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ObjectivesMost elderly patients affected by reflex vasodepressor syncope take one or more hypotensive drugs. The role of these drugs in causing syncope has not yet been established. We hypothesised that recurrence of syncope and presyncope can be reduced by discontinuing/reducing vasoactive therapy without increasing the risk of cardiovascular and neurological events.MethodsThis randomised, parallel, prospective, trial was conducted from January 2014 to March 2016 in four general hospitals. Of 328 initially screened participants, 58 patients (mean (SD) age 74±11 years) affected by vasodepressor reflex syncope, which was reproduced by tilt testing (n=54) or carotid sinus massage (n=4), were randomised to stop/reduce vasoactive therapy or to continue it. Primary end point was recurrence of syncope, presyncope or adverse events (defined as stroke, cerebral transient ischaemic attacks, worsening heart failure, myocardial infarction).ResultsOf 58 patients who were randomised, 55 completed the trial. After 1 month, systolic blood pressure was significantly higher in the ‘stop/reduce’ group than in the ‘continue’ group, in both supine (141±13 mm Hg vs 128±14 mm Hg; p=0.004) and standing (133±13 mm Hg vs 122±15 mm Hg; p=0.02) positions. During a mean follow-up of 13±7 months, the primary combined end point occurred in seven ‘stop/reduce’ patients (23%): three had syncope, three had presyncope and one had heart failure. Conversely, it occurred in 13 ‘continue’ patients (54%): 10 had syncope, 2 had presyncope and 1 had cerebral transient ischaemic attack. The log-rank p value was 0.02 and the HR was 0.37 (95% CI 0.15 to 0.91).ConclusionsRecurrence of syncope and presyncope can be reduced by discontinuing/reducing vasoactive therapy in most elderly patients affected by reflex vasodepressor syncope.Trial registration numberNCT01509534; EudraCT2013-004364-63; Results.

Cardiovascular autonomic neuropathy (CAN) predicts clinical diabetic nephropathy (DN). We investigated the relationship between DN structural lesions and CAN. Sixty three Pima Indians with type 2 diabetes underwent kidney biopsies following a 6-year clinical trial testing the renoprotective efficacy of losartan vs. placebo. CAN was assessed a median 9.2years later. CAN variables included expiration/inspiration ratio (E/I), standard deviation of the normal R-R interval (sdNN), and low and high frequency signal power and their ratio (LF, HF, LF/HF); lower values reflect more severe neuropathy. Associations of CAN with renal structural variables were assessed by linear regression adjusted for age, sex, diabetes duration, blood pressure, HbA1c, glomerular filtration rate, and treatment assignment during the trial. Global glomerular sclerosis was negatively associated with sdNN (partial r=−0.35, p=0.01) and LF (r=−0.32, p=0.02); glomerular basement membrane width was negatively associated with all measures of CAN except for LF/HF (r=−0.28 to −0.42, p<0.05); filtration surface density was positively associated with sdNN, LF, and HF (r=0.31 to 0.38, p<0.05); and cortical interstitial fractional volume was negatively associated with HF (r=−0.27, p=0.04). CAN associates with DN lesions.

Despite strong scientific evidence supporting the benefits of regular exercise for the prevention and management of cardiovascular disease (CVD), physical inactivity is highly prevalent worldwide. In addition to merely changing well-known risk factors for systemic CVD, regular exercise can also improve cardiovascular health through non-traditional mechanisms. Understanding the pathways through which exercise influences different physiological systems is important and might yield new therapeutic strategies to target pathophysiological mechanisms in CVD. This Review includes a critical discussion of how regular exercise can have antiatherogenic effects in the vasculature, improve autonomic balance (thereby reducing the risk of malignant arrhythmias), and induce cardioprotection against ischaemia–reperfusion injury, independent of effects on traditional CVD risk factors. This Review also describes how exercise promotes a healthy anti-inflammatory milieu (largely through the release of muscle-derived myokines), stimulates myocardial regeneration, and ameliorates age-related loss of muscle mass and strength, a frequently overlooked non-traditional CVD risk factor. Finally, we discuss how the benefits of exercise might also occur via promotion of a healthy gut microbiota. We argue, therefore, that a holistic view of all body systems is necessary and useful when analysing the role of exercise in cardiovascular health.

