Atrial vulnerability.

The electrophysiologic substrates of atrial flutter and fibrillation (AFF) have been studied in patients with paroxysmal arrhythmias. Atrial repetitive responses to extrastimuli are a nonspecific response, even though they can precipitate AFF. AFF inducibility is rather sensitive, but not very specific, in separating patients from controls. There is no established protocol to explore vulnerability in this fashion. Atrial refractoriness is abnormal in some patients. Some authors have found a tendency toward short effective refractory periods (AERP) and others have found a poor adaptation of AERP to decreases in cycle length. Unfortunately, these abnormalities are neither sensitive nor specific enough. Atrial conduction may be abnormal basally, but subtler abnormalities are shown by premature stimulation. Early extrastimuli are conducted with increased conduction delays in patients with paroxysmal AFF in relation to controls. Again, there is not enough sensitivity and specificity in the findings to make them of diagnostic value. Electrophysiologic abnormalities are detectable in patients with AFF, but larger studies, including reproducibility and the effect of drugs on the abnormal parameters, will be necessary to develop clinical applications.     

Right and Left Atrial Radiofrequency Catheter Therapy of Paroxysmal Atrial Fibrillation

Ablation of Paroxysmal Atrial Fibrillation. Introduction: (AF), trial fibrillation (AF), the most common arrhythmia, is due to multiple simultaneous wavelets of reentry in the atria. The only available curative treatment is surreal, using atriotomies to compartmentalize the atria. Therefore, we investigated a staged anatomical approach using radiofrequency catheter ablation lines to prevent paroxysmal AF. Methods and Results: Forty-live patients with frequent symptomatic drug-refractory episodes of paroxysmal AF were studied. Progressively complex linear lesions were created by sequential applications of radiofrequency current in the right atrium and then in the left atrium if required. The outcome of the procedure was considered a success when the episodes of AF were either eliminated or recurred at a rate of no more than one episode (lasting < 6 hours) in 3 months. Patients who had no more than one episode per month were considered “improved.” Right atrial ablation organized local electrical activity and led to stable sinus rhythm during the procedure in 18 (40%) of the 45 patients. However, sustained AF remained inducible in 40 of 45 patients, and the lesions failed to produce evidence of a significant linear conduction block/delay in all but four patients. There were no significant complications except for two transient sinus node dysfunctions. The procedure duration and fluoroscopic time were 248 ± 79 and 53 ± 11 min, respectively. Additional sessions were required in 19 patients to treat sustained right atrial flutter or arrhythmias linked to ectopic right or left atrial foci. During a mean follow-up of 11 ± 4 months, right atrial ablation was successful in 15 (33%) patients, ft without medication and 9 with a previously ineffective drug. Nine (20%) additional patients were improved. Ten patients with an unsuccessful outcome then underwent linear ablation in the left atrium. The procedure duration and fluoroscopy time were 292 ± 94 and 66 ± 24 min. A hemopericardium occurred in one patient. Two patients required reablation to treat ectopic atrial foci. Left atrial ablation terminated AF during the procedure in 8 patients, and sustained AF could not he induced in 5. Subsequent success was achieved in A (60%) patients, including 4 without medication, and 1 additional patient was improved. Conclusions: Successful radiofrequency catheter ablation of drug-refractory daily paroxysmal AF is feasible using linear atrial lesions complemented by focal ablation targeted at arrhythmogenic foci. Ablation only in the right atrium is a safe technique providing limited success, whereas linear lesions in the left atrium significantly increase the incidence of stable restoration of sinus rhythm, the inability to induce sustained AF, and the final success rate. The described technique is promising hut must he considered preliminary because significant Improvements are required to optimize lesion characteristics and shorten total procedure duration.     

