Individualized Contrast Media Application Based on Body Weight and Contrast Enhancement in Computed Tomography of Livers without Steatosis.

This study analyzes the homogeneity in liver attenuation of a body-weight-based protocol compared to a semi-fixed protocol. Patients undergoing abdominal multiphase computed tomography received 0.500 g of iodine (gI) per kilogram of body weight. Liver attenuation and enhancement were determined using regions of interest on scans in the pre-contrast and portal venous phases. The outcomes were analyzed for interpatient uniformity in weight groups. The subjective image quality was scored using a four-point Likert scale (excellent, good, moderate, and nondiagnostic). A total of 80 patients were included (56.3% male, 64 years, 78.0 kg) and were compared to 80 propensity-score-matched patients (62.5% male, 63 years, 81.7 kg). The liver attenuation values for different weight groups of the TBW-based protocol were not significantly different (p = 0.331): 109.1 ± 13.8 HU (≤70 kg), 104.6 ± 9.70 HU (70−90 kg), and 105.1 ± 11.6 HU (≥90 kg). For the semi-fixed protocol, there was a significant difference between the weight groups (p < 0.001): 121.1 ± 12.1 HU (≤70 kg), 108.9 ± 11.0 HU (70−90 kg), and 105.0 ± 9.8 HU (≥90 kg). For the TBW-based protocol, the enhancement was not significantly different between the weight groups (p = 0.064): 46.2 ± 15.1 HU (≤70 kg), 59.3 ± 6.8 HU (70−90 kg), and 52.1 ± 11.7 HU (≥90 kg). Additionally, for the semi-fixed protocol, the enhancement was not significantly different between the weight groups (p = 0.069): 59.4 ± 11.0 HU (≤70 kg), 53.0 ± 10.3 HU (70−90 kg), and 52.4 ± 7.5 HU (≥90 kg). The mean administered amount of iodine per kilogram was less for the TBW-based protocol compared to the semi-fixed protocol: 0.499 ± 0.012 and 0.528 ± 0.079, respectively (p = 0.002). Of the TBW-based protocol, 17.5% of the scans scored excellent enhancement quality, 76.3% good, and 6.3% moderate. Of the semi-fixed protocol, 70.0% scored excellent quality, 21.3% scored good, and 8.8% scored moderate. In conclusion, the TBW-based protocol increased the interpatient uniformity of liver attenuation but not the enhancement in the portal venous phase compared to the semi-fixed protocol, using an overall lower amount of contrast media and maintaining good subjective image quality.

Computed tomography-based calcium scoring in cadaver leg arteries: Influence of dose, reader, and reconstruction algorithm.

PURPOSE: Computed tomography (CT) might be a good diagnostic test to accurately quantify calcium in vascular beds but there are multiple factors influencing the quantification. The aim of this study was to investigate the influence of different computed tomography protocol settings in the quantification of calcium in the lower extremities using modified Agatston and volume scores. METHODS: Fresh-frozen human legs were scanned at different tube current protocols and reconstructed at different slice thickness. Two different iterative reconstruction protocols for conventional CT images were compared. Calcium was manually scored using modified Agatston and volume scores. Outcomes were statistically analyzed using Wilcoxon signed-rank tests and mean absolute and relative differences were plotted in Bland-Altman plots. RESULTS: Of the 20 legs, 16 had CT detectable calcifications. Differences between thick and thin slice reconstruction protocols were 129 Agatston units and 125% for Agatston and 78.4 mm3 and 57.8% for volume (all p ≤ 0.001). No significant differences were found between low and high tube current protocols. Differences between iDose4 and IMR reconstruction protocols for modified Agatston were 34.2 Agatston units and 17.7% and the volume score 33.5 mm3 and 21.2% (all p ≤ 0.001). CONCLUSIONS: Slice thickness reconstruction and reconstruction method protocols influenced the modified Agatston and volume scores in leg arteries, but tube current and different observers did not have an effect. This data emphasizes the need for standardized quantification of leg artery calcifications. Possible implications are in the development of a more universal quantification method, independent of the type of scan and vasculature.

Quantification of Calcium in Peripheral Arteries of the Lower Extremities: Comparison of Different CT Scanners and Scoring Platforms.

