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Background There is no widely accepted validated scale to assess the comprehensive symptom burden and severity of neurogenic orthostatic hypotension (NOH). The Orthostatic Hypotension Questionnaire (OHQ) was developed, with two components: the six-item symptoms assessment scale and a four-item daily activity scale to assess the burden of symptoms. Validation analyses were then performed on the two scales and a composite score of the OHQ. Methods The validation analyses of the OHQ were performed using data from patients with NOH participating in a phase IV, double blind, randomized, cross over, placebo-controlled trial of the alpha agonist midodrine. Convergent validity was assessed by correlating OHQ scores with clinician global impression scores of severity as well as with generic health questionnaire scores. Test–retest reliability was evaluated using intraclass correlation coefficients at baseline and crossover in a subgroup of patients who reported no change in symptoms across visits on a patient global impression scores of change. Responsiveness was examined by determining whether worsening or improvement in the patients’ underlying disease status produced an appropriate change in OHQ scores. Results Baseline data were collected in 137 enrolled patients, follow-up data were collected in 104 patients randomized to treatment arm. Analyses were conducted using all available data. The floor and ceiling effects were minimal. OHQ scores were highly correlated with other patient reported outcome measures, indicating excellent convergent validity. Test–retest reliability was good. OHQ scores could distinguish between patients with severe and patients with less severe symptoms and responded appropriately to midodrine, a pressor agent commonly used to treat NOH. Conclusion These findings provide empirical evidence that the OHQ can accurately evaluate the severity of symptoms and the functional impact of NOH as well as assess the efficacy of treatment.

Cognitive impairment is prevalent in patients with chronic kidney disease (CKD), but its underlying mechanisms are obscure. Here, we test the hypothesis that exaggerated orthostatic blood pressure reduction mediates the effects of renal failure on global cognition and memory. A total of 160 study subjects were recruited, including 80 dialysis patients and 80 controls. Global cognition was evaluated using the Montreal Cognitive Assessment (MoCA), and episodic memory was evaluated using the auditory verbal learning test (AVLT). Autonomic function was evaluated via the low-frequency to high-frequency ratio (LF/HF) through heart rate variability analysis. Compared with the controls, the dialysis patients had significantly lower MoCA and AVLT scores (including learning memory, short recall memory, and delayed recall memory) (all p < 0.001). They also showed exaggerated orthostatic systolic blood pressure reductions (all p ≤ 0.001). The maximum orthostatic systolic blood pressure reduction was independently and negatively associated with short (β = -0.05, p = 0.029) and delayed (β = -0.05, p = 0.035) recall memory in dialysis patients but not in controls. Mediation analysis demonstrated that maximum orthostatic systolic blood pressure reduction mediates 13.8% of the effect of end-stage renal disease (ESRD) on short recall memory (p = 0.04). After adjustment for LF/HF, the negative association between maximum orthostatic blood pressure reduction and short recall score remained significant (p = 0.049), while the association between maximum orthostatic blood pressure reduction and delayed recall score became nonsignificant, with a marginal p value of 0.062. Our study reveals that exaggerated orthostatic blood pressure reduction is a possible explanation for ESRD-associated memory deficits.

Recognition of the importance of nonmotor dysfunction as a component of Parkinson's disease has exploded over the past three decades. Autonomic dysfunction is a frequent and particularly important nonmotor feature because of the broad clinical spectrum it covers. Cardiovascular, gastrointestinal, urinary, sexual, and thermoregulatory abnormalities all can appear in the setting of Parkinson's disease. Cardiovascular dysfunction is characterized most prominently by orthostatic hypotension. Gastrointestinal dysfunction can involve virtually all levels of the gastrointestinal tract. Urinary dysfunction can entail either too frequent voiding or difficulty voiding. Sexual dysfunction is frequent and frustrating for both patient and partner. Alterations in sweating and body temperature are not widely recognized but often are present. Autonomic dysfunction can significantly and deleteriously impact quality of life for individuals with Parkinson's disease. Because effective treatment for many aspects of autonomic dysfunction is available, it is vitally important that assessment of autonomic dysfunction be a regular component of the neurologic history and exam and that appropriate treatment be initiated and maintained.

Background Recent studies have shown that ingestion of glucose water lowers blood pressure (BP) in patients with perturbed autonomic control and more modestly lowers BP in elderly normal subjects. Whether glucose water affects cardiovascular control during orthostatic stress in normal young healthy subjects is unknown. We hypothesized that glucose water ingestion will reduce orthostatic tolerance in young healthy volunteers. Methods In a randomized, controlled, within-subject study, 15 healthy male subjects (21–28 years of age) ingested water or 10% glucose water 5 min before tilt-table testing. We measured finger BP, brachial BP, heart rate, and peripheral vascular resistance. Orthostatic tolerance was measured as the time to presyncope during a 70° head-up tilt, in which the head was tilted for 45 min or until presyncopal symptoms were observed. Results During the first 45 min of tilt, 8 of 15 subjects who ingested 10% glucose water experienced presyncope, but only 2 of 15 who ingested water (P = 0.029) experienced presyncope. Ingestion of 10% glucose water increased the heart rate significantly more than pure water during head-up tilt (P = 0.026). Ingestion of water increased the peripheral vascular resistance significantly >10% glucose water during the head-up tilt test (P = 0.013). Conclusions Ingestion of 10% glucose water impairs head-up tilt tolerance relative to water ingestion. The contrasting effect of 10% glucose water vs. pure water on orthostatic tolerance is associated with increased heart rate and attenuation of the increase in peripheral vascular resistance in head-up tilt testing.

