Clinical Autonomic Research最新文献

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.

Introduction: Water intake is known to be effective in preventing orthostatic hypotension (OH). However, it is unknown whether water intake would be effective in acutely preventing exercise-induced OH.

Methods: Fourteen adults (men/women: 7/7, age: 20 ± 8 years) were recruited. Each subject underwent two protocols with and without 500 ml water intake using a randomized crossover design (Water vs. Control). Participants underwent 30 min of cycle ergometry at the 60-70% predicted VO₂ max. OH and hemodynamics were assessed before and after exercise, and immediately (Water 1) and 20 min (Water 2) after the water intake. OH was evaluated with a 1-min standing test as the criteria for systolic blood pressure (SBP) < 90 mmHg. A cross-spectral analysis for RR and SBP variability was used to evaluate the cardiac autonomic activity and baroreflex sensitivity.

Results: In both protocols, the incidence of OH increased after the exercise. The incidence of OH was lower in Water than in Control at Water 1 (OR: 0.093, 95% CI: 0.015-0.591). Heart rate was lower and SBP was higher in Water than in Control at Water 1 and 2 (P < 0.05). High-frequency power of RR variability and transfer function gains in Water were normalized and higher than in Control at Water 1 and 2 (P < 0.05). The ratio of low- to high-frequency power of RR variability in Water was normalized and lower in Water than in Control at Water 1 (P < 0.05).

Conclusion: Our findings indicate that water intake may prevent acute exercise-induced OH, accompanied by normalized cardiac autonomic activity and baroreflex sensitivity.

Purpose: Vasovagal syncope is thought to be mediated by a progressive fall in cardiac output secondary to venous pooling of blood in the splanchnic circulation. How and when this occurs before syncope has not been determined.

Methods: A total of 20 patients who became hypotensive during head-up tilt (age 40.9 ± 3.4 years; 10 females) were divided into two groups-the glyceryl trinitrate (GTN) group (n = 12) and the vasovagal syncope (VVS) group (n = 8) - on the basis of whether or not nitroglycerine provocation was required. They were compared with a control group (age 38.6 ± 3.3; 8 females; n = 13). Hemodynamics, including superior mesenteric artery blood flow (SMABF) and muscle sympathetic nerve activity (MSNA) were recorded continuously during early tilt, presyncope and recovery. We used pixel-weighting to calculate average velocity from the pulsed Doppler velocity envelope.

Results: During baseline and early tilt, resistance to mesenteric blood flow was lower in the VVS group: 0.30 ± 0.02 to 0.30 ± 0.02 mmHg/ml/min versus controls 0.30 ± 0.03 to 0.38 ± 0.04 mmHg/ml/min (p = 0.05). During presyncope, as blood pressure and stroke volume gradually fell, SMABF was higher in the VVS group, falling from 370 ± 46 to 248 ± 35 ml/min, versus controls, falling from 342 ± 51 to 233 ± 19 (p = 0.03). At this time, MSNA was lower in the VVS group than controls: 39 ± 4 to 34 ± 3 bursts/min versus 45 ± 2 to 48 ± 3 (p = 0.001).

Conclusion: During presyncope, increased splanchnic blood flow may pool more blood in capacitance vessels resulting in decreased venous return and cardiac output. This may be secondary to decreased vasoconstrictor sympathetic activity.

Purpose: Alterations of autonomic cardiovascular control are implicated in the origin of chronic low blood pressure (BP) (hypotension), but comprehensive analysis of baroreflex function is still lacking. This study explored baroreflex function in its cardiac, vascular and myocardial branches METHODS: Continuous BP was recorded at rest and during a mental arithmetic task in 40 hypotensive and 40 normotensive participants. Assessed cardiovascular variables included stroke volume (SV) (calculated by the Modelflow method), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR) and heart rate variability (HRV). Baroreflex sensitivity (BRS) was calculated using the spontaneous sequence method.

Results: Hypotensive participants exhibited greater BRS in the three baroreflex branches, in addition to lower SV, HR and CO and higher HRV and TPR. Reactivity for BP, HRV and CO during the stress task was reduced in hypotensive individuals. The greater cardiac BRS can explain the lower HR and higher HRV observed in hypotension, suggestive of increased vagal cardiac influences. The higher vasomotor BRS may contribute to the greater TPR observed in the hypotensive participants. Abnormal associations between myocardial BRS and SV arose, suggesting aberrant autonomic control of myocardial contractility in hypotension.

Conclusion: The results indicate that hemodynamic deficits in hypotension are related to preload factors, probably triggered by hypovolemia and reduced unstressed blood reserves, resulting in lower venous return, ventricular preload and SV. In contrast, afterload mechanisms seem to work appropriately.

Purpose: Cardiovascular autonomic neuropathy (CAN) is a common diabetic complication associated with excess morbidity and mortality. CAN is also seen in conditions such as Parkinson's disease. Normative reference data for cardiovascular autonomic function are used to stratify individuals into those with and without CAN. However, reference thresholds for both cardiovascular autonomic reflex tests (CARTs) and heart rate variability (HRV) are scarce and based on small sample sizes. The aim of the study was to establish contemporary normative reference thresholds based on a large non-diabetic population free of cardiovascular disease (CVD).

Methods: Cardiovascular autonomic function, CARTs and 5-min HRV indices were assessed in individuals without diabetes and CVD from the Lolland-Falster Health Study (2018-2020) by applying the point-of-care device Vagus™. Age-specific normative reference thresholds were estimated by using log-transformed quantile regression models at the 5th and 10th percentile, with adjustments made for sex. Models assessing the association between age and HRV indices were further adjusted for heart rate.

Results: We present age-specific normative reference thresholds for cardiovascular autonomic function, including CARTs and HRV, for 875 individuals (48% females) aged 15-85 years. The reference thresholds are presented for both the 5th and 10th lower percentile. Higher age was inversely associated with all outcomes. Females tended to have a higher parasympathetic drive compared to males. Pre-test conditions did not affect CARTs significantly.

Conclusions: The presented age-related normative reference thresholds for both CARTs and HRV indices based on a large Danish cohort may facilitate improved quality of research and treatment.