Atrial Pacing Rate Research Articles

A less aggressive therapeutic option for electrical storm.

Electrical storm (ES) describes the rapidly clustering ventricular fibrillation (VF) that requires multiple cardioversions. Emerging evidence suggests that Purkinje arborization and sympathetic nerve regeneration play a major role in initiating malignant arrhythmias. We report the case of two patients who, after having survived an acute myocardial infarction (MI), developed repetitive episodes of polymorphic ventricular tachycardia and VF one week after percutaneous revascularization, triggered by monomorphic premature ventricular contractions (PVCs). Owing to repetitive and drug-refractory VF episodes, temporary atrial overdrive pacing was attempted with complete suppression of VF. In the following month, recurrence of ventricular arrhythmia was inversely related to the atrial pacing rate. Although antiarrhythmic drugs other than beta-blockers had been discontinued, neither PVCs nor ventricular arrhythmias recurred at one-month follow-up when the lower pacing rate was set at 60 bpm. In conclusion in these patients, ES was likely related to nerve sprouting after ischemic injury. This chaotic phenomenon occurs early after tissue damage and shows a peak seven days after acute MI with degeneration of superfluous axon branches. High pacing rates can reduce early after depolarizations and suppress PVCs, thus preventing ES. On these grounds, ES patients may be treated with temporary overdrive pacing rather than early radiofrequency ablation.

Facilitating assessment of QT interval duration during ventricular pacing

We aimed to facilitate the assessment of the QT interval duration during conventional right ventricular pacing (VP) by uncovering relationships with the underlying QT interval during intrinsic atrioventricular conduction (IC). The study patients (n = 122, age 68 ± 11 years) were dual-chamber device recipients with preserved IC and narrow QRS complexes. Patients were classified into either 'normal-QT' (n = 70) or 'prolonged-QT' (n = 52) group. Incremental atrial pacing rates were exercised to record serial QT/JT intervals over 5 min periods in IC mode and then in VP mode. Six different QT correction methods for heart rate were applied to assess the effect (i) of pacing mode (IC vs. VP) and (ii) of heart rate on the derived QT(c)/JT(c) intervals by mixed-effects linear models. Following VP, the uncorrected QT/JT intervals as well as the JTc intervals shortened (P < 0.001), whereas the QTc intervals prolonged (P < 0.001). In both patient groups, the Framingham and Nomogram methods demonstrated the optimal balance to assess QTc, with low heart rate dependence during VP and minimal interaction between pacing mode and heart rate. The Rautaharju formula provided excellent correction for the QT changes induced by VP, but the QTc interval responded differently to rate changes in IC vs. VP mode. Bazett's formula exaggerated QTc/JTc rate dependency during VP. The Framingham and Nomogram correction methods perform most reliably in assessing the underlying QT interval during IC from the ventricular paced QT interval.

THE TIME COURSE OF ELECTRICAL REMODELLING, STRUCTURAL REMODELLING, NEURAL REMODELLING AND ENDOTHELIN-1 LEVEL IN ATRIAL FIBRILLATION

ObjectivesThe consistency between electrical remodelling, structural remodelling, neural remodelling and endothelin-1 level in atrial fibrillation (AF) has not been reported. The present study aimed to investigate the time course of...

Central versus peripheral control of cardiac output in humans: insight from atrial pacing

Central <i>versus</i> peripheral control of cardiac output in humans: insight from atrial pacing

Shortening of atrioventricular delay at increased atrial paced heart rates improves diastolic filling and functional class in patients with biventricular pacing