Cardiovascular (CV) issues after spinal cord injury (SCI) are of paramount importance considering they are the leading cause of death in this population. Disruption of autonomic pathways leads to a highly unstable CV system, with impaired blood pressure (BP) and heart rate regulation. In addition to low resting BP, on a daily basis the majority of those with SCI suffer from transient episodes of aberrantly low and high BP (termed orthostatic hypotension and autonomic dysreflexia, respectively). In fact, autonomic issues, including resolution of autonomic dysreflexia, are frequently ranked by individuals with high-level SCI to be of greater priority than walking again. Owing to a combination of these autonomic disturbances and a myriad of lifestyle factors, the pernicious process of CV disease is accelerated post-SCI. Unfortunately, these secondary consequences of SCI are only beginning to receive appropriate clinical attention. Immediately after high-level SCI, major CV abnormalities present in the form of neurogenic shock. After subsiding, new issues related to BP instability arise, including orthostatic hypotension and autonomic dysreflexia. This review describes autonomic control over the CV system before injury and the mechanisms underlying CV abnormalities post-SCI, while also detailing the end-organ consequences, including those of the heart, as well as the systemic and cerebral vasculature. The tertiary impact of CV dysfunction will also be discussed, such as the potential impediment of rehabilitation, and impaired cognitive function. In the recent past, our understanding of autonomic dysfunctions post-SCI has been greatly enhanced; however, it is vital to further develop our understanding of the long-term consequences of these conditions, which will equip us to better manage CV disease morbidity and mortality in this population.

Autonomic symptoms and orthostatic syndromes have been reported in Long COVID, but few studies have characterized findings using head up tilt table testing. To characterize autonomic responses to positional changes among individuals with Long COVID. We assessed autonomic symptoms using the Composite Autonomic Symptom Scale 31 (COMPASS 31) instrument and performed head up tilt table testing for 30 minutes at 70 degrees among individuals with Long COVID and recovered comparators. We included 26 participants (median age 56 years, 50% female median 25 months after first COVID): 16 with Long COVID and 10 recovered comparators. COMPASS 31 scores (0-100, higher is worse) were higher among those with Long COVID (median 30.5 vs 8, p = 0.003). Heart rate was 8 beats per minutes higher throughout tilt among those with Long COVID (95% CI 1.1 to 14.4; p = 0.02); there were no differences in blood pressure. Ten (63%) with Long COVID had symptoms during tilt compared to none among recovered participants (p = 0.003). Three (19%) with Long COVID had clinically abnormal findings: one each with orthostatic hypotension, and delayed orthostatic hypotension, and cardioinhibitory/vasovagal presyncope. Among those with chronic autonomic symptoms in the setting of Long COVID, symptoms were common during tilt testing, and heart rate was increased, but most did not meet diagnostic criteria for a clinically abnormal hemodynamic response. Further research into mechanisms of autonomic symptoms in Long COVID is urgently needed.

Despite autonomic dysfunction after spinal cord injury (SCI) being the major cause of death and a top health priority, the clinical management options for these conditions are limited to drugs with delayed onset and nonpharmacological interventions with equivocal effectiveness. We tested the capacity of electrical stimulation, applied transcutaneously over the spinal cord, to manage autonomic dysfunction in the form of orthostatic hypotension after SCI. We assessed beat-by-beat blood pressure (BP), stroke volume, and cardiac contractility (dP/dt; Finometer), as well as cerebral blood flow (transcranial Doppler) in 5 individuals with motor-complete SCI (4 cervical, 1 thoracic) during an orthostatic challenge with and without transcutaneous electrical stimulation applied at the TVII level. During the orthostatic challenge, all individuals experienced hypotension characterized by a 37 ± 4 mm Hg decrease in systolic BP, a 52 ± 10% reduction in cardiac contractility, and a 23 ± 6% reduction in cerebral blood flow (all p < 0.05), along with severe self-reported symptoms. Electrical stimulation completely normalized BP, cardiac contractility, cerebral blood flow, and abrogated all symptoms. Noninvasive transcutaneous electrical spinal cord stimulation may be a viable therapy for restoring autonomic cardiovascular control after SCI.

