Standard Deviation of Sequential Five-Minute R-R Interval Means (SDANN) is a prognostic marker, but not necessarily an autonomic marker.
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Autonomic Nervous System↗
Biomedical subjects
Robert S Sheldon
Publications and source records attributed to Robert S Sheldon.
Vasovagal syncope in medical students and their first-degree relatives.
AIMS: To determine the effect of family history on the likelihood of vasovagal syncope. METHODS AND RESULTS: Sixty-two medical students and 228 first-degree relatives were studied. Vasovagal syncope was ascertained with the Calgary syncope symptom score. The effects of the sex of the subject and parental syncope history on the likelihood of offspring fainting were described using Kaplan-Meier estimates and analysed using proportional hazards regression. The prevalence of vasovagal syncope was 32% and the median age of first faint in those who fainted was 14 years. More females than males fainted [42 vs. 31%; P=0.02; hazard ratio (HR) 1.34 (95% CI 1.07-1.68)]. An individual with two fainting parents was more likely to faint than one with no fainting parents [P<0.0001; HR 3.4 (95% CI 1.7-7.03)]. In the proportional hazards model, offspring of either sex whose mother faints are more likely to faint than those whose mother does not faint [HR 2.86 (95% CI 1.54-5.31)]. Having a father who faints significantly increases the risk of syncope in sons [HR 4.12 (95%CI 1.39-12.31)], but not in daughters [HR 1.18 (95% CI 0.56-3.34)]. CONCLUSION: Family history and sex of subject are important predictors of vasovagal syncope in offspring.
Adult↗
The Second Prevention of Syncope Trial (POST II)--a randomized clinical trial of fludrocortisone for the prevention of neurally mediated syncope: rationale and study design.
BACKGROUND: Neurally mediated syncope is a common and frequently distressing problem. It is associated with a poor quality of life, which improves when the frequency of syncope is reduced. Few therapies for neurally mediated syncope have been proven effective. Fludrocortisone is commonly used to prevent recurrences of syncope but with little evidence to support its use. A placebo-controlled clinical trial of fludrocortisone for the prevention of neurally mediated syncope is needed. STRUCTURE OF STUDY: POST II is a multicenter, international, randomized, placebo-controlled study of fludrocortisone in the prevention of neurally mediated syncope. The primary end point is the time to first recurrence of syncope. Patients will be randomized 1:1 to receive fludrocortisone 0.05 to 0.2 mg or matching placebo and followed for 1 year. Secondary end points include syncope frequency, presyncope, and quality of life. Primary analysis will be performed with an intention-to-treat approach, with a secondary on-treatment analysis. POWER CALCULATIONS: Assuming a 40% risk of syncope in the control arm, a relative reduction of 40% by fludrocortisone, and a dropout rate of 20%, the enrollment of 310 patients will give an 80% power of reaching a positive conclusion about fludrocortisone therapy, with P = .05. REGISTRATION: POST II is registered with both (ISRCTN 51802652) and (NCT00118482). IMPLICATIONS: This study will be the first adequately powered trial to determine whether fludrocortisone is effective in preventing neurally mediated syncope. If it is effective, then fludrocortisone may become the first-line medical therapy for this condition.
Fludrocortisone↗
Age of first faint in patients with vasovagal syncope.
INTRODUCTION: Understanding whether vasovagal syncope is a lifelong disorder might shed insight into its physiology and affect management strategies. Accordingly, we determined the age of the first syncopal spell in adult patients who sought care for syncope. METHODS AND RESULTS: Patients were 42 +/- 18 years old with 64% women. They had had a median 8 syncope spells (interquartile range [IQR]: 4, 20) with a median frequency of 1.0 syncopal spells per year. The range of syncopal spells was 1-3,375, and the range of duration of history of syncope was 0.003-70 years. The first syncopal spell occurred at ages 0-81 in a skewed distribution, with a marked mode age of 13 years, a median age of 18 years (IQR 12, 37), and a mean age of 26 +/- 20 years. The distributions were statistically indistinguishable across countries (P = 0.50), among Canadian regions (P = 0.69), and between the studies (P = 0.49). The same modal values were seen in males and females, and in patients <40 and > or =40 years old. However, patients > or =40 years had median ages of onset older than patients <40 years (36 +/- 23 vs 17 +/- 8 years). Patients had a recalled history of syncopal spells of median duration of 10 years (IQR: 2, 23), with a range of 0.003-70 years. An age of onset <44 years was 86% accurate for vasovagal syncope. CONCLUSION: The most common age at which vasovagal syncope first presents is 13 years, and patients remain at risk of syncope for many years. Lifelong coping strategies may be desirable.