Electrophysiologic Characteristics of Complex Fractionated Atrial Electrograms in Patients with Atrial Fibrillation

Introduction: The underlying mechanisms of complex fractionated atrial electrogram (CFAE) during radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) have not yet been clearly elucidated. We explored the relationships between CFAE and left atrial (LA) voltage, or conduction velocity (CV).
Methods and Results: In 50 patients with AF (23 paroxysmal AF [PAF], 41 males, mean age 55.76 ± 10.16 years), the CFAE (average index of fractionation of electrograms during AF by interval-analysis algorithm, cycle length [CL]≤ 120 ms) areas, voltage, and CV were measured at eight different quadrants in each patient's LA by analyzing a NavX-guided, color-coded CFAE CL map, a voltage map, and an isochronal map (500 ms pacing) generated by contact bipolar electrograms (70–100 points in the LA). The results were: (1) CFAE areas were predominantly located in the septum, roof, and LA appendage; (2) CFAE area had lower voltage than those in non-CFAE area and was surrounded by the areas of high voltage (P < 0.0001); (3) The CFAE areas had low CVs compared with non-CFAE areas (P < 0.001); and (4) The percentage of CFAE area was lower in patients with persistent atrial fibrillation (PeAF) compared with those with PAF (P < 0.05).
Conclusions: The CFAE area, which is primarily located at the septum, has a low voltage with a lower CV, and is surrounded by high-voltage areas. Underlying electroanatomical complexity is associated with clustering of CFAEs.     

Mechanisms of Atrial Fibrillation

Based on experimental studies in the canine heart and an early computer model, atrial fibrillation (AF) has been thought to be due to multiple reentrant wavelets. However, subsequent studies in animal models are most consistent with a mechanism of AF due to a stable reentrant circuit of short cycle length or unstable reentrant circuits of short cycle length that drive the atria so fast that much or most of the atrial tissue manifests fibrillatory conduction. Limited mapping studies in patients during open heart surgery and during electrophysiologic studies using endocardial catheter electrodes also are most consistent with the concept of a driver, seemingly most often a focus in or near one or more of the pulmonary veins, precipitating and maintaining AF. However, a precise understanding of the mechanism(s) of AF in patients is not yet available. (J Cardiovasc Electrophysiol, Vol. 14, pp. S267-S274, December 2003, Suppl.)     

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex-trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)     

Conduction Velocity in the Tricuspid Valve-Inferior Vena Cava Isthmus is Slower in Patients With Type I Atrial Flutter Compared to Those Without a History of Atrial Flutter

Slower Conduction in the TV-IVC Isthmus. Introduction : In human type I atrial flutter, the electrophysiologic substrate is unclear. In order to determine if slow conduction is mechanistically important, we evaluated conduction velocity in the tricuspid valve-inferior vena cava (TV-IVC) isthmus, right atriai free wall, and interatrial septum in patients with and without a history of atrial flutter undergoing electrophysiologic study.
Methods and Results : Nine patients with (group 1) and nine without a history of type I atrial flutter (group 2) were studied. Conduction time (msec) in the right atrial free wall. TV-IVC isthmus (bidirectional), and interatrial septum was measured during pacing in sinus rhythm at cycle lengths of 600, 500, 400, and 300 msec from the low lateral right atrium and coronary sinus ostium. Conduction velocity (cm/sec) was calculated by dividing the distance between pacing electrodes and sensing electrodes (cm) by the conduction time (sec). Conduction velocity was slower in the TV-IVC isthmus in group 1 (range 37 ± 8 to 42 ± 8 cm/sec) versus group 2 (range 50 ± 8 to 55 ± 9 msec) at all pacing cycle lengths (P < 0.05). However, conduction velocity was not different in the right atrial free wall or interatrial septum between groups 1 and 2. Conduction velocity was also slower in the TV-IVC isthmus than in the right atrial free wall and interatrial septum in group 1 patients, at all pacing cycle lengths (P < 0.05). Atrial flutter cycle length correlated with total atrial conduction time (r ≥ 0.832, P < 0.05).
Conclusion : Slow conduction in the TV-IVC isthmus may be mechanistically important for the development of human type I atrial flutter.     

VVI起搏术后心房颤动与心钠素和室房逆传的关系

长期心脏起搏的患者,有部分并发心房颤动,尤其是VVI起搏者。本文主要阐述VVI起搏术后心房颤动与血心钠素和室房逆传的关系,为选择适当的起搏器和起搏方式以及临床干预措施提供理论依据,从而减少起搏术后心房颤动的发生。     

P Wave Dispersion: A Valuable Electrocardiographic Marker for the Prediction of Paroxysmal Lone Atrial Fibrillation

