Sinus Tachycardia: a Multidisciplinary Expert Focused Review.

Sinus tachycardia (ST) is ubiquitous, but its presence outside of normal physiological triggers in otherwise healthy individuals remains a commonly encountered phenomenon in medical practice. In many cases, ST can be readily explained by a current medical condition that precipitates an increase in the sinus rate, but ST at rest without physiological triggers may also represent a spectrum of normal. In other cases, ST may not have an easily explainable cause but may represent serious underlying pathology and can be associated with intolerable symptoms. The classification of ST, consideration of possible etiologies, as well as the decisions of when and how to intervene can be difficult. ST can be classified as secondary to a specific, usually treatable, medical condition (eg, pulmonary embolism, anemia, infection, or hyperthyroidism) or be related to several incompletely defined conditions (eg, inappropriate ST, postural tachycardia syndrome, mast cell disorder, or post-COVID syndrome). While cardiologists and cardiac electrophysiologists often evaluate patients with symptoms associated with persistent or paroxysmal ST, an optimal approach remains uncertain. Due to the many possible conditions associated with ST, and an overlap in medical specialists who see these patients, the inclusion of experts in different fields is essential for a more comprehensive understanding. This article is unique in that it was composed by international experts in Neurology, Psychology, Autonomic Medicine, Allergy and Immunology, Exercise Physiology, Pulmonology and Critical Care Medicine, Endocrinology, Cardiology, and Cardiac Electrophysiology in the hope that it will facilitate a more complete understanding and thereby result in the better care of patients with ST.

Characteristics of heart rate reduction with resumption of supine position in the postural tachycardia syndrome: factors influencing recovery.

OBJECTIVES: Postural orthostatic tachycardia syndrome (POTS), a heart rate (HR) rise with upright positioning, is dependent on autonomic influences. HR recovery (HR decrease after exercise cessation) is a measure of autonomic function. Characteristics of HR reduction during supine Recovery after head-up Tilt in POTS patients have not been elucidated. METHODS: 113 subjects (mean age 41.7 years, 86 female), diagnosed with POTS on head-up Tilt were analyzed. HR's were recorded during baseline supine position, 70-degree Tilt, and 20 sec, 1 min and 2 min of supine Recovery. Percent HR reduction during Recovery was calculated. RESULTS: Baseline HR was 68.7±13.4 bpm. Maximum HR during Tilt was 109±16.9 bpm. Mean HR was 84.2±20 bpm at 20 sec, 78.5±18.9 bpm at 1-min, and 77.1±18.3 bpm at 2 min of Recovery. Younger age and slower baseline HR were associated with greater HR reductions at 20 sec (p=0.006, p=0.000, respectively). Younger age, slower baseline HR and less time to achieve POTS were associated with greater HR reductions at 1 min (p=0.025, p=0.000, p=0.000, respectively) and at 2 min (p=0.004, p=0.000, p=0.000, respectively). Gender and baseline blood pressures were not significant. CONCLUSIONS: In POTS patients, HR quickly decreases upon resuming supine position. Younger age, slower baseline HR and less time to achieve POTS were associated with greater HR reductions during supine Recovery. Further study is needed to determine mechanisms, as well as analyze differences in symptoms or prognosis.

POTS due to excessive venous pooling in an enlarged inferior vena cava.

Postural tachycardia syndrome (POTS) is a form of orthostatic intolerance characterized by a marked increase in heart rate within the first 10 min of head-up tilt (HUT). We present a patient whose enlarged inferior vena cava that appears to be a contributing mechanism to her POTS and presyncopal symptoms.

Effect of metoprolol on quality of life in the Prevention of Syncope Trial.

