ArticleCirculation. Arrhythmia and electrophysiology2020
When Sinus Tachycardia Becomes Too Much: Negative Effects of Excessive Upright Tachycardia on Cardiac Output in Vasovagal Syncope, Postural Tachycardia Syndrome, and Inappropriate Sinus Tachycardia.
Article in Circulation. Arrhythmia and electrophysiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Ivabradine in Postural Orthostatic Tachycardia Syndrome. Is That All We Need?Arquivos brasileiros de cardiologia · 2026Article
- The Role of the Autonomic Nervous System in Vasovagal Syncope.Cardiac electrophysiology clinics · 2024Review
- SleepBP-Net: A Time-Distributed Convolutional Network for Nocturnal Blood Pressure Estimation from Photoplethysmogram.IEEE sensors journal · 2024Article
- Phenylephrine alters phase synchronization between cerebral blood velocity and blood pressure in ME/CFS with orthostatic intolerance.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Understanding how closed-loop stimulation pacing suppresses cardioinhibition in vasovagal syncope.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Article
- Sinus Tachycardia: a Multidisciplinary Expert Focused Review.Circulation. Arrhythmia and electrophysiology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundUpright posture reduces venous return, stroke volume, and cardiac output (CO) while causing reflex sinus rate (heart rate [HR]) increase. Yet, in inappropriate sinus tachycardia (IST), postural tachycardia syndrome (POTS), and vasovagal syncope (VVS), symptomatic excessive HR occurs. We hypothesized that CO reaches maximum as function of HR in all.
methodsWe recruited 12 healthy controls, 9 IST, 30 VVS, and 30 POTS patients (13-23years) selected randomly by disorder not by HR, each fulfilled appropriate diagnostic criteria. Subjects were instrumented for electrocardiography, beat-to-beat blood pressure, respiratory rate, CO-Modelflow algorithm, and central blood volume from impedance cardiography; 10-minute data were collected supine; subjects were tilted head-up for ≤10 minutes. We computed phase differences, ΔΦ, between fluctuations of HR (ΔHR) and CO (ΔCO) tabulating data when phases were synchronized, determined by a squared nonlinear phase synchronization index >0.5, describing extent/validity of CO/HR coupling. We graphed results supine, 1-minute post-tilt-up, mid-tilt, and pre-tilt-down using polar coordinates (HR-radius, ΔΦ-angle) plotting cos(ΔΦ) versus HR to determine if transition HR exists at which in-phase shifts to antiphase above which CO decreases when HR further increases.
resultsAt baseline HR, diastolic and mean arterial pressures in IST and POTS were higher versus controls. Upright HR increased most in POTS then IST and VVS, with diverse changes in CO, SVR, and central blood volume. Each patient grouping was separately and collectively analyzed for HR change showing transition from in-phase to anti-phase (ΔΦ) as HR increased: HR
conclusionsExcessive HR independently and equivalently reduces upright CO, in IST, POTS, and VVS.
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Registered trials
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