BackgroundUse of rate adaptive atrioventricular (AV) delay remains controversial in patients with biventricular (Biv) pacing. We hypothesized that a shortened AV delay would provide optimal diastolic filling by allowing separation of early and late diastolic filling at increased heart rate (HR) in these patients.Methods34 patients (75 ± 11 yrs, 24 M, LVEF 34 ± 12%) with Biv and atrial pacing had optimal AV delay determined at baseline HR by Doppler echocardiography. Atrial pacing rate was then increased in 10 bpm increments to a maximum of 90 bpm. At each atrial pacing HR, optimal AV delay was determined by changing AV delay until best E and A wave separation was seen on mitral inflow pulsed wave (PW) Doppler (defined as increased atrial duration from baseline or prior pacemaker setting with minimal atrial truncation). Left ventricular (LV) systolic ejection time and velocity time integral (VTI) at fixed and optimal AV delay was also tested in 13 patients. Rate adaptive AV delay was then programmed according to the optimal AV delay at the highest HR tested and patients were followed for 1 month to assess change in NYHA class and Quality of Life Score as assessed by Minnesota Living with Heart Failure Questionnaire.Results81 AV delays were evaluated at different atrial pacing rates. Optimal AV delay decreased as atrial paced HR increased (201 ms at 60 bpm, 187 ms at 70 bpm, 146 ms at 80 bpm and 123 ms at 90 bpm (ANOVA F-statistic = 15, p = 0.0010). Diastolic filling time (P < 0.001 vs. fixed AV delay), mitral inflow VTI (p < 0.05 vs fixed AV delay) and systolic ejection time (p < 0.02 vs. fixed AV delay) improved by 14%, 5% and 4% respectively at optimal versus fixed AV delay at the same HR. NYHA improved from 2.6 ± 0.7 at baseline to 1.7 ± 0.8 (p < 0.01) 1 month post optimization. Physical component of Quality of Life Score improved from 32 ± 17 at baseline to 25 ± 12 (p < 0.05) at follow up.ConclusionsIncreased heart rate by atrial pacing in patients with Biv pacing causes compromise in diastolic filling time which can be improved by AV delay shortening. Aggressive AV delay shortening was required at heart rates in physiologic range to achieve optimal diastolic filling and was associated with an increase in LV ejection time during optimization. Functional class improved at 1 month post optimization using aggressive AV delay shortening algorithm derived from echo-guidance at the time of Biv pacemaker optimization.

ORAL PRESENTATION

ORAL PRESENTATION

Effects of Pacing Rates on Global and Regional Myocardial Blood Flow

Information is scarce on the effects of right ventricular apical (RVA) pacing on regional and global myocardial blood flow (MBF). The purpose of this study was to assess the relationship between pacing rate and both regional and global MBF. Four patients with exclusive atrial pacing and six patients with exclusive RVA pacing underwent three consecutive H(2) (15)O positron emission tomography scans at 60, 90, and 130 pulses per minute (ppm). For each pacing rate, regional and global MBF was determined. In all patients, the left ventricular (LV) function was normal. By varying the atrial pacing rate from 60 to 130 ppm, the mean global MBF increased from 0.94 to 1.40 mL/g/min, whereas the mean septal to lateral MBF ratio decreased from 1.09 to 0.83. In ventricular-paced patients at corresponding rates, the mean global MBF also increased from 1.07 to 1.52 mL/g/min but here the mean septal to lateral MBF ratio increased from 0.83 to 1.0. During both acute atrial and RVA pacing, regional and global MBF increases with higher pacing rates. However, the septal to lateral MBF ratio decreases with atrial pacing and increases with RVA pacing in patients with normal LV function. In RVA pacing, these different rate-dependent effects on regional MBF can be considered as a favorable factor that helps to understand why in some long-term paced patients, LV function is preserved.