Adolescent↗
Letter regarding article by Adamson et al, "Continuous autonomic assessment in patients with symptomatic heart failure: prognostic value of heart rate variability measured by an implanted cardiac resynchronization device".
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Activities of Daily Living↗
Role of hypotension in heart rate turbulence physiology.
BACKGROUND: Heart rate turbulence is a recently described cardiac prognostic marker that may be mediated by arterial baroreceptor sensitivity, suggesting it is induced by a brief initial hypotension. OBJECTIVES: The purpose of this study was to assess whether heart rate turbulence could be noninvasively induced through a previously implanted defibrillator and whether hypotension modulates turbulence physiology. METHODS: Premature ventricular paced beats was delivered during continuous ECG and blood pressure monitoring in patients with implanted defibrillators. Heart rate turbulence parameters from paced beats were compared with those from spontaneous premature ventricular beats. Subsequently, turbulence hemodynamic parameters were compared in 11 subjects with turbulence induced by pacing trains of 1, 3, 5, and 8 beats at a cycle length of 400 ms. RESULTS: Heart rate turbulence was very similar whether it followed a spontaneous premature ventricular complex or a paced beat. Induced and spontaneous turbulence slopes correlated well (R(s) = 0.917, P = .001). With increasing pacing train length, the magnitude of hypotension, cumulative hypotension time from the last sinus beat, turbulence tachycardia magnitude, magnitude of hypertension in recovery, and turbulence onset (but not turbulence slope) all increased. The cumulative hypotension time, but not the magnitude of hypotension, was tightly correlated with the magnitude of tachycardia (R2 = 0.999, P = .003) and turbulence onset (R2 = 0.975, P = .01). CONCLUSION: Heart rate turbulence can be induced noninvasively through an implanted device. Turbulence parameters are physiologically modulated by the duration of the initial hypotension, suggesting a possible important role for arterial baroreceptors.
Aged↗
Activity-responsive pacing produces long-term heart rate variability.
INTRODUCTION: Long-term heart rate variability (HRV) measures, including the standard deviation of means of successive 5-minute epochs of R-R interval intervals (SDANN) and the power law slope (beta), are important prognostic measures, yet their physiologic basis is unknown. We tested the hypothesis that long-term HRV arises from physical activity in a randomized cross-over study in patients with rate-responsive pacemakers. METHODS AND RESULTS: Ten patients with complete heart block and dual-chamber pacemakers underwent 24-hour periods of ambulatory ECG in each of three pacing modes: atrially tracked, fixed-rate, and rate-responsive pacing. SDANN, ultra low frequency (ULF; frequencies <0.0033 Hz), and beta slope were calculated; and high-frequency power and root mean square of consecutive normal R-R intervals (rMSSD) were calculated as measures of short-term HRV, which have autonomic origins. Long-term HRV measures were similar with atrially tracked and rate-responsive pacing and were much greater than in fixed-rate pacing (SDANN P = 0.0001; ULF P = 0.0001; beta slope P = 0.0002). Short-term HRV measures were similarly low in fixed-rate and rate-responsive pacing (P = NS) and were significantly lower than with atrially tracked pacing (P = 0.0034). CONCLUSION: Rate-responsive pacing reproduces long-term, but not short-term, measures of HRV, suggesting that they may be markers of heart rate responses to patient activity.
Adult↗
Measuring transient systemic conductance and capacitance responses using a modified Brooksby-Donald technique in anesthetized, autonomically intact rabbits.
BACKGROUND: The Brooksby-Donald approach uses two flow probes to measure the inflow and outflow from an organ or vascular bed; the difference in flow can be time-integrated to assess changes in venous capacitance. OBJECTIVES: To measure changes in subdiaphragmatic venous capacitance and arterial conductance in acutely instrumented rabbits, and to document the acute vascular responses to intravenous injections of pharmacological agents. METHODS: In artificially ventilated, fentanyl-anesthetized New Zealand female rabbits, ultrasonic flow probes were attached to the descending thoracic aorta and inferior vena cava to measure subdiaphragmatic inflow and outflow. Systemic arterial and venous pressures were measured. Conductance was calculated as aortic flow divided by the difference between systemic arterial and venous pressures. Changes in capacitance were assessed by integrating flow differences. Nitroglycerin (NG), isoproterenol hydrochloride, phenylephrine hydrochloride (PE) and vasopressin (VP) were administered intravenously in stepwise injections, and transient conductance and capacitance responses were determined. RESULTS: NG significantly increased conductance and capacitance, while isoproterenol hydrochloride had significant effects only on conductance. Both VP and PE significantly decreased conductance and capacitance. CONCLUSIONS: The modified Brooksby-Donald approach used in the present study was validated by the observed concordant increases in conductance and capacitance caused by NG, and decreases caused by VP and PE. This approach may be useful to characterize specific comparative conductance-capacitance properties of various vasoactive agents.