OBJECTIVES: The aim of this study was to investigate the interscanner and interscoring platform variability of calcium quantification in peripheral arteries of the lower extremities. MATERIALS AND METHODS: Twenty human fresh-frozen legs were scanned using 3 different computed tomography (CT) scanners. The radiation dose (CTDIvol) was kept similar for all scanners. The calcium scores (Agatston and volume scores) were quantified using 4 semiautomatic scoring platforms. Comparative analysis of the calcium scores between scanners and scoring platforms was performed by using the Friedman test; post hoc analysis was performed by using the Wilcoxon signed rank test with Bonferroni correction. RESULTS: Sixteen legs had calcifications and were used for data analysis. Agatston and volume scores ranged from 12.1 to 6580 Agatston units and 18.2 to 5579 mm3. Calcium scores differed significantly between Philips IQon and Philips Brilliance 64 (Agatston: 19.5% [P = 0.001]; volume: 14.5% [P = 0.001]) and Siemens Somatom Force (Agatston: 18.1% [P = 0.001]; volume: 17.5% [P = 0.001]). The difference between Brilliance 64 and Somatom Force was smaller (Agatston: 5.6% [P = 0.778]; volume: 7.7% [P = 0.003]). With respect to the interscoring platform variability, OsiriX produced significantly different Agatston scores compared with the other 3 scoring platforms (OsiriX vs IntelliSpace: 14.8% [P = 0.001] vs Syngo CaScore: 13.9% [P = 0.001] vs iX viewer: 13.2% [P < 0.001]). For the volume score, the differences between all scoring platforms were small ranging from 2.9% to 4.0%. Post hoc analysis showed a significant difference between OsiriX and IntelliSpace (3.8% [P = 0.001]). CONCLUSIONS: The use of different CT scanners resulted in notably different Agatston and volume scores, whereas the use of different scoring platforms resulted in limited variability especially for the volume score. In conclusion, the variability in calcium quantification was most evident between different CT scanners and for the Agatston score.

Liver Enhancement on Computed Tomography Is Suboptimal in Patients with Liver Steatosis.

This study's aim was twofold. Firstly, to assess liver enhancement quantitatively and qualitatively in steatotic livers compared to non-steatotic livers on portal venous computed tomography (CT). Secondly, to determine the injection volume of contrast medium in patients with severe hepatic steatosis to improve the image quality of the portal venous phase. We retrospectively included patients with non-steatotic (n = 70), the control group, and steatotic livers (n = 35) who underwent multiphase computed tomography between March 2016 and September 2020. Liver enhancement was determined by the difference in attenuation in Hounsfield units (HU) between the pre-contrast and the portal venous phase, using region of interests during in three different segments. Liver steatosis was determined by a mean attenuation of ≤40 HU on unenhanced CT. Adequate enhancement was objectively defined as ≥50 ΔHU and subjectively using a three-point Likert scale. Enhancement of non-steatotic and steatotic livers were compared and associations between enhancement and patient- and scan characteristics were analysed. Enhancement was significantly higher among the control group (mean 51.9 ± standard deviation 11.5 HU) compared to the steatosis group (40.6 ± 8.4 HU p for difference < 0.001). Qualitative analysis indicated less adequate enhancement in the steatosis group: 65.7% of the control group was rated as good vs. 8.6% of the steatosis group. We observed a significant correlation between enhancement, and presence/absence of steatosis and grams of iodine per total body weight (TBW) (p < 0.001; adjusted R2 = 0.303). Deduced from this correlation, theoretical contrast dosing in grams of Iodine (g I) can be calculated: g I = 0.502 × TBW for non-steatotic livers and g I = 0.658 × TBW for steatotic livers. Objective and subjective enhancement during CT portal phase were significantly lower in steatotic livers compared to non-steatotic livers, which may have consequences for detectability and contrast dosing.

Towards Personalised Contrast Injection: Artificial-Intelligence-Derived Body Composition and Liver Enhancement in Computed Tomography.