Background: The prolongation of atrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiological characteristics in patients with paroxysmal atrial fibrillation. Methods: The aim of this study was to test the ability of a new ECG marker to discriminate between patients with a prior history of paroxysmal lone atrial fibrillation and healthy controls. Maximum P wave duration (Pmax) and the difference between the maximum and the minimum P wave duration, which was defined as P-wave dispersion (Pdisp) were calculated from the 12-lead surface ECGs of 75 patients with a history of paroxysmal lone atrial fibrillation and 50 age-matched healthy controls. Results: Pmax was in patients 122 ± 17 ms and in controls 101 ± 10 ms (t = 7.935, P > 0.001). Pdisp was in patients 48 ± 16 ms and in controls 29 ± 8 ms (t = 7.616, P > 0.001). A Pmax value of 110 ms separated patients from controls with a sensitivity 85%, a specificity 72%, and a positive predictive accuracy of 82%. A Pdisp value of 40 ms separated patients from controls with a sensitivity of 81%, a specificity of 80%, and a positive predictive accuracy of 85%. Conclusions: (1) Pmax and Pdisp values were found to be significantly higher in patients with a prior history of paroxysmal lone atrial fibrillation than in age-matched healthy controls, and (2) Pdisp is a new simple ECG marker that could be possibly used for the identification of patients with a previous history of paroxysmal lone atrial fibrillation. A.N.E. 1999;4(1):39–45     

Competitive Anterograde and Retrograde Atrioventricular Junctional Activation in Atrial Fibrillation

Reset and Cancellation. In eight medically-treated patients with chronic atrial fibrillation and a random ventricular rhythm, we studied the effect of single right ventricular stimuli delivered after each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the “compensatory” pauses following the ventricular extrasystoles were calculated. Analyses of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanism.s: (1) reset of the timing cycle of atrioventricular nodal activation by relatively early retrograde impulses: and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular nodal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results of this study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation. ( J Cardiovasc Electrophysiol, Vol. 1. pp. 448–456, October 1990 )     

Apparent Bidirectional Conduction Block Following Radiofrequency Catheter Ablation of Typical Atrial Flutter

Objective: The purpose of this study is to determine the reliability of activation sequence mapping in assessing the presence of bidirectional conduction block (BCB) in typical atrial flutter (AFL) ablation. Introduction: Radiofrequency ablation (RFA) can cure typical AFL by creating BCB across the right atrial isthmus. Effective conduction block across this region can prevent AFL recurrence, but accurate assessment of isthmus conduction may be flawed. Methods: BCB was measured before and after RFA by pacing at multiple rates on both sides of the isthmus during sinus rhythm. Pacing was performed from a low lateral tricuspid annulus site (proximal to the isthmus) and a coronary sinus Os site (distal to the isthmus), while recording simultaneously from 8–10 right atrial sites bordering the isthmus (4–5 free wall sites; 4–5 septal sites) as well as from an isthmus site. After ablation reinduction of atrial flutter was attempted from both sides of the block with rapid atrial pacing after BCB was established in all patients. In some patients lines of conduction block were evident at the isthmus (using the ablation catheter to map). Results: Of 65 patients undergoing RFA of AFL, 59 had typical AFL. In all 59 patients, BCB was demonstrated at all pacing cycle lengths 30[emsp4 ]min after RFA applications. In 6 of these 59, AFL was inducible with atrial pacing despite apparent BCB. Further RFA resulted in non inducibility in all 6 patients. In the remaining 53/59 patients, BCB was associated with noninducibility at 30[emsp4 ]min. A total of 8 recurrences were seen during a mean 19.3[emsp4 ]±[emsp4 ]8.3 (SD) month follow-up. Conclusion: Apparent BCB as determined by activation sequence mapping outside of the isthmus is an excellent marker, but, as measured, may be a misleading method of assessing the presence or absence of conduction through the isthmus. It is necessary to attempt reinduction of AFL after apparent success. Elimination of typical AFL does not preclude other AFLs.     