Effects of Autonomic Interventions on Atrial Restitution Properties

Atrial Restitution Properties. The restitution hypothesis suggests that action potential duration (APD) restitution slope >1 predicts the development of alternans and fibrillation. This study aimed to investigate the effects of autonomic interventions on the restitution properties on the atria. In 10 anesthetized open-chest dogs, multiple electrode catheters were sutured at pulmonary vein and atrial sites. The monophasic APD was recorded by an Ag-AgCl catheter. The restitution curve at each site was constructed by plotting each APD(90) against the preceding diastolic interval at incremental atrial pacing rates before and after vagal nerve stimulation (VNS) or ganglionated plexi (GP) ablation. Before GP ablation, VNS significantly shortened the APD, flattened the restitution curves and suppressed the APD alternans at each site, while increasing the atrial fibrillation (AF) inducibility and duration (P < 0.05 for all). These effects were eliminated by GP ablation. Compared with the baseline, GP ablation significantly increased the APD, steepened the restitution curves, and facilitated the APD alternans at each site while decreasing the AF inducibility and duration (P < 0.05 for all). VNS significantly increased (0.5 ± 0.2 vs 0.3 ± 0.1, P < 0.05) and GP ablation decreased (0.2 ± 0.1 vs 0.3 ± 0.1, P < 0.05) the spatial dispersion of the slopes of APDR curves, respectively. The maximal slope of APDR curve alone does not fully account for the changes of AF inducibility and duration induced by autonomic interventions; instead, the spatial dispersion of the APDR kinetics may be an important determinant for susceptibility of AF.

Rate Response Function of Pacemaker with Closed-Loop Stimulation (CLS) to Blood Pressure Variation during Dialysis in a Bradycardia Patient

Purpose: The patient was a 70-year old male under maintenance dialysis because of diabetic nephropathy. For his advanced atrioventricular block, we implanted a pacemaker (PM) with CLS function (Entovis DR/CLS, Nihon Kohden, BIOTRONIK) (DDD-CLS, basic rate 60 ppm) and then monitored heart rate response during dialysis. Results: Until 120 minutes after start of dialysis, systolic blood pressure (Ps) and heart rate (HR) shifted in the ranges of 158 to 167 mmHg and 60 to 63 bpm in the pacing behavior of As-Vp. About 130 to 140 minutes after start of dialysis, Ps suddenly dropped from 178 to 159 mmHg, then As-Vp changed to Ap-Vp with an increased atrial paing rate of up to 69 ppm earlier than an increase of patient’s sinus rate, so that Ps had a tendency of early recovery. Discussion: It may be possible that when Ps dropped suddenly, CLS function detected intracardiac impedance changes which reflected changes in myocardial contraction dynamics yielded by circulating blood volume reduction due to water removal during dialysis. Conclusion: When blood pressure drops during dialysis with little body motion, an increase of atrial pacing rate by PM with CLS function may help recover blood pressure early. We will accumulate data further in order to investigate effectiveness of cardiac pacing for dialysis hypotension.

Roles of Autonomic Nerve System on the Evolution of PAF to PRAF

Atrial fibrillation (AF) can be either paroxysmal or sustained. Not all patients with paroxysmal AF progress to sustained forms. The mechanisms by which paroxysmal AF progresses to sustained AF remain poorly understood. Intermittent rapid atrial pacing in large animals can initially induce paroxysmal AF followed by transition to persistent AF. Pacing-induced shortening of the effective refractory periods were thought to underlie the mechanisms of AF progression. However, the time course of changes in atrial refractoriness did not completely run parallel with the time course of development of sustained AF. We analyzed long-term recording of nerve activities in ambulatory dogs, and used an intermittent high rate atrial pacing protocol to determine the duration of pacing needed to induce sustained (>48 hrs) of AF. We found that differential patterns of interactions among cardiac autonomic structures naturally exist at baseline (before pacing). We also noted that dogs with good linear sympathovagal correlation and higher vagal tone at baseline have more paroxysmal atrial tachycardias at baseline and faster induction of sustained AF by rapid pacing, as compared to dogs with an L-shaped sympathovagal correlation and lower vagal tone at baseline. These findings suggest that simultaneous sympathovagal discharges, which simultaneously increase Ca2+ entry and shortens the action potential duration, are important in the development of persistent AF.