INTRODUCTION: Vasovagal syncope is common, often recurrent, and reduces quality of life. No therapies have proven useful to improve quality of life in adequately designed randomized clinical trials. Beta-blockers have mixed evidence for effectiveness in preventing syncope. METHODS: The Prevention of Syncope Trial was a randomized, placebo-controlled, double-blind, multinational, clinical trial that tested the hypothesis that metoprolol improves quality of life in adult patients with vasovagal syncope in a 1-year observation period. Randomization was stratified in strata of patients <42 and > or =42 years old. The quality of life questionnaires Short Form-36 (SF-36) and Euroqol EQ-5D were completed at baseline and after 6 and 12 months of treatment by 204, 132, and 121 patients, respectively. RESULTS: There were 208 patients, mean age 42 +/- 18, of whom 134 (64%) were females. All had positive tilt tests. There was no improvement in quality of life during the trial in the entire group or in either treatment arm. Patients in the metoprolol treatment arm did not have improved quality of life compared to the patients in the placebo arm using either the SF-36 or EQ5D after either 6 or 12 months. Finally, there was no improvement in quality of life associated with metoprolol use in patients either <42 or > or =42 years of age. CONCLUSION: Metoprolol does not improve quality of life in patients with recurrent vasovagal syncope and a positive tilt test.

The incidence of coexistent autonomic and vestibular dysfunction in patients with postural dizziness.

PURPOSE: To evaluate the incidence of coexistent peripheral vestibular dysfunction and cardiovascular autonomic dysfunction in patients undergoing evaluation for dizziness exacerbated by postural changes. MATERIALS AND METHODS: Retrospective case review of 56 sequential patients seen from 2003 to 2006 at a tertiary center for a primary complaint of dizziness who underwent both passive tilt table testing for evaluation of neurocardiogenic etiology and quantitative vestibular testing. The vestibular test battery consisted of alternating bithermal caloric testing; computerized sinusoidal vertical axis rotation (at frequencies 0.01-0.64) with infrared videonystagmography; and oculomotor and positional testing including bilateral Dix-Hallpike, head center supine, and 30-degree supine head turns right and left. RESULTS: Eight of the 56 subjects had caloric weakness. Forty-five subjects (80%) had abnormal tilt table test findings. The incidence of coexistent neurocardiogenic and vestibular test abnormalities was 10.7%. There was no significant association between abnormal tilt table test result and caloric weakness (Fisher exact test; P = .64). The degree of compensation seen on vestibule-ocular reflex gain testing did not affect tilt table findings (chi2; P = .872). CONCLUSIONS: There is no difference in the rate of postural orthostatic intolerance in subjects with evidence of caloric weakness compared with those with normal caloric function.

Design and use of a quantitative scale for measuring presyncope.

INTRODUCTION: Vasovagal syncope is common and distressing. One important symptom is presyncope, but there are no clinimetric measures of this. We developed the Calgary Presyncope Form (CPF) and used it to test whether metoprolol reduces presyncope in a randomized trial. METHODS: The CPF captures the frequency, duration, and severity of presyncope. We administered it to participants in the Prevention of Syncope Trial (POST), a randomized clinical trial that tested the hypothesis that metoprolol reduces syncope and presyncope in adult patients with vasovagal syncope. RESULTS: The CPF was completed by 44 patients on metoprolol and 39 patients on placebo, of a total of 208 subjects. Completion of the CPF for each of the threedimensions was 84-87% in the 83 respondents. Results were centrally distributed in duration and severity dimensions, but not in frequency. Patients had a median of 1.2 presyncopal spells per day, with a median moderate severity, lasting a median 10 minutes. The 3 scales were statistically independent of each other. These results were independent of subject age, and results in all 3 dimensions were stable over the observation period. There was no significant difference between patients on metoprolol and placebo in any dimension. CONCLUSION: The 3-dimensional CPF is simple, easy to use, stable over time, measures 3 independent variables, and documents that metoprolol does not reduce presyncope.

Early versus late postural tachycardia: a re-evaluation of a syndrome.