Patients with COPD might be particularly susceptible to hypoxia-induced autonomic dysregulation. Decreased baroreflex sensitivity (BRS) and increased blood pressure (BP) variability (BPV) are markers of impaired cardiovascular autonomic regulation and there is evidence for an association between decreased BRS/increased BPV and high cardiovascular risk. The aim of this study was to evaluate the effect of short-term exposure to moderate altitude on BP and measures of cardiovascular autonomic regulation in COPD patients. Continuous morning beat-to-beat BP was noninvasively measured with a Finometer device for 10 minutes at low altitude (490 m, Zurich, Switzerland) and for 2 days at moderate altitude (2,590 m, Davos Jakobshorn, Switzerland) - the order of altitude exposure was randomized. Outcomes of interest were mean SBP and DBP, BPV expressed as the coefficient of variation (CV), and spontaneous BRS. Changes between low altitude and day 1 and day 2 at moderate altitude were assessed by ANOVA for repeated measurements with Fisher's exact test analysis. Thirty-seven patients with moderate to severe COPD (mean±SD age 64±6 years, FEV 60%±17%) were included. Morning SBP increased by +10.8 mmHg (95% CI: 4.7-17.0, =0.001) and morning DBP by +5.0 mmHg (95% CI: 0.8-9.3, =0.02) in response to altitude exposure. BRS significantly decreased ( =0.03), whereas BPV significantly and progressively increased ( <0.001) upon exposure to altitude. Exposure of COPD patients to moderate altitude is associated with a clinically relevant increase in BP, which seems to be related to autonomic dysregulation. ClinicalTrials.gov (NCT01875133).

The aim of the present study was to investigate reactions in trapezius muscle blood flow (MBF), muscle activity, heart rate variability (HRV) and systemic blood pressure (BP) to autonomic tests in subjects with chronic neck–shoulder pain and healthy controls. Changes in muscle activity and blood flow due to stress and unfavourable muscle loads are known underlying factors of work-related muscle pain. Aberration of the autonomic nervous system (ANS) is considered a possible mechanism. In the present study, participants ( n  = 23 Pain, n  = 22 Control) performed autonomic tests which included a resting condition, static hand grip test (HGT) at 30% of maximal voluntary contraction, a cold pressor test (CPT) and a deep breathing test (DBT). HRV was analysed in time and frequency domains. MBF and muscle activity were recorded from the upper trapezius muscles using photoplethysmography and electromyography (EMG). The pain group showed reduced low frequency-HRV (LF) and SDNN during rest, as well as a blunted BP response and increased LF-HRV during HGT (∆systolic 22 mm Hg; ∆LF(nu) 27%) compared with controls (∆systolic 27; ∆LF(nu) 6%). Locally, the pain group had attenuated trapezius MBF in response to HGT (Pain 122% Control 140%) with elevated trapezius EMG following HGT and during CPT. In conclusion, only HGT showed differences between groups in systemic BP and HRV and alterations in local trapezius MBF and EMG in the pain group. Findings support the hypothesis of ANS involvement at systemic and local levels in chronic neck–shoulder pain.

Patients with chronic obstructive pulmonary disease (COPD) exhibit aerobic function, autonomic nervous system, and mucociliary clearance alterations. These parameters can be attenuated by aerobic training, which can be applied with continuous or interval efforts. However, the possible effects of aerobic training, using progressively both continuous and interval sessions (ie, linear periodization), require further investigation. To analyze the effects of 12-week aerobic training using continuous and interval sessions on autonomic modulation, mucociliary clearance, and aerobic function in patients with COPD. Sixteen patients with COPD were divided into an aerobic (continuous and interval) training group (AT) (n=10) and a control group (CG) (n=6). An incremental test (initial speed of 2.0 km·h(-1), constant slope of 3%, and increments of 0.5 km·h(-1) every 2 minutes) was performed. The training group underwent training for 4 weeks at 60% of the peak velocity reached in the incremental test (vVO2peak) (50 minutes of continuous effort), followed by 4 weeks of sessions at 75% of vVO2peak (30 minutes of continuous effort), and 4 weeks of interval training (5×3-minute effort at vVO2peak, separated by 1 minute of passive recovery). Intensities were adjusted through an incremental test performed at the end of each period. The AT presented an increase in the high frequency index (ms(2)) (P=0.04), peak oxygen uptake (VO2peak) (P=0.01), vVO2peak (P=0.04), and anaerobic threshold (P=0.02). No significant changes were observed in the CG (P>0.21) group. Neither of the groups presented changes in mucociliary clearance after 12 weeks (AT: P=0.94 and CG: P=0.69). Twelve weeks of aerobic training (continuous and interval sessions) positively influenced the autonomic modulation and aerobic parameters in patients with COPD. However, mucociliary clearance was not affected by aerobic training.