Implantable Sensors for Heart Failure

Heart failure (HF) affects more than 5 million Americans, and acute decompensated heart failure (ADHF) has emerged as the leading cause of hospitalization among people over the age of 65 years.1 Importantly, HF is a leading public health concern, and hospitalization expenses related to management of ADHF impose a substantial financial burden on the health care system. Additionally, readmission rates after hospitalization for ADHF may be as high as 50% at 6 months,2 and insights from the ADHERE registry suggest that a majority of patients admitted with ADHF have a history of heart failure.1 These data demonstrate that the majority of patients admitted with ADHF are known to the medical system and to medical providers, thereby creating an opportunity for upstream strategies that may be capable of detecting early HF destabilization and implementing therapies to restabilize the patient and avert hospitalization. The anticipated changes in the health care system—with a focus on bundled payments for disease management—will necessitate robust disease management programs to optimize therapy and minimize recurrent admissions once patients have been diagnosed with HF. Perhaps even more importantly, averting repeat episodes of ADHF is likely to have a stabilizing effect on the progression of HF and may improve long-term morbidity and mortality. The transition from chronic HF to ADHF involves perturbations in multiple intersecting processes including neurohormonal circuits, inflammatory mediators, cardiorenal interactions, and myocardial performance. Concurrently, derangements in comorbid illnesses such as coronary disease, atrial and ventricular arrhythmias, and hypertension also contribute to the pathophysiology of ADHF.3 Ultimately, these multiple pathways lead to an elevation in ventricular filling pressures and signs of vascular congestion, which, in concert with symptoms from impaired cardiac output, lead to the clinical constellation of ADHF. This pathophysiologic paradigm highlights multiple opportunities for detecting early changes in the processes that …

Distinct restitution properties in vagally mediated atrial fibrillation and six-hour rapid pacing-induced atrial fibrillation

The atrial potential duration (APD) restitution has been suggested to play an important role in ventricular fibrillation; however, its role in atrial fibrillation (AF) has not been determined. This study sought to investigate the APD restitution properties in two different AF models: vagally mediated AF and 6-h rapid atrial pacing-induced AF. Twenty anaesthetized open-chest dogs were assigned to Group I, vagally mediated AF (n= 8) or Group II, 6-h rapid atrial pacing-induced AF (n= 12). In both groups, the monophasic APD was subsequently recorded at multiple pulmonary vein and atrial sites. The APD restitution curve was constructed using a dynamic pacing protocol and determined by plotting each APD(90) against the preceding diastolic interval at incremental atrial pacing rates at eight sites. In Group I, vagal stimulation significantly shortened the APD(90), flattened the APD restitution curve (slopes <1), and suppressed the APD alternans at each site, while increasing the AF inducibility and duration (P<0.05 for all). In Group II, 6-h rapid pacing-induced APD shortening steepened the restitution curves (slopes >1), facilitated the APD alternans, and also increased the incidence and duration of AF (P< 0.05 for all). The spatial dispersion of APD restitution was significantly increased in both groups. This study showed distinct atrial APD restitution properties in vagally mediated AF and 6-h rapid pacing-induced AF, indicating specific restitution kinetics in different mechanisms of AF.

Chronic Augmentation of the Parasympathetic Tone to the Atrioventricular Node: A Nonthoracotomy Neurostimulation Technique for Ventricular Rate Control During Atrial Fibrillation

The right inferior ganglionated plexus (RIGP) selectively innervates the atrioventricular node. Temporary electrical stimulation of this plexus reduces the ventricular rate during atrial fibrillation (AF). We sought to assess the feasibility of chronic parasympathetic stimulation for ventricular rate control during AF with a nonthoracotomy intracardiac neurostimulation approach. In 9 mongrel dogs, the small endocardial area inside the right atrium, which overlies the RIGP, was identified by 20 Hz stimulation over a guiding catheter with integrated electrodes. Once identified, an active-fixation lead was implanted. The lead was connected to a subcutaneous neurostimulator. An additional dual-chamber pacemaker was implanted for AF induction by rapid atrial pacing and ventricular rate monitoring. Continuous neurostimulation was delivered for 1-2 years to decrease the ventricular rate during AF to a range of 100-140 bpm. Implantation of a neurostimulation lead was achieved within 37 +/- 12 min. The latency of the negative dromotropic response after on/offset or modulation of neurostimulation was <1 s. Continuous neurostimulation was effective and well tolerated during a 1-2 year follow-up with a stimulation voltage <5 V. The neurostimulation effect displayed a chronaxie-rheobase behavior (chronaxie time of 0.07 +/- 0.02 ms for a 50% decrease of the ventricular rate during AF). Chronic parasympathetic stimulation can be achieved via a cardiac neurostimulator. The approach is safe, effective, and well tolerated in the long term. The atrioventricular nodal selectivity and the opportunity to adjust the negative dromotropic effect within seconds may represent an advantage over pharmacological rate control.

