Counter pressure maneuvers for syncope prevention: A semi-systematic review and meta-analysis.

Physical counter pressure maneuvers (CPM) are movements that are recommended to delay or prevent syncope (fainting) by recruiting the skeletal muscle pump to augment cardiovascular control. However, these recommendations are largely based on theoretical benefit, with limited data evaluating the efficacy of CPM to prevent syncope in the real-world setting. We conducted a semi-systematic literature review and meta-analysis to assess CPM efficacy, identify literature gaps, and highlight future research needs. Articles were identified through a literature search (PubMed, April 2022) of peer-reviewed publications evaluating the use of counter pressure or other lower body maneuvers to prevent syncope. Two team members independently screened records for inclusion and extracted data. From 476 unique records identified by the search, 45 met inclusion criteria. Articles considered various syncopal conditions (vasovagal = 12, orthostatic hypotension = 8, postural orthostatic tachycardia syndrome = 1, familial dysautonomia = 2, spinal cord injury = 1, blood donation = 10, healthy controls = 11). Maneuvers assessed included hand gripping, leg fidgeting, stepping, tiptoeing, marching, calf raises, postural sway, tensing (upper, lower, whole body), leg crossing, squatting, "crash" position, and bending foreword. CPM were assessed in laboratory-based studies (N = 28), the community setting (N = 4), both laboratory and community settings (N = 3), and during blood donation (N = 10). CPM improved standing systolic blood pressure (+ 14.8 ± 0.6 mmHg, p < 0.001) and heart rate (+ 1.4 ± 0.5 bpm, p = 0.006), however, responses of total peripheral resistance, stroke volume, or cerebral blood flow were not widely documented. Most patients experienced symptom improvement following CPM use (laboratory: 60 ± 4%, community: 72 ± 9%). The most prominent barrier to employing CPM in daily living was the inability to recognize an impending faint. Patterns of postural sway may also recruit the skeletal muscle pump to enhance cardiovascular control, and its potential as a discrete, proactive CPM needs further evaluation. Physical CPM were successful in improving syncopal symptoms and producing cardiovascular responses that may bolster against syncope; however, practical limitations may restrict applicability for use in daily living.

Cardiovascular responses to vibrostimulation for sperm retrieval in men with spinal cord injury.

BACKGROUND/OBJECTIVE: Cardiovascular abnormalities and arrhythmias are common in individuals with spinal cord injury (SCI) who are undergoing vibrostimulation for sperm retrieval. The study aimed to examine cardiovascular control in men with SCI undergoing this procedure. METHODS: Individuals with chronic cervical (n=8; age: 33.1 +/- 1.9 years) and upper thoracic SCI (n=5; age: 35.2 +/- 2.9 years) volunteered for vibrostimulation, with continuous blood pressure (Finometer) and electrocardiographic monitoring. Patients were characterized further by sympathetic skin responses (SSR) to assess descending autonomic spinal pathways and American Spinal Injury Association (ASIA) scores to assess motor and sensory pathways. RESULTS: All but one subject with cervical SCI were ASIA A or B and were negative for SSR in the hands and feet. All subjects with upper thoracic SCI were ASIA A or B and were positive for SSR in the hands. Systolic blood pressure was lower in men with cervical injury at rest. Vibrostimulation induced an increase in systolic blood pressure >20 mmHg in all patients with cervical SCI (range = 125/65 - 280/152; median = 167/143 mmHg) and in 2 thoracic subjects (151/104 and 170/121 mmHg). During ejaculation, 6 cervical and 3 thoracic subjects developed arrhythmias (5 with bradycardia, 6 with premature atrial contractions, 4 with ventricular excitation, 1 with junctional rhythm, and 1 with heart block). CONCLUSION: The vibrostimulation procedure induced electrocardiographic abnormalities and autonomic dysreflexia in subjects with either cervical or high thoracic SCI.

Waist circumference is the best index for obesity-related cardiovascular disease risk in individuals with spinal cord injury.