Postural tachycardia syndrome (POTS) involves an HR-rise within 10 minutes of head-up tilt. Hypokinetic circulation, older age, and ACE-inhibitor or Angiotensin-Receptor Blockers were associated with "Late" POTS (after 10 minutes of tilt) versus "Early" POTS (within 10 minutes of tilt).

Dynamic changes in T-wave amplitude during tilt table testing: correlation with outcomes.

BACKGROUND: Changes in autonomic tone may play a role in syncope. Autonomic tone has been shown to affect cardiac repolarization in the ECG. Changes in the T wave can be seen during head-up tilt table (HUT) testing with unknown significance or relationship to outcomes. METHODS: Twelve-lead ECGs during HUT testing from 150 patients were reviewed from a prospectively collected registry database. ECGs during supine-rest, 30-45-70 degrees tilt, and 5-minute supine recovery were reviewed. Changes in the T wave, that is, decreased amplitude with or without becoming negative or flipping from negative to positive, were recorded for each stage. Outcomes of the HUT test include nondiagnostic, postural orthostatic hypotension (POH), postural orthostatic tachycardia syndrome (POTS), and vasovagal response (VVR). Age (Younger: <50 year old; Older: > or = 50 year old) and gender were analyzed. RESULTS: Of 150 patients (108 women; 80 Younger), 135 had T-wave changes during HUT; changes resolved in 114 patients during supine recovery. Changes mostly occurred in inferior and anterolateral leads. POH occurred in 114 patients, POTS in 67, and VVR in 30. T-wave changes in V1 inversely correlated with POH (P = 0.005). T-wave changes in inferior leads II, III, aVF and in anterolateral leads V3-V6 positively correlated with POTS (P < 0.05). Female gender and younger age correlated with POTS independent of the leads (P < 0.05). Concomitant T-wave changes in V5 and V6 correlated with VVR; changes in aVF also correlated with VVR (P < 0.05). CONCLUSIONS: Dynamic T-wave changes during HUT testing in inferior and anterolateral leads are associated with POTS and VVR independent of age and gender. Changes in autonomic tone may play a role and need further study.

Blood volume measurement as a tool in diagnosing syncope.

BACKGROUND: The cause of syncope remains unknown in 24% to 37% of cases even after standard diagnostic tests. Measuring blood volume may elucidate the mechanisms of syncope in the individual patient and prove helpful in determining optimal therapy. This report includes the largest set of blood volume measurements performed in syncope patients to date. METHODS: We performed radioisotopic blood volume measurement (Daxor BVA-100) on 539 patients who presented to our center with syncope/presyncope of unclear etiology. There were 202 men and 337 women, ages 16 to 88 years; many were receiving treatment at the time they were referred to our center. We also measured blood pressure, heart rate, and cardiac index before and during tilt, with complete data available for 411 patients. RESULTS: Blood volume derangements ranged from -32% to +116% deviation from normal. Hematocrit could not be used to predict volume status. Volume depletion was found in 241 (44.7%) patients and volume expansion was found in 63 (11.7%). Blood pressure, heart rate, and cardiac index before and during tilt did not correlate with any component of blood volume and could not be used to predict volume status. CONCLUSIONS: Syncope patients are heterogeneous with respect to blood volume, and blood volume derangements are common and are not identified through tilt table testing. Empirically prescribed pharmacological treatment for syncope is frequently inappropriate. Blood volume measurement should be included in syncope diagnosis.

Prevention of Syncope Trial (POST): a randomized, placebo-controlled study of metoprolol in the prevention of vasovagal syncope.