In contrast-enhanced computed tomography, total body weight adapted contrast injection protocols have proven successful in achieving a homogeneous enhancement of vascular structures and liver parenchyma. However, because solid organs have greater perfusion than adipose tissue, the lean body weight (fat-free mass) rather than the total body weight is theorised to cause even more homogeneous enhancement. We included 102 consecutive patients who underwent a multiphase abdominal computed tomography between March 2016 and October 2019. Patients received contrast media (300 mgI/mL) according to bodyweight categories. Using regions of interest, we measured the Hounsfield unit (HU) increase in liver attenuation from unenhanced to contrast-enhanced computed tomography. Furthermore, subjective image quality was graded using a four-point Likert scale. An artificial intelligence algorithm automatically segmented and determined the body compositions and calculated the percentages of lean body weight. The hepatic enhancements were adjusted for iodine dose and iodine dose per total body weight, as well as percentage lean body weight. The associations between enhancement and total body weight, body mass index, and lean body weight were analysed using linear regression. Patients had a median age of 68 years (IQR: 58-74), a total body weight of 81 kg (IQR: 73 - 90), a body mass index of 26 kg/m2 (SD: ±4.2), and a lean body weight percentage of 50% (IQR: 36 - 55). Mean liver enhancements in the portal venous phase were 61 ± 12 HU (≤ 70 kg), 53 ± 10 HU (70 - 90 kg), and 53 ± 7 HU (≥ 90 kg). The majority (93%) of scans were rated as good or excellent. Regression analysis showed significant correlations between liver enhancement corrected for injected total iodine and total body weight (r = 0.53; p < 0.001) and between liver enhancement corrected for lean body weight and the percentage of lean body weight (r = 0.73; p < 0.001). Most benefits from personalising iodine injection using %LBW additive to total body weight would be achieved in patients under 90 kg. Liver enhancement is more strongly associated with the percentage of lean body weight than with the total body weight or body mass index. The observed variation in liver enhancement might be reduced by a personalised injection based on the artificial-intelligence-determined percentage of lean body weight.

Longitudinal changes in the control mechanisms for blood pressure and cerebral blood flow in Alzheimer's disease: Secondary results of a randomized controlled trial.

Objective: Dynamic cerebral autoregulation (dCA) and baroreflex sensitivity (BRS) are key mechanisms involved in the homeostasis of blood pressure (BP) and cerebral blood flow. We assessed changes in these mechanisms in Alzheimer's disease (AD) during a 1.5 year follow-up. Methods: In this secondary analysis of a randomized controlled trial we measured beat-to-beat BP, heart rate, and cerebral blood flow velocity at baseline, 0.5 and 1.5 years, during: rest (spontaneous oscillations), repeated sit-stand maneuvers (induced oscillations), an orthostatic challenge, and hypo- and hypercapnia. dCA was estimated using transfer function analysis and the autoregulatory index on spontaneous and induced oscillations. BRS was estimated by calculating the heart rate response to BP changes during induced oscillations. Linear mixed models were used to assess changes over time. Results: 56 patients were included (mean age:73 ± 6 years, 57% female). BRS did not change over time. dCA parameters showed small changes after 0.5 years, suggestive of a reduction in efficiency (e.g. higher gain [linear mixed effect model: B = 0.09, SE = 0.03, P = 0.008] and lower phase [B = -9.7, SE= 3.2, P = 0.004] in the very low frequency domain, and lower autoregulatory index during induced oscillations [B = -0.69, SE = 0.26, P = 0.010]). These changes did not show further progression after 1.5 years of follow-up. Discussion: In this sample of patients with dementia due to AD we found no evidence that dCA or BRS become impaired during AD progression. This paves the way for further studies that investigate the safety and benefits of antihypertensive treatment in patients with AD.

Orthostatic Blood Pressure Recovery Is Associated With the Rate of Cognitive Decline and Mortality in Clinical Alzheimer's Disease.

BACKGROUND: Impaired recovery of blood pressure (BP) after standing has been shown to be related to cognitive function and mortality in people without dementia, but its role in people with Alzheimer's disease (AD) is unknown. The aim of this study was to investigate the association of the orthostatic BP response with cognitive decline and mortality in AD. METHODS: In this post hoc analysis of a randomized controlled trial (Nilvad), we measured the beat-to-beat response of BP upon active standing in mild-to-moderate AD. This included the initial drop (nadir within 40 seconds) and recovery after 1 minute, both expressed relative to resting values. We examined the relationship between a small or large initial drop (median split) and unimpaired (≥100%) or impaired recovery (<100%) with 1.5-year change in Alzheimer's Disease Assessment-cognitive subscale (ADAS-cog) scores and all-cause mortality. RESULTS: We included 55 participants (age 73.1 ± 6.2 years). Impaired BP recovery was associated with higher increases in ADAS-cog scores (systolic: ß [95% confidence interval] = 5.6 [0.4-10.8], p = .035; diastolic: 7.6 [2.3-13.0], p = .006). During a median follow-up time of 49 months, 20 participants died. Impaired BP recovery was associated with increased mortality (systolic: HR [95% confidence interval] = 2.9 [1.1-7.8], p = .039; diastolic: HR [95% confidence interval] = 5.5 [1.9-16.1], p = .002). The initial BP drop was not associated with any outcome. Results were adjusted for age, sex, and intervention group. CONCLUSIONS: Failure to fully recover BP after 1 minute of standing is associated with cognitive decline and mortality in AD. As such, BP recovery can be regarded as an easily obtained marker of progression rate of AD.