Obesity is an important identifier of cardiovascular disease (CVD) risk, but is challenging to determine accurately in individuals with spinal cord injury (SCI). Body mass index (BMI) is used worldwide as a simple indicator of obesity, but is difficult to measure in individuals with SCI. Furthermore, standard BMI cutoffs underestimate obesity in this population. Therefore, we aimed to identify the best marker of obesity in individuals with SCI, considering both practicality, and ability to detect adiposity and CVD risk. Five anthropometric measures were evaluated: BMI; waist circumference (WC); waist-to-height ratio (WHtR); waist-to-hip ratio; and neck circumference. We evaluated relationships between these measures and abdominal and total body-fat percentage, seven cardiovascular metabolic risk factors (fasting insulin, glucose, glucose tolerance, triglycerides, high-density lipoprotein, low-density lipoprotein, and total cholesterol), and the Framingham risk score. BMI, WC, and WHtR were correlated with abdominal fat percentage. WC and WHtR were correlated with five metabolic risk factors as well as the Framingham risk score. WC is a more practical measure for an SCI population. The optimal cutoff for identifying adverse CVD risk in individuals with SCI was identified as WC ≥94 cm, with 100% sensitivity and 79% specificity. We propose that WC is a simple, more sensitive alternative to BMI in this population that is easy to use in multiple settings. The cutoff provides a simple tool to predict adverse CVD risk profiles that can be used to guide risk management, as well as as a practical aid for individuals with SCI to maintain a healthy body composition.

Are compression stockings an effective treatment for orthostatic presyncope?

BACKGROUND: Syncope, or fainting, affects approximately 6.2% of the population, and is associated with significant comorbidity. Many syncopal events occur secondary to excessive venous pooling and capillary filtration in the lower limbs when upright. As such, a common approach to the management of syncope is the use of compression stockings. However, research confirming their efficacy is lacking. We aimed to investigate the effect of graded calf compression stockings on orthostatic tolerance. METHODOLOGY/PRINCIPAL FINDINGS: We evaluated orthostatic tolerance (OT) and haemodynamic control in 15 healthy volunteers wearing graded calf compression stockings compared to two placebo stockings in a randomized, cross-over, double-blind fashion. OT (time to presyncope, min) was determined using combined head-upright tilting and lower body negative pressure applied until presyncope. Throughout testing we continuously monitored beat-to-beat blood pressures, heart rate, stroke volume and cardiac output (finger plethysmography), cerebral and forearm blood flow velocities (Doppler ultrasound) and breath-by-breath end tidal gases. There were no significant differences in OT between compression stocking (26.0±2.3 min) and calf (29.3±2.4 min) or ankle (27.6±3.1 min) placebo conditions. Cardiovascular, cerebral and respiratory responses were similar in all conditions. The efficacy of compression stockings was related to anthropometric parameters, and could be predicted by a model based on the subject's calf circumference and shoe size (r = 0.780, p = 0.004). CONCLUSIONS/SIGNIFICANCE: These data question the use of calf compression stockings for orthostatic intolerance and highlight the need for individualised therapy accounting for anthropometric variables when considering treatment with compression stockings.

Phase of the menstrual cycle does not affect orthostatic tolerance in healthy women.

Women of child-bearing age have a lower orthostatic tolerance (OT) than older women or men, and women suffering from frequent syncopal episodes often comment that their symptoms occur at certain times of the menstrual cycle. However, it is not known whether, in asymptomatic women, OT varies at different phases of the menstrual cycle. We studied 8 healthy asymptomatic women aged 26.8 +/- 3.4 years. We determined OT using a test of combined head-up tilting and lower body suction. We continuously monitored beat-to-beat blood pressure (Finapres), heart rate (ECG), and cerebral and forearm blood flow velocities (Doppler ultrasound). On each test day we assessed carotid baroreceptor sensitivity from suction/pressure applied to a neck chamber. We also determined estradiol and progesterone levels from a venous blood sample. Tests were performed in early follicular and late luteal phases, and during ovulation. Serum concentrations of estradiol (pmol x l(-1)) and progesterone (nmol x l(-1)) were in follicular phase 464.1 +/- 63 and 6.3 +/- 2.8; ovulation 941.6 +/- 298 and 5.8 +/- 1.2; luteal phase 698 +/- 188 and 32.3 +/- 9.6. Progesterone levels were significantly higher in the luteal phase (p < 0.001). OT was not different on any test day: follicular 31.9 +/- 1.6 min, ovulation 31.3 +/- 0.7 min; luteal 31.1 +/- 2.2 min. Supine and tilted heart rates and blood pressures, the maximum heart rate, and the cerebral autoregulatory and forearm vascular resistance responses to the orthostatic stress were similar during all studies. Both cardiac and vascular resistance carotid baroreceptor sensitivities were also similar on all test days. These results suggest that there is no difference in either OT or cardiovascular control at the tested phases of the menstrual cycle in healthy women.

