Clinical Autonomic Research最新文献

Purpose: The semiautomated carbon monoxide (CO) rebreathing method has been introduced as a noninvasive and radiation-free blood volume estimation method. We tested whether the semiautomated CO rebreathing method can detect the blood volume deficit in postural orthostatic tachycardia syndrome (POTS). In addition, we explored the relationship between blood volume estimated from CO rebreathing and body impedance.

Patients and methods: We recruited 53 subjects (21 female patients with POTS, 19 healthy female participants, and 13 healthy male participants) to record blood volumes and hemodynamic data. Blood volumes were measured by CO rebreathing and segmental body impedance. Linear regression models to predict normal values of red blood cell volume (RBCV), plasma volume (PV), and total blood volume (BV) were developed. Percentage deviations from the predicted normal volumes were calculated.

Results: Patients with POTS had lower RBCV (25.18 ± 3.95 versus 28.57 ± 3.68 mL/kg, p = 0.008, patients with POTS versus healthy female participants), BV (64.53 ± 10.02 versus 76.78 ± 10.00 mL/kg, p < 0.001), and BV deviation (-13.92 ± 10.38% versus -0.02 ± 10.18%, p < 0.001). Patients with POTS had higher supine heart rate (HR) (84 ± 14 versus 69 ± 11 bpm, p < 0.001) and upright HR (123 ± 23 versus 89 ± 22 bpm, p < 0.001). We found a correlation between BV deviation and upright HR in patients with POTS (r = -0.608, p = 0.003), but not in healthy participants. Volumes from the CO rebreathing and body impedance were well correlated (r = 0.629, p < 0.001).

Conclusions: The CO rebreathing method can detect BV deficit, as well as the RBCV deficit in patients with POTS. The negative correlation between BV deviation and upright HR indicates that hypovolemia is one of the pathophysiological causes of POTS. Correlations between body impedance and CO rebreathing volume suggest its usefulness for measurements of volume changes.

Purpose: The use of circulatory assist devices has been shown to improve glomerular filtration rate and reduce the incidence of acute kidney injury in patients following acute cardiac pathology. However, the mechanisms of improvement in kidney function are not clear. We tested the hypothesis that mechanical circulatory support would result in a decrease in directly recorded renal sympathetic nerve activity (RSNA) and mediate the improvement in renal blood flow (RBF) in a setting of acute myocardial infarction (AMI)-induced left ventricular systolic dysfunction.

Methods: An anaesthetized ovine model was used to induce AMI (n = 8) using injections of microspheres into the left coronary artery in one group. The second group did not undergo embolization (n = 6). The effects of mechanical circulatory support using the Impella CP on directly recorded renal sympathetic nerve activity were examined in these two groups of animals.

Results: Injection of microspheres resulted in a drop in mean arterial pressure (MAP) of 21 ± 4 mmHg compared to baseline values (p < 0.05; n = 8). This was associated with a 67% increase in renal sympathetic nerve activity (RSNA; from 16 ± 5 to 21 ± 5 spikes/s; p < 0.05; n = 7). Impella CP support significantly increased MAP by 13 ± 1.5 mmHg at pump level 8 (p < 0.05) in the AMI group. Incremental pump support resulted in a significant decrease in RSNA (p < 0.05) in both groups. At pump level P8 in the AMI group, RSNA was decreased by 21 ± 5.5% compared to pump level P0 when the pump was not on.

Conclusion: Our data indicate that the improvement in kidney function following mechanical circulatory support may be mediated in part by renal sympathoinhibition.

Purpose: We compared standing and upright tilt in patients with postural tachycardia syndrome (POTS) and healthy volunteers to determine whether standing accurately tests for POTS in youngsters < 19 years. POTS in adolescents is defined by orthostatic intolerance plus sustained excessive upright tachycardia, without hypotension during upright tilt. We examined whether active standing is a valid classifier for POTS in adolescents compared to tilt.

Methods: Patients with POTS (N = 36, 12.2-18.8 years) and healthy volunteers (N = 39, 13.1-18.9 years) performed stand for a minimum of 5-min and were tilted to 70° for 10 min. Receiver operating characteristics analyses (ROC) were performed at 5-min stand, and at 5  and 10 min tilt for optimal threshold for heart rate (HR) increase (ΔHR), and test sensitivity and specificity.

Results: Most subjects were unable to stand for 10 min. ΔHRs at 5 min stand were higher in POTS (31 ± 3) compared with control (21 ± 2) and elevated at 5- or 10-min tilt in POTS (51 ± 3 and 51 ± 2) versus control (26 ± 2 and 25 ± 2) compared with standing. ΔHR in POTS and controls for 10 min were not different from 5 min. For 5 min stand ROC threshold was 26 beats per min (bpm), sensitivity of 70.6%, and specificity of 68.2% compared with 39 bpm, 88.2%, and 95.1% for 5 min tilt, and 40 bpm, 94.1%, and 95.1% for 10-min tilt. A precision-recall graph confirmed the superior discriminating ability of 5 min and 10 min tilt compared to 5 min stand.