The immediate effects of pacemaker-related electric remodelling on left ventricular function in patients with sick sinus syndrome

The immediate effects of electric remodelling on the left ventricular (LV) function by dual-chamber pacemakers remain unknown. The purpose of our study was to assess the interaction between heart rates and right ventricular pacing (VP) on LV contractility and diastolic function. Twenty-five patients with dual-chamber pacemakers and sick sinus syndrome were evaluated. Echocardiographic examinations included standard and tissue-Doppler echocardiography at bilateral mitral annulus margins under either the intrinsic atrio-ventricular sequential conduction (ventricular sensing; VS) mode or right ventricular apical pacing (VP) mode. Under either mode, we accelerated the pacing rate at an increment of 15 b.p.m. step-by-step from 60 to 90/min. The tissue-Doppler echocardiography of mitral annulus showed that under the VS status, accelerating atrial pacing rate from 60 to 90 b.p.m. enhanced A'-wave velocity (P < or =0.002), whereas no significant change of LV ejection fraction (LVEF) and E'-wave velocity were noted. Under the VP status, acceleration of pacing rates exerted no effect on the LVEF, E'-, and A'-wave (P = NS). While shifting the pacemaker mode from VS to VP, the E'-wave velocity (P < or =0.002) and E'/A' ratio decreased significantly (P < or = 0.001). The A'-wave velocity also increased significantly during shifting to VP mode at 60 b.p.m. (P < or =0.004). At fixed pacing rates, shifting from VS to VP mode impaired LV diastolic function immediately with preserved LV contractility. The acceleration of heart rate impaired LV diastolic function under VS mode.

A Prospective Randomized Study to Assess the Efficacy of Rate and Site of Atrial Pacing on Long‐Term Development of Atrial Fibrillation

The Septal Pacing for Atrial Fibrillation Suppression Evaluation (SAFE) study is a single-blinded, parallel randomized designed multicenter study in pacemaker indicated patients with paroxysmal atrial fibrillation (AF). The objective is to evaluate whether the site of atrial pacing--conventional right atrial appendage versus low atrial septal--with or without atrial overdrive pacing will influence the development of persistent AF. The study will provide a definitive answer to whether a different atrial pacing site or the use of AF suppression pacing or both can give incremental antiarrhythmic benefit when one is implanting a device for a patient with a history of paroxysmal AF.

Atrial Flutter with Spontaneous 1:1 Atrioventricular Conduction in Adults: An Uncommon but Frequently Missed Cause for Syncope/Presyncope

To compare patients with atrial flutter (AFl) and 1:1 atrioventricular conduction (AVC) with patients with AFl and higher AVC. The characteristics of 19 patients with AFl and 1:1 AVC (group A) were compared with those of 116 consecutive patients with AFl and 2:1 AVC or higher degree AV block (group B). Age, gender, and left ventricular function were similar in the two groups. In group A versus group B, more patients had no structural heart disease (42% vs 17%, P < 0.05) and syncope/presyncope (90% vs 12%, P < 0.05). The AFl cycle length (CL) in group A was longer than in group B (265 +/- 24 ms vs 241 +/- 26 ms, P < 0.01). The transition from AFl with 1:1 to 2:1 AVC or vice versa was associated with small but definite changes in AFl CL, which showed larger variations in response to sympathetic stimulation. In group A patients who were studied off drugs, the atrial-His interval was not different from group B, but maximal atrial pacing rate with 1:1 AVC was faster. In group A, five patients were misdiagnosed as ventricular tachyarrhythmias, and three with a defibrillator received inappropriate shocks. Four patients had ablation of AVC and six had ablation of AFl circuit. The main difference between groups A and B may be an inherent capacity of the AV node for faster conduction, especially in response to increased sympathetic tone. The latter affects not only AVC but also the AFl CL. One should be aware of the different presentations of AFl with 1:1 AVC to avoid misdiagnosis/mismanagement and to consider the diagnosis in patients with narrow or wide QRS tachycardia and rates above 220/min.