R-R interval-blood pressure interaction in subjects with different tolerances to orthostatic stress.

In addition to the gain, the time delay in the input-output response in a feedback system is crucial for the maintenance of its stability. Patients with posturally related (vasovagal) syncope have inadequate control of blood pressure and one possible explanation for this could be prolonged latency of the baroreflex. We studied 14 patients with histories of syncope and poor orthostatic tolerance (assessed by a progressive orthostatic stress test) and 16 healthy controls. We performed spontaneous sequence analysis of the fluctuations of R-R period (ECG) and systolic arterial pressure (SAP, Finapres) recorded during a 20 min supine period and during 20 min 60 deg head-up tilt (HUT). The baroreflex latency was determined by identifying the lag between the changes in SAP and in R-R interval from which the highest correlation coefficient was obtained. During the supine period, 74% of sequences in control subjects and 54% in patients occurred with zero beats of delay (i.e. R-R interval changed within the same R-R interval). The remaining sequences occurred with delays of up to four beats. HUT shifted the baroreflex delay to be approximately one heartbeat slower and again patients showed more sequences with prolonged response. The delay in heartbeats was transformed into delay in time. In control subjects, 75% of baroreflex responses occurred within 1 s. In patients, 75% of baroreflex responses took more than 2 s to occur. The results showed that syncopal patients with poor orthostatic tolerance have increased baroreflex latency. This may lead to instability and inadequate blood pressure control and may predispose to vasovagal syncope.

Prolonged latency in the baroreflex mediated vascular resistance response in subjects with postural related syncope.

In addition to the gain, the delay of the baroreflex response plays an important role in the maintenance of cardiovascular system stability. Additionally when postural changes induce sudden drops in blood pressure, a delayed response may fail to maintain sufficient cerebral perfusion pressure. We tested the hypothesis that the delay of the carotid baroreceptor reflex is impaired in subjects with poor orthostatic tolerance. An orthostatic test with 60 degrees head-up tilt, and progressive lower-body negative pressure was performed on 27 patients with histories of unexplained syncope and 13 control subjects. The test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Twelve patients had normal tolerance and thirteen patients had low tolerance. We measured beat-to-beat blood pressure (Finapres) and brachial artery blood flow velocity (Doppler ultrasonography). Before the test, we determined the response of forearm vascular resistance (mean arterial pressure/mean brachial artery velocity) to loading/unloading of carotid baroreceptors by the application of neck suction/pressure (-/+30 mmHg) to a chamber fitted overlying the carotid sinus. We measured the gain in the response (maximum percentage change from baseline value in vascular resistance divided by the neck collar pressure) and the latency in the response (delay of the maximum change in vascular resistance after neck-collar stimulation). Results are reported as means +/- SEM. In the three groups, there were no differences in the sensitivity of the vascular resistance response after baroreceptor loading/unloading. Following baroreceptor unloading, the latency of the response was 14.0+/-1.3 seconds in early fainters, 9.3+/-0.7 seconds in normal patients and 10.1+/-1.2 seconds in controls. The latency in blood pressure rise was 11.1+/-1.3 seconds in early fainters, 7.9+/-0.9 seconds in normal patients and 7.2+/-1.0 seconds in controls. The results following baroreceptor loading were more scattered. The early fainters still had a tendency to show prolonged latency. These results suggest that the delay in the baroreflex response plays an important role in postural related syncope.