Analysis of Variance↗
Outcome of patients with dual-chamber pacemakers implanted for the prevention of neurally mediated syncope.
Dual-chamber pacemaker insertion (PI) has been found to reduce the recurrence of neurally mediated syncope (NMS) in 3 randomized trials. However, the long-term benefits of PI are unknown. To assess the natural history of NMS, we followed a cohort of 40 patients who underwent PI for frequent NMS for 46 to 75 months. We assessed the reduction in syncope frequency after PI and the time to first recurrence of syncope. Sixty months after PI, 32.5% of patients remained free of NMS. The frequency of syncope decreased from 0.46 to 0.06 spells/month (before to after PI, p = 0.04). Two groups of patients were identified, with responders to PI defined as having a 75% decrease in the frequency of NMS. Responders (n = 22) experienced a significant decrease in the frequency of NMS (0.31 to 0.01 spells/month, p <0.0001), whereas nonresponders did not experience a similar reduction (p = 0.8). Responders could not be identified by either baseline or tilt-test parameters. Patients without an early recurrence of syncope after PI (within 6 months) experienced a significant reduction in the frequency of NMS (0.24 to 0.02 spells/month, p = 0.0002), although the reduction was not significant (p = 0.3) in patients with an early recurrence of syncope. Some, but not all, patients respond to permanent PI for NMS. The long-term benefit of permanent PI can be predicted by timing of the first recurrence of syncope, but not by preimplantation factors.
Cohort Studies↗
Paced QT dispersion and QT morphology after radiofrequency atrioventricular junction ablation: impact of left ventricular function.
Catheter ablation of the atrioventricular junction (AVJ) is a widely accepted treatment for drug refractory atrial fibrillation. Unfortunately, there have been some reports of pause dependent ventricular arrhythmias associated with QT interval prolongation, mainly in patients with reduced LV function. The present investigation evaluates the association of LV function with QT dispersion in response to a sudden rate drop. ECGs were' recorded on 20 patients (13 with normal LV function) on the day following AVJ ablation while paced at a range of ventricular rates (40-120 beats/min), and during a sudden drop from 80 to 40 beats/min. The maximum QT interval (QTmax), minimum QT interval (QTmin), and QT interval dispersion (QTdisp) were compared. In both groups, the QTmax and QTmin increased at slower paced heart rates while the QTdisp did not change. In response to a sudden rate drop from 80 to 40 beats/min, the QTmax increased in both groups of LV function (trend), while the QTmin increased in those with normal LV function (24 +/- 22 ms), but not in those with reduced LV function (0 +/- 14 ms; P = 0.01). Consequently, the QTdisp increased significantly in those with reduced LV function (31 +/- 23 ms) but not in normal LV function (-5 +/- 29 ms; P = 0.01). Morphological QTU changes developed following the sudden rate drop in 67% of the reduced LV versus 8% of the normal LV (P = 0.02) function groups. Following AVJ ablation, QTdisp increased during a sudden rate drop in patients with reduced LV function, but not in patients with normal LV function.
Atrial Fibrillation↗
Clinical and electrophysiologic predictors of ventricular tachyarrhythmia recurrence in patients with implantable cardioverter defibrillators.
INTRODUCTION: Not all patients experience recurrent sustained ventricular tachyarrhythmias after placement of an implantable cardioverter defibrillator (ICD). We evaluated the clinical and electrophysiologic predictors of ventricular tachycardia (VT) and ventricular fibrillation (VF) recurrence following ICD implantation. METHODS AND RESULTS: Consecutive patients (n = 133) underwent 4 +/- 3 serial electrophysiologic studies (EPS) over 50 +/- 26 months following ICD implantation. Sustained VT/VF could always be induced during follow-up EPS in 49 patients; sustained VT/VF was sometimes induced during follow-up EPS in 47 patients; and sustained VT/VF could never be induced during follow-up EPS in 37 patients. Spontaneous VT/VF requiring ICD therapy occurred in 107 patients during follow-up. Patients with sustained VT/VF that was always inducible or sometimes inducible during follow-up experienced more frequent episodes of VT/VF following ICD implant (20.5, 95% CI 12.7-33.0; and 17.8, 95% CI 11.3-28.1 episodes/patient respectively; vs 3.0, 95% CI 2.0-4.6 episodes/patient for patients with VT/VF never induced, P < 0.001). Inducibility of sustained VT/VF post-ICD implant (P < 0.001) and sustained VT as the presenting arrhythmia (P = 0.02) were independent predictors of spontaneous VT/VF recurrence. CONCLUSION: Reproducibly inducible VT/VF following ICD implantation predicts a high probability of VT/VF recurrence and identifies a cohort of patients who experience frequent episodes of VT/VF over time. Persistent noninducibility of sustained VT/VF identifies a group of patients who experience no or very few episodes of VT/VF recurrence.