Left Atrial Conduction Along the Coronary Sinus During Ectopic Atrial Tachycardia and Atrial Fibrillation:

Introduction: Correlation function analysis was applied to endocardial electrograms to investigate conduction patterns along the coronary sinus (CS) during sinus rhythm (SR) and atrial tachycardias.
Methods and Results: Eighteen recordings were obtained from 14 patients with supraventricular tachycardias. Five atrial fibrillation (AF) recordings were compared to 10 SR recordings and 3 ectopic atrial tachycardia (EAT) recordings. The maximum correlation coefficient was used to assess similarity between signals, i.e., if they originate from the same wavefront. The cumulative time delay, calculated as pairwise summation of interelectrode time delays, was used as an indicator of activation sequence along the CS. Method validation using SR showed right-to-left conduction with high correlations in 8 of 10 recordings indicating one single wavefront. EAT recordings showed consistent left-to-right conduction with left atrial foci and right-to-left with right atrial focus and lower correlations than SR. All 5 AF recordings showed predominantly left-to-right conduction direction, also with correlations lower than SR.
Conclusion: (1) Correlation function analysis can be used to assess agreement between signals and direction of activation spread. (2) Due to the position of CS, the results can be used to derive mechanisms of interatrial conduction. (3) Consistency in electrical activity propagation along CS is common in AF. (J Cardiovasc Electrophysiol, Vol. 14, pp. S148-S153, October 2003, Suppl.)     

Slowing of the Atrial Flutter Rate During 1:1 Atrioventricular Conduction in Humans and Dogs: An Effect Mediated Through Atrial Pressure and Volume

Atrial Flutter Rate and Atrial Pressure . Introduction: During atrial flutter the effects of 1:1 atrioventricular (AV) conduction on the rate of atrial flutter was studied in 12 patients and 14 dogs. Methods and Results: (A) In all patients, the development of 1:1 AV conduction was associated with a significant increase in flutter cycle length (261.7 ± 9.9 to 281.8 ± 12.1 msec, mean increase 20.3 ± 3.2 msec, P < 0.001). The flutter cycle length returned to control values when 1:1 AV conduction ceased. In four patients in whom atrial pressure was monitored, the prolongation of the atrial flutter cycle interval during 1:1 AV conduction was associated with an immediate rise in atrial pressure (4.0 ± 0.4 to 6.5 ±0.7 mmHg, P < 0.003). (B) In order to examine the mechanism of this phenomenon, similar studies were carried out in dogs with experimentally induced atrial flutter. 1:1 AV conduction consistently lengthened the flutter cycle length during control conditions or following vagotomy and during the administration of isoproterenol. This was always associated with a rise in atrial filling pressure. Inferior vena cava occlusion consistently shortened the flutter cycle length and this was also independent of vagotomy and isoproterenol administration. The atrial filling pressure fell during inferior vena cava occlusion. During 1:1 AV conduction, the prolonged flutter cycle length was shortened by inferior vena cava occlusion to values prior to 1:1 AV conduction. Conclusion: The rate of atrial flutter is accelerated by reductions in atrial pressure, and slowed by increased atrial pressure. These effects are independent of the vagus nerve or an adrenergic agonist. Changes in atrial pressure and volume affect characteristics of the atrial flutter circuit, and thus can modulate the rate of atrial flutter.     

An Algorithm to Measure Beat‐to‐Beat Cycle Lengths for Assessment of Atrial Electrogram Rate and Regularity During Atrial Fibrillation

AF Cycle Length Detection Analysis . Introduction: Experimental models have demonstrated that atrial fibrillation (AF) may be due to one or more rapid drivers (source) producing AF. These drivers may be characterized by rapid and regular cycle lengths (CLs), producing fibrillatory conduction to the rest of the atria. The ability to reliably identify such drivers would be invaluable. The purpose of this study was to develop and validate a CL variability detection (CLVD) analysis capable of accurately determining beat‐to‐beat CLs of atrial electrograms (AEGs) during AF, and then to compare this analysis with dominant frequency (DF) analysis. Methods and Results: We analyzed 6 episodes of AF in 6 dogs (sterile pericarditis model) due either to a single, stable left atrial reentrant circuit, or unstable reentrant circuits causing fibrillatory conduction to the rest of the atria. During AF, AEGs were recorded simultaneously from 400 to 420 electrodes on both atria. CLs from over 20,000 AEGs were manually measured, and compared to CLs detected using both the CLVD and DF analyses. There was significant correlation between (1) CLs measured manually and the CLVD analysis (mean CL: correlation coefficient [CC]= 0.96, standard deviation [SD]: CC = 0.89); and (2) mean CL measured manually and the DF analysis (CC = 0.84). However, there was poor correlation between SD of CLs measured manually and the organization index (OI) by DF analysis (CC =–0.59). Conclusion: The CLVD analysis was validated as being accurate for detecting both rate and degree of regularity of AEGs during AF, and more accurate than DF analysis. (J Cardiovasc Electrophysiol, Vol. 24, pp. 199‐206, February 2013)     