Gravity, an invisible but constant force , challenges the regulation of blood pressure when transitioning between postures. As physiological reserve diminishes with age, individuals grow more susceptible to such stressors over time, risking inadequate haemodynamic control observed in orthostatic hypotension. This prevalent condition is characterized by drops in blood pressure upon standing; however, the contrary phenomenon of blood pressure rises has recently piqued interest. Expanding on the currently undefined orthostatic hypertension, our study uses continuous non‐invasive cardiovascular data to explore the full spectrum of blood pressure profiles and their associated frailty outcomes in community‐dwelling older adults. Given the richness of non‐invasive beat‐to‐beat data, artificial intelligence (AI) offers a solution to detect the subtle patterns within it. Applying machine learning to an existing dataset of community‐based adults undergoing postural assessment, we identified three distinct clusters (iOHYPO, OHYPO and OHYPER) akin to initial and classic orthostatic hypotension and orthostatic hypertension, respectively. Notably, individuals in our OHYPER cluster exhibited indicators of frailty and sarcopenia, including slower gait speed and impaired balance. In contrast, the iOHYPO cluster, despite transient drops in blood pressure, reported fewer fallers and superior cognitive performance. Surprisingly, those with sustained blood pressure deficits outperformed those with sustained rises, showing greater independence and higher Fried frailty scores. Working towards more refined definitions, our research indicates that AI approaches can yield meaningful blood pressure morphologies from beat‐to‐beat data. Furthermore, our findings support orthostatic hypertension as a distinct clinical entity, with frailty implications suggesting that it is worthy of further investigation. What is the central question of this study? Can blood pressure morphologies akin to those found in dysregulated postural blood pressure conditions be identified from continuous non‐invasive cardiovascular data using artificial intelligence? What are the main findings and their importance? The findings revealed differences in frailty phenotypes between morphologies indicative of orthostatic hypotension and orthostatic hypertension, with increased frailty being associated with orthostatic hypertension. These results add to the emerging evidence for the clinical significance of the currently undefined condition of orthostatic hypertension.

Orthostatic hypertension—a condition characterized by a hyper-reactive pressor response to orthostatic stress—is an emerging new risk factor for the development of hypertension, hypertensive target-organ damage and subsequent cardiovascular events. In this Review, Kazuomi Kario describes the diagnosis, epidemiology and pathophysiology of orthostatic hypertension and discusses its clinical implications. Orthostatic hypertension—a condition characterized by a hyperactive pressor response to orthostatic stress—is an emerging risk factor for cardiovascular disease and is associated with hypertensive target-organ damage (resulting in silent cerebrovascular disease, left ventricular hypertrophy, carotid atherosclerosis and/or chronic kidney disease) and cardiovascular events (such as coronary artery disease and lacunar stroke). The condition is also considered to be a form of prehypertension as it precedes hypertension in young, normotensive adults. Orthostatic blood pressure changes can be assessed using orthostatic stress tests, including clinic active standing tests, home blood pressure monitoring and the head-up tilting test. Devices for home and for ambulatory blood pressure monitoring that are equipped with position sensors and do not induce a white-coat effect have increased the sensitivity and specificity of diagnosis of out-of-clinic orthostatic hypertension. Potential major mechanisms of orthostatic hypertension are sympathetic hyperactivity (as a result of hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyperactivation. Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome. Key Points Orthostatic hypertension is characterized by a hyper-reactive pressor response to orthostatic stress and is an emerging risk factor for organ damage and cardiovascular disease The condition increases the pulsatile haemodynamic stress of central arterial pressure and blood flow, resulting in progression of systemic haemodynamic atherothrombotic syndrome Orthostatic hypertension precedes hypertension and is considered to be a form of prehypertension and a biomarker of masked hypertension in patients with normal sitting blood pressure levels Sympathetic hyperactivity (resulting from hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyper-reactive vascular disease are potential major mechanisms of orthostatic hypertension Further studies are needed to demonstrate whether orthostatic hypertension is only a marker or one of the leading causes of target-organ damage and cardiovascular events

Orthostatic hypotension (OH) is a common inpatient condition associated with falls, syncope, and mortality. However, standardized approaches for inpatient management of OH are lacking and may vary across clinical specialties. In this retrospective observational cohort study, we reviewed the electronic medical records of patients admitted to Beth Israel Deaconess Medical Center between April 1, 2015 and June 1, 2021 with a diagnosis of OH or medication‐related hypotension. Variables of interest included admitting service, presenting symptoms, suspected etiology, and management. Among the 400 inpatients with OH, one‐third had OH documented on admission. Dizziness and lightheadedness were the most common symptoms; medical patients experienced dizziness, falls, and other symptoms more frequently than surgical patients. Volume depletion and medications were the leading suspected causes of OH. Surgical patients were less likely to have medication‐related OH and were more likely to lack an identified etiology. Cardiovascular disease was more frequently implicated in cardiology patients. Volume depletion, neurodegenerative disease, and other conditions were more often suspected among medical patients. Management commonly involved volume resuscitation and medication adjustment, though medication changes were less frequent in surgical patients. Nonpharmacologic interventions were more common among medical patients. By discharge, OH had resolved in only one‐third of patients. In summary, inpatient OH was most often identified after admission, attributed to hypovolemia, treated with fluids, and unresolved at discharge, with differences in symptoms, etiology, and management between specialties. Prospective studies are needed to formalize diagnostic and treatment strategies for OH in the hospital setting.