Aged↗
Randomized controlled trial of fixed rate versus rate responsive pacing after radiofrequency atrioventricular junction ablation: quality of life, ventricular refractoriness, and paced QT dispersion.
INTRODUCTION: Ablation of the AV junction is a widely accepted treatment of drug-refractory atrial fibrillation. Long-term pacing of the right ventricular (RV) apex following AV junction ablation can result in adverse cardiac remodeling. However, anecdotal studies report that pacing too slowly following AV junction ablation was associated with propensity to sudden cardiac death. The aim of this study was to provide information about the balance between measures of quality of life versus measures of electrical remodeling achieved by pacing with different rate modalities in a randomized pilot clinical trial. METHODS AND RESULTS: Patients with permanent atrial fibrillation were randomized to VVI (80 beats/min) versus VVIR (minimum rate 80 beats/min), whereas patients with paroxysmal atrial fibrillation were randomized to DDI versus DDDR pacing at discharge from hospital. Serially, measurements of exercise capacity, quality of life, cycle length dependence of QT dispersion (QTdisp), RV refractoriness, and the incidence of nonsustained ventricular tachycardia were made in 28 patients over a 6-month follow-up period. Time-dependent increases in QTdisp were observed in patients randomized to the rate responsive mode (RR-ON) but only when paced at 40 beats/min. This was paralleled by time-dependent increases in RV refractoriness (270 +/- 11 ms at baseline to 302 +/- 5 ms at 6 months) in patients with RR-ON. RR-ON also was associated with trends to an increasing incidence of episodes of nonsustained ventricular tachycardia and worsening of some measures of quality of life. Exercise capacity was not substantially different in the randomized groups. CONCLUSION: Rate responsive pacing results in electrical remodeling of the ventricle following AV junction ablation, but exercise capacity was similar in groups with RR-ON or RR-OFF.
Aged↗
Role of pacemakers in treating neurocardiogenic syncope.
Patients with frequent vasovagal syncope have a poor quality of life and often resist treatment with standard pharmacologic approaches. Clinical vasovagal syncope may be associated with some degree of bradycardia. Studies of temporary pacing during tilt table tests showed that pacing prevented syncope in a little more than half of patients who developed a vasovagal response. Six open-label studies of permanent pacing show that permanent pacemaker therapy is associated with substantial improvement over medical therapy. The roles of specific pacemaker modes have not been determined, although there is some evidence that rate-drop responsiveness helps. The second Vasovagal Pacemaker Study will quantify the true benefits of pacing for vasovagal syncope and assess the role of rate-drop response algorithms.
Cardiac Pacing, Artificial↗
Selective knockout of mouse ERG1 B potassium channel eliminates I(Kr) in adult ventricular myocytes and elicits episodes of abrupt sinus bradycardia.
The ERG1 gene encodes a family of potassium channels. Mutations in human ERG1 lead to defects in cardiac repolarization, referred to as the long QT syndrome. Through homologous recombination in mouse embryonic stem cells the ERG1 B potassium channel transcript was eliminated while the ERG1 A transcript was maintained. Heterologous expression of ERG1 isoforms had previously indicated that the deactivation time course of ERG1 B is 10-fold more rapid than that of ERG1 A. In day-18 fetal +/+ myocytes, I(Kr) exhibited two time constants of deactivation (3,933 +/- 404 and 350 +/- 19 ms at -50 mV), whereas in age-matched ERG1 B(-/-) mice the rapid component was absent. Biexponential deactivation rates (2,039 +/- 268 and 163 +/- 43 ms at -50 mV) were also observed in adult +/+ myocytes. In adult ERG1 B(-/-) myocytes no I(Kr) was detected. Electrocardiogram intervals were similar in +/+ and -/- mice. However, adult -/- mice manifested abrupt spontaneous episodes of sinus bradycardia (>100 ms of slowing) in 6 out of 21 mice. This phenomenon was never observed in +/+ mice (0 out of 16). We conclude that ERG1 B is necessary for I(Kr) expression in the surface membrane of adult myocytes. Knockout of ERG1 B predisposes mice to episodic sinus bradycardia.