Effects of Nilvadipine on Cerebral Blood Flow in Patients With Alzheimer Disease.

Cerebrovascular changes, including reduced cerebral blood flow (CBF), occur early in the development of Alzheimer disease and may accelerate disease progression. This randomized, double-blind, placebo-controlled study investigated how 6 months of treatment with the calcium antagonist nilvadipine would affect CBF in patients with mild-to-moderate Alzheimer disease. CBF was measured with magnetic resonance arterial spin labeling in whole-brain gray matter and in a priori defined regions of interest including the hippocampus. Fifty-eight patients were randomly assigned (29 in each group), of whom 22 in both groups had no magnetic resonance exclusion criteria and were medication compliant over 6 months. Mean age was 72.8±6.2 years, mean mini-mental state examination was 20.4±3.4. Nilvadipine treatment lowered systolic blood pressure (Δ=-11.5 [95% CI, -19.7 to -3.2] mm Hg; P<0.01), while whole-brain gray-matter CBF remained stable (Δ=5.4 [95% CI, -6.4 to 17.2] mL/100 g per minute; P=0.36). CBF in the hippocampus increased (left: Δ=24.4 [95% CI, 4.3-44.5] mL/100 g per minute; P=0.02; right: Δ=20.1 [95% CI, -0.6 to 40.8] mL/100 g per minute; P=0.06). There was no significant change in CBF in the posterior cingulate cortex (Δ=5.2 [95% CI, -16.5 to 27.0] mL/100 g per minute; P=0.63) or other regions of interest. In conclusion, nilvadipine reduced blood pressure and increased CBF in the hippocampus, whereas other regions showed stable or small nonsignificant increases in CBF. These findings not only indicate preserved cerebral autoregulation in Alzheimer disease but also point toward beneficial cerebrovascular effects of antihypertensive treatment. Clinical Trial Registration- URL: http://www.clinicaltrials.gov . Unique identifier: NCT02017340.

Dynamic Regulation of Cerebral Blood Flow in Patients With Alzheimer Disease.

Cerebral autoregulation and baroreflex sensitivity are key mechanisms that maintain cerebral blood flow. This study assessed whether these control mechanisms are affected in patients with dementia and mild cognitive impairment due to Alzheimer disease, as this would increase the risks of antihypertensive treatment. We studied 53 patients with dementia (73.1 years [95% confidence interval (CI), 71.4-74.8]), 37 patients with mild cognitive impairment (69.2 years [95% CI, 66.4-72.0]), and 47 controls (69.4 years [95% CI, 68.3-70.5]). Beat-to-beat blood pressure (photoplethysmography), heart rate, and cerebral blood flow velocity (transcranial Doppler) were measured during 5-minute rest (sitting) and 5 minutes of orthostatic challenges, using repeated sit-to-stand maneuvers. Cerebral autoregulation was assessed using transfer function analysis and the autoregulatory index. Baroreflex sensitivity was estimated with transfer function analysis and by calculating the heart rate response to blood pressure changes during the orthostatic challenges. Dementia patients had the lowest cerebral blood flow velocity (P=0.004). During rest, neither transfer function analysis nor the autoregulatory index indicated impairments in cerebral autoregulation. During the orthostatic challenges, higher autoregulatory index (P=0.011) and lower transfer function gain (P=0.017), indicating better cerebral autoregulation, were found in dementia (4.56 arb. unit [95% CI, 4.14-4.97]; 0.59 cm/s per mm Hg [95% CI, 0.51-0.66]) and mild cognitive impairment (4.59 arb. unit [95% CI, 4.04-5.13]; 0.51 cm/s per mm Hg [95% CI, 0.44-0.59]) compared with controls (3.71 arb. unit [95% CI, 3.35-4.07]; 0.67 cm/s per mm Hg [95% CI, 0.59-0.74]). Baroreflex sensitivity measures did not differ between groups. In conclusion, the key mechanisms to control blood pressure and cerebral blood flow are not reduced in 2 stages of Alzheimer disease compared with controls, both in rest and during orthostatic changes that reflect daily life challenges.