Elimination of Pulse Deficit During Atrial Fibrillation by Left Vagal Stimulation

Six anesthetized dogs (17–25 kg) were used to test the hypotheses that low-frequency, left-vagal stimulation can be used to reduce or eliminate pulse deficit during atrial fibrillation. Atrial fibrillation was induced and sustained by rapid electrical stimulation of the right atrium using a J-lead placed in the right atrial appendage. A bipolar sleeve electrode was placed around the left vagus nerve in the cervical region and low-frequency 1-ms rectangular current pulses were applied. Pulse deficit was completely eliminated in 28 of the 29 trials and was reduced in all 29. Additionally, an increase in mean blood pressure was observed at the commencement of vagal stimulation and a decrease in mean blood pressure was observed after cessation of left vagal stimulation, when the pulse deficit reappeared. We conclude that controlled low-frequency left vagal stimulation is an effective way to eliminate the pulse deficit in atrial fibrillation.     

Atrial tachycardia originating from the upper left atrial septum: demonstration of transseptal interatrial conduction using the infolded atrial walls

We report a rare case of atrial tachycardia (AT) originating from the upper left atrial septum. Electroanatomic mapping of both atria demonstrated that the earliest atrial activation during AT occurred at the upper left atrial septum 26 msec before the onset of the P wave, followed by the mid-right atrial septum (10 msec before the onset of the P wave) and then the upper right atrial septum just adjacent to the left septal AT site (1 msec before the onset of the P wave), indicating detour pathway conduction from the upper left to the upper right atrium. Embryologically, it was suggested that the superior components of the secondary atrial septum are made by the infolded atrial walls and could develop a transseptal detour pathway involving the left-side atrial septal musculature, the superior rim of the oval fossa and the right-side atrial septal musculature. A single radiofrequency application targeting the upper left atrial septum successfully abolished the AT.     

Frequency Analysis of Atrial Electrograms Identifies Conduction Pathways from the Left to the Right Atrium During Atrial Fibrillation—Studies in Two Canine Models

Studies of atrial fibrillation (AF) have demonstrated that a stable rhythm of very short cycle length in the left atrium (LA) can cause fibrillatory conduction in the rest of the atria. We tested the hypothesis that fast Fourier transform (FFT) analysis of atrial electrograms (AEGs) during this AF will rapidly and reliably identify LA-to-right atrium (RA) conduction pathway(s) generated by the driver.
Methods and Results: During induced atrial tachyarrhythmias in the canine sterile pericarditis and rapid ventricular pacing-induced congestive heart failure models, 380–404 AEGs were recorded simultaneously from epicardial electrodes on both atria. FFT analysis of AEGs during AF demonstrated a dominant frequency peak in the LA (driver), and multiple frequency peaks in parts of the LA and the most of the RA. Conduction pathways from the LA driver to the RA varied from study-to-study. They were identified by the presence of multiple frequency peaks with one of the frequency peaks at the same frequency as the driver, and traveled (1) inferior to the inferior vena cava (IVC); (2) between the superior vena cava and the right superior pulmonary vein (RSPV); (3) between the RSPV and the right inferior pulmonary vein (RIPV); (4) between the RIPV and the IVC; and (5) via Bachmann's bundle. Conduction pathways identified by FFT analysis corresponded to the conduction pathways found in classical sequence of activation mapping. Computation time for FFT analysis for each AF episode took less than 5 minutes.
Conclusion: FFT analysis allowed rapid and reliable detection of the LA-to-RA conduction pathways in AF generated by a stable and rapid LA driver.     

P‐Wave Dispersion: A Novel Predictor of Paroxysmal Atrial Fibrillation

Background: The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P‐wave duration in 12‐lead surface electrocardiograms (ECG) and signal‐averaged ECG recordings. Methods: The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P‐wave dispersion. P‐wave dispersion is defined as the difference between the longest and the shortest P‐wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P‐wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P‐wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P‐wave dispersion. The methodology used for the calculation of P‐wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P‐wave dispersion measurements are needed. Conclusions: P‐wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction. A.N.E. 2001;6(2):159–165     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).