Conclusions: The stand test is relatively non-specific and imprecise compared to tilt and does not satisfactorily distinguish POTS from control in patients aged < 19 years old.

Introduction: Syncope is common, with bimodal distribution through life, peaking in adolescence and in the elderly, and overall increases in incidence with age among both men and women. In this context, syncope-related visits to emergency departments (ED), hospitalizations, and testing are a significant healthcare cost burden. Ultimately, understanding the volume of testing types and settings of syncope encounters may aid in more effective healthcare utilization and high value care for this patient population.

Methods: Data for this study were collected from the Truven Health Analytics MarketScan Database from 2006 to 2019. This database contains both commercially insured patients and those with Medicare coverage. Patients with the diagnosis of syncope were identified using International Classification of Diseases (ICD)-9 and -10 codes. We assessed the incidence of various tests for syncope evaluation and ED disposition for the study period.

Results: The incidence of syncope among the study cohort rose from nine per 1000 patients to 13 per 1000 patients during the study period. The incidence of testing for syncope among multiple domains (neurologic, cardiac, blood testing) decreased in some categories, but routine testing remained prevalent. Women had a significantly lower incidence of testing in most testing domains. Discharge rate from the ED for patients presenting with syncope remained stable during the study period. However, admission rate to the hospital for those aged > 65 years increased during the study time.

Conclusion: Testing and admissions for syncope remain prevalent and are drivers of healthcare-associated costs. There is a clear need for further work in developing a focused approach in the evaluation of syncope patients in order to mitigate healthcare costs and improve outcomes.

Purpose: The prevailing hypothesis posits that Takotsubo syndrome (TTS) is caused by massive sympathetic activation, yet supporting evidence remains inconsistent. The objectives of the present study were to determine whether sympathetic activity and reactivity are enhanced in the recovery phase of TTS, and to evaluate the effect of selective β1-receptor blockade on sympathetic reactivity.

Methods: We conducted a case-control study that included 18 female patients with TTS and 13 age- and sex-matched controls. Muscle sympathetic nerve activity was measured through microneurography of the peroneal nerve at rest and during the cold pressor test. In the TTS group, recordings were repeated after randomisation to intravenous metoprolol or placebo. In 10 TTS patients, cardiac sympathetic activity was assessed using iodine 123-metaiodobenzylguanidine scintigraphy. Blood samples were collected during hospitalisation.

Results: Microneurography was performed a median of 27.5 days after patient admission. There were no significant differences in burst incidence, burst frequency, burst height or burst area between the TTS patients and the controls at rest, during stress or after administration of intravenous metoprolol. Iodine 123-metaiodobenzylguanidine scintigraphy was performed a median of 12.5 days after admission, revealing decreased early 1.54 ± 0.13 and late 1.40 ± 0.13 heart-to-mediastinum ratios, and an increased washout rate of 41.8 ± 12.1%. Catecholamine metabolites were comparable between the study groups.

Conclusion: General sympathetic hyperactivity or hyperreactivity unlikely contributes to TTS, as catecholamine levels and muscle sympathetic nerve activity at rest and during stress were similar between the TTS patients and the controls. As scintigraphy showed increased cardiac sympathetic activity, a pathological cardiac adrenergic response and vulnerability to sympathetic activation may be crucial for the development of the syndrome.

Purpose: Patients with chronic kidney disease (CKD) are more than twice as likely to die from a cardiovascular event than those with normal kidney function. Although CKD may increase resting sympathetic activity, quantification of resting sympathetic outflow alone does not account for the ensuing vasoconstriction, and blood pressure (BP) change (i.e., sympathetic transduction). Patients with CKD have been reported to exhibit elevated α-adrenergic receptor sensitivity, which may predispose this population to greater sympathetic transduction. We tested the hypothesis that patients with CKD have augmented sympathetic transduction to BP.

Methods: In 16 patients with CKD, 17 bodyweight-matched (BWM) controls, and 11 lean controls of a similar age muscle sympathetic nerve activity (MSNA) and beat-to-beat BP were continuously recorded during quiet supine rest. Signal averaging was used to quantify changes in mean arterial pressure (MAP) and total vascular conductance (TVC) following spontaneous bursts of MSNA.

Results: Peak increases in MAP following MSNA bursts were not different among patients with CKD and the control groups (CKD: 2.3 ± 1.1 mmHg; BWM controls: 2.1 ± 1.0 mmHg; lean controls: 1.7 ± 0.9 mmHg; P = 0.28). Likewise, nadir reductions in TVC following all bursts of MSNA were not different among patients with CKD and either control group (P = 0.69). Both patients with CKD and controls had graded increases in MAP and decreases in TVC with increasing burst size, which were not different among groups (all P > 0.05).

Conclusion: In summary, these data indicate that patients with CKD do not have augmented sympathetic transduction to BP.