What is the role of the pacing rate in the prevention of atrial tachyarrhythmias?

In 1998, Delfaut et al. 1 reported about 30 patients with drug-refractory atrial fibrillation (AF) which recurred in all individuals despite continuation of antiarrhythmic drugs within approximately 1 month, but was suppressed by pacing for a mean of 143 days. Although the main scope of this study was the assessment of dual-site right atrial pacing (which further prolonged the arrhythmia-free interval to 195 days), this observation stimulated interest in atrial overdrive pacing as a potential therapy of AF. Of note, all patients in this study had spontaneous or drug-induced bradycardia, and the investigators carefully adjusted pacing rate and drug dose until a proportion of atrial pacing during sinus rhythm of >80% was achieved. Similarly, Garrigue et al. 2 calculated the mean 24 h heart rate in 22 patients with a dual-chamber pacemaker via the memory of the device and programmed the lower pacing rate just 10 bpm above this value to perform atrial overdrive at an individually optimized rate. Again, overdrive pacing, in this case at a mean of 75 bpm, was associated with a reduction or complete prevention of AF recurrences. These and other observations led to the hypothesis that atrial overdrive pacing, i.e. pacing faster than the sinus rate, for a significant proportion of time may prevent AF. As the PA3 trial showed, atrial pacing in the DDDR mode with 70 bpm achieved atrial pacing for only 67% of the time in patients without sinus bradycardia and was unable to prolong the time to AF recurrence.3 Pacing at higher rates such as 90 bpm can achieve atrial overdrive for >80% of the time but is not tolerated by a number of patients.4 Therefore, pacing algorithms that maintain the atrial pacing rate just above the … *Corresponding author. Tel:+49 69 6301 6512; fax:+49 69 6301 6341. E-mail address: c.w.israel{at}em.uni-frankfurt.de

Increased base rate of atrial pacing for prevention of atrial fibrillation after implantation of a dual-chamber pacemaker: insights from the Atrial Overdrive Pacing Study

Different pacing sites and various algorithms have been utilized to prevent atrial fibrillation (AF) in pacemaker recipients. However, the optimal pacing rate settings have not yet been established. In this randomized, prospective, multicentre, single-blinded, cross over study, rate-adaptive pacing at a high base rate (BR) in patients, age 60 years or above, or a history of paroxysmal AF, who underwent dual-chamber (DDD) pacemaker implantation for standard pacing indications, was evaluated for prevention of AF. In the study cohort of 145 patients implanted with DDD pacemakers with a programmable rest rate (RR) feature, the BR/RR settings were sequentially but randomly adjusted as follows: 60 bpm/Off for the baseline quarter (initial 3 months) and then to either 'A-B-C' or 'C-B-A' settings (A = 70/65 bpm, B = 70/Off, C = 80/65 bpm) for the subsequent quarters each of 3 months duration. Data on automatic mode switch episodes, device diagnostics, and a questionnaire evaluating pacemaker awareness and palpitations were collected. Ninety-nine patients, mean age 77 +/- 10 years, who completed the study protocol and followed for 12 months did not show significant differences in the number of mode switch episodes between any settings used. The percentage of atrial pacing was lower during baseline pacing compared to settings A, B, and C (P < 0.0001). Setting C produced a higher percentage of atrial pacing than A and B (P < 0.01). Although a higher percentage of atrial pacing correlated with a lower incidence of mode switch episodes, there was no statistically significant difference in the number of mode switch episodes between settings A, B, and C. There were no significant differences in the questionnaire scores relating to pacemaker awareness or palpitation. Overdrive single-site pacing in the right atrium achieved by programming analysed settings in the present study did not reduce AF as assessed by mode switch episodes. Additionally, no change in the symptoms of arrhythmia or awareness of pacing was seen.

