hypotension in patients with supine hypertension may have multiple etiologies. Hemodynamic assessment with determination of cardiopulmonary volume and systemic vascular resistance differentiated between venous pooling and autonomic insufficiency in these patients; head-up tilt and plasma catecholamine levels did not. These findings may have important therapeutic implications.     

Is orthostatic hypotension in the elderly due to autonomic failure?

In order to investigate whether orthostatic hypotension in elderly people is due to autonomic nervous system dysfunction or blood vessel abnormalities, we have measured platelet and lymphocyte adrenoceptor numbers and agonist binding in addition to venous plasma catecholamine concentrations. Eight elderly subjects with orthostatic hypotension and six control elderly subjects were studied. None of the subjects had other symptoms of autonomic failure. There was no significant difference between the heart rate or plasma catecholamine responses to standing of the two groups. The orthostatic hypotension subjects had a significant rise of their plasma vasopressin levels whereas the control group had no significant change. The number of alpha 2-adrenoceptor sites in platelets was lower in the orthostatic hypotensive group compared to the controls and the binding affinity was greater than in the controls. There were no significant differences in beta-adrenoceptor binding sites or affinities in isolated lymphocytes between the two groups. The similar changes in heart rate and catecholamines together with the vasopressin changes suggest that, in these elderly patients with an abnormal drop of blood pressure on standing, there is no dysfunction of autonomic pathways concerned with cardiovascular function. The lower numbers of alpha 2-adrenoceptor sites on isolated platelets in subjects with orthostatic hypotension could indicate reduced alpha 2-adrenoceptor numbers on their blood vessels which could contribute to their inability to maintain blood pressure while standing.     

The role of body position and gravity in the symptoms and treatment of various medical diseases

Postural medicine studies the effects of gravity on human body functions and the ability to influence various diseases by changing the body's position. Orthostasis requires numerous cardiovascular and neurohumoral adaptations to prevent hypotension and a resulting decrease in cerebral perfusion. Sitting upright or in a semi-sitting position reduces venous return in patients with heart failure, intracranial pressure in patients with intracranial hypertension, intraocular pressure in glaucoma patients and may decrease gastro-oesophageal reflux. A left recumbent posture also decreases reflux. A right lateral position results in a lower sympathetic tone than lying on the left side and is beneficial in patients with heart failure or after an infarction without bradycardia. A 40 to 70% decreased prevalence of the sudden infant death syndrome has been observed since the recommendation to avoid laying infants to sleep in a prone position. Sleeping in a supine posture increases the severity of sleep apnoea compared to a lateral position. In patients with acute respiratory distress syndrome, a prone position can rapidly improve blood oxygenation. Idiopathic oedema, orthostatic proteinuria, intradiscal pressure and venous circulation in legs are improved in the decubitus position, whereas arterial flow is reduced. Health risks due to microgravity and prolonged bed rest, such as osteoporosis, venous thrombosis or pressure sores, are discussed.     

Orthostatic hypotension and supine hypertension in pure autonomic failure]

Orthostatic hypotension is associated with significant morbidity and mortality in elderly patients. In orthostatic hypotension caused by central and peripheral nervous system disorders (neurogenic orthostatic hypotension), the release of catecholamine in the standing posture is insufficient to compensate adequately for decreased venous return to the heart. Primary autonomic failure exhibits, often, supine hypertension, that can be worsened by pressor agents, such as midodrine, used to prevent syncope episodes. Salt-retaining steroid fludrocortisone, also, used to treat orthostatic hypotension, increases blood pressure both in supine and in standing position. We describe 3 patients with neurogenic orthostatic hypotension caused by pure autonomic failure. They complained of several syncope episodes. On examination, orthostatic hypotension and supine hypertension were detected in the absence of pharmacological therapy. All the patients presented hypertensive organ disease. Fludrocortisone acetate was started in one patient, and short-acting vasopressor agents during the day and dihydropyridine-calcium antagonist during the night in the other two. During the follow-up a transient ischemic attack occurred in the patient treated with fludrocortisone. When fludrocortisone was titrated down and short-acting antihypertensive drugs were started, the patient did not complain of any symptoms. Supine hypertension is part of pure autonomic failure, and short-acting antihypertensive agents should be associated with vasopressor agents to prevent hypertensive target organ disease.     

Gender differences in orthostatic hypotension

Orthostatic hypotension is a decrease in systolic blood pressure of more than 20 mm Hg or a decrease in diastolic blood pressure of at least 10 mm Hg, within 3 minutes of changing from a supine to an upright position. The typical clinical presentation of orthostatic hypotension includes dizziness, syncope, blurry vision and loss of balance. Symptoms may be more frequent in women, but the complicating roles played by comorbid factors and the estrogen mechanisms are not well understood. Women have a more active parasympathetic system, higher estrogen levels and a lower center of gravity. Thus, women less effectively compensate for the drop of blood pressure in response to positional change. An understanding of these mechanisms contributing to orthostatic hypotension may improve diagnosis and treatment of the problem.     

Twenty four hour continuous non-invasive finger blood pressure monitoring: a novel approach to the evaluation of treatment in patients with autonomic failure.

Occasional sphygmomanometric readings are not an effective way of evaluating the effect of treatment in patients with hypoadrenergic orthostatic hypotension. A novel non-invasive portable device (Portapres) was used to monitor 24 hour continuous finger blood pressure before and during chronic volume expansion in a 66 year old woman with severe orthostatic hypotension. In both conditions pressures while she was standing were lowest in the morning. Her tolerance to standing and walking increased during the day and, as a consequence of a higher upright mean blood pressure, was improved after treatment. Mean blood pressure during sleep was increased after treatment. Continuous 24 hour non-invasive finger blood pressure monitoring is a promising technique for the evaluation of the effect of treatment in patients with autonomic failure. It provides information about situations in daily life that cannot be obtained by laboratory tests or conventional sphygmomanometric measurements.