Age Factors↗
Learning needs of patients with vasovagal syncope.
This exploratory, descriptive study was undertaken to identify common questions and concerns that patients with vasovagal syncope have about their condition. A semistructured interview format was used to survey patients' subjective learning needs. Interview transcripts were analyzed qualitatively for content themes using the grounded theory procedure of open coding. A convenience sample of 10 patients referred to a university-based syncope clinic at a tertiary care centre for investigation of unexplained syncope was used. The diagnosis of vasovagal syncope was confirmed based on clinical features and tilt table testing. Patients universally communicated broad areas of learning needs with regard to their condition, including etiology, management, natural history, and prognosis. A number of more specific subcategories of learning needs were also found in the majority of patients sampled. Patients with vasovagal syncope share a number of well-defined categories of subjectively identified learning needs. These categories should guide attempts to provide patients with relevant counselling, reassurance, and education.
Adult↗
Syncope: investigation and treatment.
Syncope is a common condition that can be both disabling and expensive to treat. Although investigative modalities are sometimes required, a diagnosis can often be made with a good history and physical exam. Recent reports have identified specific historic features that are more suggestive of cardiac syncope as compared with vasovagal syncope and seizures. Advances in ambulatory electrocardiography (in particular the implantable loop recorder) have proven invaluable in both difficult-to-diagnose syncope, and in advancing our knowledge of its mechanisms. When clear dysrhythmias are manifest, appropriate therapies are self-evident. However, recurrent vasovagal syncope continues to be a condition that can be difficult to treat. Fortunately, there are well-conducted trials of both pharmacologic therapies (b-blockers, alpha agonists, and selective serotonin reuptake inhibitors) and nonpharmacologic treatments (orthostatic physical training and dual-chamber pacemakers) that should provide more guidance in the near future.
Humans↗
Precordial QT dispersion does not predict inducibility of ventricular tachyarrhythmias at post-revascularization electrophysiologic study.
OBJECTIVES: We tested the hypothesis that revascularization would decrease QT interval dispersion and that QT interval dispersion would predict the outcome of the electrophysiologic study following revascularization. BACKGROUND: QT interval dispersion may be a measure of the inhomogeneity of ventricular repolarization. The value of the QT interval dispersion for predicting inducibility of ventricular tachyarrhythmias (VT) during electrophysiologic studies after coronary artery revascularization in patients with hemodynamically significant VT is unknown. METHODS AND RESULTS: QT interval dispersions were measured from electrocardiograms recorded before and after coronary artery revascularization, but before an electrophysiologic study during the same hospitalization. Fifty-six patients (93% male, 65.1 +/- 9.6 years) were studied. QT interval dispersion decreased significantly following revascularization from 69 +/- 31 ms to 53 +/- 23 ms (p=0.002). Inducibility of VT could not be predicted by the QT interval dispersion following revascularization (50 +/- 30 ms in patients with VT induced vs. 58 +/- 25 ms in patients without VT induced at electrophysiologic study; p=0.2). The change in QT interval dispersion with revascularization (-15 +/- 33 ms vs. -17 +/- 46 ms; p=0.9) could not predict VT inducibility. Actuarial survival after 80 months follow-up was similar in the patients in whom VT was induced (82%) and those patients in whom VT was not induced (83%; p=NS). CONCLUSIONS: Coronary artery revascularization decreased QT interval dispersion in patients with hemodynamically significant VT, but QT interval dispersion was not predictive of inducibility of VT at follow-up electrophysiologic study. Actuarial survival was similar in patients in whom VT was induced and patients in whom VT was not induced.
Aged↗
Permanent cardiac pacing to prevent vasovagal syncope.
Patients with frequent vasovagal syncope have a poor quality of life and often resist treatment with standard pharmacologic approaches. Although the evidence is weak, clinical vasovagal syncope is probably associated with some degree of bradycardia. Studies of temporary pacing during tilt table tests showed that pacing prevented syncope in a little over half of patients who developed a vasovagal response. Six open-label studies of permanent pacing show that permanent pacemaker therapy is associated with substantial improvement over medical therapy. The roles of specific pacemaker modes have not been determined, although there is some evidence that rate-drop responsiveness helps. The second Vasovagal Pacemaker Study will quantify the true benefits of pacing for vasovagal syncope and assess the role of rate-drop response algorithms.
Bradycardia↗