Lack of linear correlation between dynamic and steady-state cerebral autoregulation.

KEY POINTS: For correct application and interpretation of cerebral autoregulation (CA) measurements in research and in clinical care, it is essential to understand differences and similarities between dynamic and steady-state CA. The present study found no correlation between dynamic and steady-state CA indices in healthy older adults. There was variability between individuals in all (steady-state and dynamic) autoregulatory indices, ranging from low (almost absent) to highly efficient CA in this healthy population. These findings challenge the assumption that assessment of a single CA parameter or a single set of parameters can be generalized to overall CA functioning. Therefore, depending on specific research purposes, the choice for either steady-state or dynamic measures or both should be weighed carefully. ABSTRACT: The present study aimed to investigate the relationship between dynamic (dCA) and steady-state cerebral autoregulation (sCA). In 28 healthy older adults, sCA was quantified by a linear regression slope of proportionate (%) changes in cerebrovascular resistance (CVR) in response to proportionate (%) changes in mean blood pressure (BP) induced by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infusion. Cerebral blood flow (CBF) was measured at the internal carotid artery (ICA) and vertebral artery (VA) and CBF velocity at the middle cerebral artery (MCA). With CVR = BP/CBF, Slope-CVRICA , Slope-CVRVA and Slope-CVRiMCA were derived. dCA was assessed (i) in supine rest, analysed with transfer function analysis (gain and phase) and autoregulatory index (ARI) fit from spontaneous oscillations (ARIBaseline ), and (ii) with transient changes in BP using a bolus injection of SNP (ARISNP ) and PhE (ARIPhE ). Comparison of sCA and dCA parameters (using Pearson's r for continuous and Spearman's ρ for ordinal parameters) demonstrated a lack of linear correlations between sCA and dCA measures. However, comparisons of parameters within dCA and within sCA were correlated. For sCA slope-CVRVA with Slope-CVRiMCA (r = 0.45, P < 0.03); for dCA ARISNP with ARIPhE (ρ = 0.50, P = 0.03), ARIBaseline (ρ = 0.57, P = 0.03) and PhaseLF (ρ = 0.48, P = 0.03); and for GainVLF with GainLF (r = 0.51, P = 0.01). By contrast to the commonly held assumption based on an earlier study, there were no linear correlations between sCA and dCA. As an additional observation, there was strong inter-individual variability, both in dCA and sCA, in this healthy group of elderly, in a range from low to high CA efficiency.

European multicentre double-blind placebo-controlled trial of Nilvadipine in mild-to-moderate Alzheimer's disease-the substudy protocols: NILVAD frailty; NILVAD blood and genetic biomarkers; NILVAD cerebrospinal fluid biomarkers; NILVAD cerebral blood flow.

INTRODUCTION: In conjunction with the NILVAD trial, a European Multicentre Double-Blind Placebo Controlled trial of Nilvadipine in Mild-to-Moderate Alzheimer's disease (AD), there are four NILVAD substudies in which eligible NILVAD patients are also invited to participate. The main NILVAD protocol was previously published in BMJ Open (2014). The objectives of the NILVAD substudies are to determine whether frailty, cerebrospinal fluid (CSF), blood biomarker profile and Apolipoprotein E (APOE) status predict response to Nilvadipine, and to investigate the effect of Nilvadipine on cerebral blood flow and blood biomarkers. METHODS AND ANALYSIS: All participants who fulfil criteria for the main NILVAD study are eligible for participation in the NILVAD substudies. Participation is subject to informed consent and whether the substudy is available at a particular NILVAD study site. Each substudy entails extra measurements during the course of the main NILVAD study. For example, in the blood and genetic biomarkers substudy, extra blood (30 mL) will be collected at week 0, week 13, week 52 and week 78, while in the cerebral blood flow substudy, participants will receive an MRI and transcranial Doppler measurements at week 0, week 26 and week 78. In the CSF substudy, 10 mL CSF is collected at week 0 and week 78. ETHICS AND DISSEMINATION: All NILVAD substudies and all subsequent amendments have received ethical approval within each participating country, according to national regulations. Each participant provides written consent to participate. All participants remain anonymised throughout and the results of each substudy will be published in an international peer reviewed journal. TRIAL REGISTRATION NUMBER: EUDRACT 2012-002764-27; Pre-results.