BACKGROUND: Previous studies that assessed the effects of beta-blockers in preventing vasovagal syncope provided mixed results. Our goal was to determine whether treatment with metoprolol reduces the risk of syncope in patients with vasovagal syncope. METHODS AND RESULTS: The multicenter Prevention of Syncope Trial (POST) was a randomized, placebo-controlled, double-blind, trial designed to assess the effects of metoprolol in vasovagal syncope over a 1-year treatment period. Two prespecified analyses included the relationships of age and initial tilt-test results to any benefit from metoprolol. All patients had >2 syncopal spells and a positive tilt test. Randomization was stratified according to ages <42 and > or =42 years. Patients received either metoprolol or matching placebo at highest-tolerated doses from 25 to 200 mg daily. The main outcome measure was the first recurrence of syncope. A total of 208 patients (mean age 42+/-18 years) with a median of 9 syncopal spells over a median of 11 years were randomized, 108 to receive metoprolol and 100 to the placebo group. There were 75 patients with > or =1 recurrence of syncope. The likelihood of recurrent syncope was not significantly different between groups. Neither the age of the patient nor the need for isoproterenol to produce a positive tilt test predicted subsequent significant benefit from metoprolol. CONCLUSIONS: Metoprolol was not effective in preventing vasovagal syncope in the study population.

Blood volume and brain natriuretic peptide in congestive heart failure: a pilot study.

BACKGROUND: Brain natriuretic peptide (BNP) levels rise in response to stretch of ventricular myocytes or increases in wall tension, as in congestive heart failure (CHF). Brain natriuretic peptide can be released in bursts, but nonetheless, BNP levels may lag behind clinical changes. We postulated that concomitant measurement of blood volume (BV), BNP, and hemodynamics during treatment of CHF may elucidate interrelationships among changes in these parameters. METHODS: We studied 10 male patients, aged 60 +/- 8 years, who were admitted for pulmonary catheter-guided treatment of CHF. Hemodynamics, venous BNP, and blood and plasma volumes were measured at baseline before treatment and again on the following morning after 12 to 24 hours of acute treatment for CHF. RESULTS: At baseline, all 10 patients exhibited marked expansion of BV at 29% +/- 19%. At baseline, increased systolic pulmonary artery pressure correlated with BV (r = 0.615) and diastolic pulmonary artery pressure (PAD) with BV (r = 0.609). After treatment, there was an inverse correlation between change (decline) in expanded BV and change (improvement) in mixed venous oxygenation (r = -0.775) and a positive correlation with central venous pressure (CVP) (r = 0.710). Poor correlation was found between BNP and any hemodynamic parameter. Little correlation was found between absolute BNP and BV before or after treatment (r = -0.127 and -0.126, respectively). CONCLUSION: In this pilot study, changes in BV with treatment correlate better with hemodynamics than do changes in BNP, likely reflecting the lag in BNP response to treatment and its tendency to reflect long-term rather than instantaneous volume status. These preliminary data suggest that BV may be a more accurate guide in optimizing CHF treatment than BNP.

Plasma volume and outcome in pulmonary hypertension.

Poor survival in pulmonary hypertension is known to be associated with unfavorable hemodynamic variables, including elevated right atrial pressure, elevated mean pulmonary artery pressure, and low cardiac index. However, the effect of plasma volume on outcome has not been evaluated. Our goal was to study the spectrum of plasma volume distribution in patients with pulmonary hypertension and to determine whether plasma volume could provide any prognostic insight in these patients. Our pilot study comprised 11 patients (aged 46 +/- 16 years; 7 women) who were undergoing pulmonary artery catheterization before vasodilator therapy. In all 11 patients, plasma volume was measured, with use of < 25 microCi 131I-radioiodinated serum albumin. Patient follow-up averaged 19 months. There were 2 deaths. The 2 patients who died had the highest right atrial pressures in the group: > or = 17 mmHg. Those 2 patients also had 2 of the 3 highest plasma volumes at > or = 8.4%. None of the patients underwent lung transplantation. The propensity for elevated plasma volume and right atrial pressure in patients who died in this pilot study is consistent with the advanced right-sided heart failure that occurs in the terminal stages of pulmonary hypertension. Elevated plasma volume may be a useful prognosticator; further studies are needed to assess whether manipulation of plasma volume affects prognosis.