Diabetes mellitus is not just a simple metabolic disorder, however, it is considered to be a cardiovascular disease of a metabolic origin. This is apparent especially when speaking about type 2 diabetes (DM II). The objective of our study was to determine whether a comprehensive spa treatment (procedures and drinking cure) may affect the level of the sympathetic tone of patients suffering from DM II. As an indicator of the sympathetic tone, selected electrocardiographic parameters derived from the heart rate variability and microwave alternans were chosen. There were 96 patients enrolled in our study: 38 patients with poorly controlled DM II and two control groups: 9 patients with compensated DM II and 49 patients, average age without diabetes or other disorders of the glucose metabolism. All received an identical spa treatment and continued their medical therapy. The electrophysiological examination of patients was performed before and after a three-week spa treatment using the KARDiVAR system. Parameters derived from the analysis of heart rate variability (HRV), microvolt T-wave alternans, and microvolt R-wave alternans were analyzed in order to evaluate the tones of the autonomic nervous system (ANS). The control group showed a slight increase of parameter the index of activity of regulatory systems (IRSA) (4.4±1.3 vs. 3.8±1.4; p=0.006) after the spa treatment, while increased heart rate (80.9±11.0 vs. 74.6±9.6; p=0.028), reduced index of centralization (IC) (1.3±0.6 vs. 2.9±1.4; p=0.027) and reduced index of myocardium (IM) (9.9±7.4 vs. 18.0±6.3; p=0.041) were found in patients with a compensated DM II. Patients with a poorly compensated DM II showed a decreased IM (10.9±8.6 vs. 16.9±5.2; p=0.001) and also a reduced IRSA (4.1±3.5 vs. 6.3±1.9; p=0.001). The results proved favorable changes in ANS cardiovascular control of patients with DM II after a spa treatment, especially in terms of reducing the sympathoadrenal system activity (decreased IRSA), improving electrical stability of the myocardium and increasing centrally controlled heart rate variability without overloading the cardiovascular system (drop of IM).

This study investigates how various hypoxic interventions affect cardiac autonomic activity and hemodynamic control during posture change and the Valsalva maneuver. Ten healthy sedentary men exposed to 12, 15 and 21% O 2 for 1 h in a normobaric hypoxia chamber in a random order. Before and after various O 2 concentrations were administered, subjects performed the sit-up test and Valsalva maneuver, respectively. An impedance plethysmography was utilized to measure blood pressure (BP) and vascular hemodynamics, whereas spectral analysis of heart rate variability (HRV) was performed to determine cardiac autonomic activity. Analytical results can be summarized as follows: while the patient rests in a supine position, exposure to 12% O 2 reduces the ratio of lower to upper extremity systolic BP, which is accompanied by (1) suppressed arterial reactive hyperemia and increased venous flow resistance, as well as (2) decreased total power and high frequency (HF) and increased low frequency (LF) and the ratio of LF to HF. Moreover, the hypoxia-induced changes of time and frequency domains in HRV at resting supine disappear following the sit-up test, whereas this hypoxic exposure attenuates the BP and heart rate responses to the Valsalva maneuver. Conversely, resting and physical stimuli-mediated HRV and vascular hemodynamic values are unaltered by both 15 and 21% O 2 exposures. We conclude that acute hypoxic exposure affects cardiovascular autonomic functions, with reactions determined by the intervening O 2 concentrations. Moreover, the BP and cardiac autonomic responses to 12% O 2 , but not 15% O 2 , exposure are depressed while performing posture change and the Valsalva maneuver.

Sympathetic restraint in exercising muscle is currently viewed as required to prevent ‘excess’ vasodilatation from exceeding the cardiac output (Q̇ ${\\dot{Q}} $ ) response, even in submaximal exercise. Certainly, muscle vasodilatory capacity dictates the requirement for sympathetic restraint when cardiac pumping capacity is approached. However, a similar role in submaximal exercise has at least two important implications for integrated cardiovascular control in exercise that have not been considered. First, such a role means that there is a ‘set’ Q̇ ${\\dot{Q}} $response to a given exercise challenge that dictates the cardiovascular circuit flow and therefore the vasodilatation allowed such that Q̇ ${\\dot{Q}} $ –peripheral blood flow balance and target arterial blood pressure are achieved. This represents a ‘cardiocentric’ model of integrated cardiovascular control, whereby the heart leads and the peripheral resistance vessel tone is modulated accordingly. Second, what is commonly described as ‘tight’ matching of exercising muscle oxygen delivery relative to demand would therefore require that the Q̇ ${\\dot{Q}} $response is closely ‘calibrated’ to exercising muscle metabolic demand. This would require a means of driving cardiac activation via precise communication of exercising muscle metabolic demand. However, considerable evidence demonstrates that ‘excess’ vasodilatation in a healthy system simply leads to a matching increased Q̇ ${\\dot{Q}} $without arterial blood pressure compromise. This review re‐examines the evidence for existence of sympathetic restraint in exercising muscle and its currently proposed role. We propose that key questions remain unanswered and that renewed investigation into sympathetic restraint and its role can lead to important advances in understanding integrated cardiovascular control in exercise. What is the topic of this review? This review examines the current proposed role of sympathetic restraint in exercising muscle, i.e., to prevent ‘excess’ vasodilatation from exceeding the cardiac output response, even in submaximal exercise. What advances does it highlight? This review points out two implications of the current proposed role of sympathetic restraint that have been ignored. It also identifies important evidence suggesting that the current view might be incorrect.