Load-sensitivity of regional tissue deformation in the right ventricle: isovolumic versus ejection-phase indices of contractility

Objective:Doppler myocardial imaging is increasingly being used to evaluate regional and global cardiac function. Quantitative measurements of tissue deformation obtained during ejection as well as isovolumic contraction have been proposed...

Effect of acute volume overload on the magnitude of T-wave alternans

LETTERS TO THE EDITOREffect of acute volume overload on the magnitude of T-wave alternansJohn E. MadiasJohn E. MadiasPublished Online:01 Aug 2007https://doi.org/10.1152/japplphysiol.00346.2007MoreSectionsPDF (25 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations To the Editor: I read with great interest the contribution by Narayan et al. (1) on the effect of acute volume loading on the magnitude of the T-wave alternans (TWA) in five dogs without structural heart disease. The authors showed that the acute saline infusion led to a rise of pulmonary capillary wedge pressure and an increase of the magnitude of TWA in comparison with the value of TWA found prior to the acute volume infusion. Importantly, the increased magnitude of the TWA after the volume occurred at a lower atrial paced rate than the one noted at baseline. In addition, there was a linear relationship between the volume loading and the increased magnitude of TWA. Although these findings were noted in normal anesthetized dogs undergoing fluid loading, there may be clinical implications for patients with structural heart disease and associated fluid overload. The findings are also of interest in the light of the current climate that the magnitude of TWA and the heart rate at its onset matter and suggest a higher arrhythmic risk than the one associated with TWA of lower magnitude, elicited at higher heart rates. However, one wonders whether the increase in the TWA magnitude following the fluid overload was of primary nature (indicative of a more advanced electrophysiological destabilization), or secondary, due to changes in the overall T-wave magnitude/morphology/axis consequent to the volume overload and resultant heart enlargement. No data on heart volumes were acquired, but the magnitude of the administered fluid infusions would be expected to produce some heart dilation (indeed the authors refer repeatedly to a plausibly induced “stretch,” and its repolarization and arrhythmic consequences), and such increases in end-diastolic volumes elicit the “Brodie effect” (2), characterized electrocardiographically by an augmentation of the QRS complexes; also changes in the corresponding T-waves (secondary) may be noted. Were changes noted after volume infusion in the ECG QRS and/or T-waves, both before and during atrial pacing? Was the increase in magnitude of TWA after fluid infusion totally or partially secondary to the changes in the amplitude (or other attributes) of the T-waves, and could a “crude” adjustment (notwithstanding the complexity of the spectral TWA method) of the increased TWA magnitude values by possibly increased T-wave amplitude render the magnitude of the TWA after the fluid loading less impressively elevated?REFERENCES1 Narayan SM, Drinan DD, Lackey RP, Edman CF. Acute volume overload elevates T-wave alternans magnitude. J Appl Physiol 102: 1462–1468, 2007.Link | ISI | Google Scholar2 Brody DA. A theoretical analysis of intracavitary blood mass influence on the heart-lead relationship. Circ Res 4: 731–738, 1956.Crossref | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: J. E. Madias, Division of Cardiology, Elmhurst Hospital Center, 79–01 Broadway, Elmhurst, NY 11373 (e-mail:[email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByReply to MadiasSanjiv M. Narayan, Darrel D. Drinan, Robert P. Lackey, and Carl F. Edman1 August 2007 | Journal of Applied Physiology, Vol. 103, No. 2 More from this issue > Volume 103Issue 2August 2007Pages 728-728 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00346.2007PubMed17666734History Published online 1 August 2007 Published in print 1 August 2007 Metrics