How measurement artifacts affect cerebral autoregulation outcomes: A technical note on transfer function analysis.

Cerebral autoregulation (CA) is the mechanism that aims to maintain adequate cerebral perfusion during changes in blood pressure (BP). Transfer function analysis (TFA), the most reported method in literature to quantify CA, shows large between-study variability in outcomes. The aim of this study is to investigate the role of measurement artifacts in this variation. Specifically, the role of distortion in the BP and/or CBFV measurementon TFA outcomes was investigated. The influence of three types of artifacts on TFA outcomes was studied: loss of signal, motion artifacts, and baseline drifts. TFA metrics of signals without the simulated artifacts were compared with those of signals with artifacts. TFA outcomes scattered highly when more than 10% of BP signal or over 8% of the CBFV signal was lost, or when measurements contained one or more artifacts resulting from head movement. Furthermore, baseline drift affected interpretation of TFA outcomes when the power in the BP signal was 5 times the power in the LF band. In conclusion, loss of signal in BP and loss in CBFV, affects interpretation of TFA outcomes. Therefore, it is vital to validate signal quality to the defined standards before interpreting TFA outcomes.

Central artery stiffness, baroreflex sensitivity, and brain white matter neuronal fiber integrity in older adults.

Cerebral hypoperfusion elevates the risk of brain white matter (WM) lesions and cognitive impairment. Central artery stiffness impairs baroreflex, which controls systemic arterial perfusion, and may deteriorate neuronal fiber integrity of brain WM. The purpose of this study was to examine the associations among brain WM neuronal fiber integrity, baroreflex sensitivity (BRS), and central artery stiffness in older adults. Fifty-four adults (65 ± 6 years) with normal cognitive function or mild cognitive impairment (MCI) were tested. The neuronal fiber integrity of brain WM was assessed from diffusion metrics acquired by diffusion tensor imaging. BRS was measured in response to acute changes in blood pressure induced by bolus injections of vasoactive drugs. Central artery stiffness was measured by carotid-femoral pulse wave velocity (cfPWV). The WM diffusion metrics including fractional anisotropy (FA) and radial (RD) and axial (AD) diffusivities, BRS, and cfPWV were not different between the control and MCI groups. Thus, the data from both groups were combined for subsequent analyses. Across WM, fiber tracts with decreased FA and increased RD were associated with lower BRS and higher cfPWV, with many of the areas presenting spatial overlap. In particular, the BRS assessed during hypotension was strongly correlated with FA and RD when compared with hypertension. Executive function performance was associated with FA and RD in the areas that correlated with cfPWV and BRS. These findings suggest that baroreflex-mediated control of systemic arterial perfusion, especially during hypotension, may play a crucial role in maintaining neuronal fiber integrity of brain WM in older adults.

Geriatric hypotensive syndromes are not explained by cardiovascular autonomic dysfunction alone.

BACKGROUND: Though highly prevalent, the pathophysiology of orthostatic hypotension (OH), postprandial hypotension (PPH), and carotid sinus hypersensitivity (CSH) are rarely studied together. Therefore, we conducted such a comprehensive study focusing on the common role of the cardiovascular autonomic system. We hypothesized that in geriatric patients, OH, PPH, and CSH are manifestations of cardiovascular autonomic dysfunction and investigated state-of-the-art cardiovascular autonomic function indices in a group of geriatric falls or syncope patients. METHODS: In a cross-sectional study of 203 consecutive eligible falls clinic patients, we compared heart rate variability (HRV), blood pressure variability (BPV), and baroreflex sensitivity (BRS) as potential autonomic function determinants of the three different hypotensive syndromes. RESULTS: OH, PPH, and CSH were diagnosed in 53%, 57%, and 50% of the patients, respectively. In a population relevant for geriatric practice, we found no differences in HRV, BPV, and BRS between patients with and without OH, with and without PPH, and with and without CSH, respectively, nor between patients with and without falls, dizziness, or syncope as presenting symptom, respectively. CONCLUSIONS: In geriatric patients with hypotensive syndromes, cardiovascular autonomic function as measured by HRV, BPV, and BRS is comparable to patients without such syndromes. These findings argue against a single or dominant etiological factor, that is, cardiac autonomic dysfunction and underline the structured, broad, and multifactorial approach to elderly patients with falls and/or syncope as proposed in the current evidence-based syncope guidelines.