Effects of atrial electromechanical delay and ventriculoatrial conduction over the atrial functions in patients with frequent extrasystole and preserved ejection fraction.

BACKGROUND: The deterioration of left atrial and ventricular functions was demonstrated in patients with frequent ventricular extrasystole (fVES). The exact pathophysiology of left atrial dysfunction in patients with fVES is unclear. Retrograde ventriculoatrial conduction (VAC) often accompanies fVES, which may contribute to atrial dysfunction. We investigated whether atrial electromechanical delay and VAC are related to these atrial functions in patients with frequent right ventricular outflow tract (RVOT) VES and preserved ejection fraction (pEF). METHODS: This study included 21 patients with pEF (eight males, 48 ± 11 years), who had experienced more than 10 000 RVOT-VES during 24-h Holter monitoring and had undergone electrophysiological study/ablation. The study also included 20 healthy age- and sex-matched control subjects. Transthoracic echocardiography was performed on all of the subjects. Atrial conduction time was obtained by using tissue Doppler imaging. Strain analysis was performed with two-dimensional speckle tracking echocardiography. RESULTS: The peak atrial longitudinal strain was significantly impaired in patients with fVES (P = 0.01). In addition, although the interatrial and left atrial conduction delay times were significantly different between each group (P < 0.001, P < 0.001), the right atrial conduction delay times were similar. When patients with fVES were divided into groups depending on the existence of retrograde VAC, atrial deformation parameters and conduction delay time did not significantly differ between either group. CONCLUSION: Frequent RVOT-VES causes left atrial dysfunction. This information is obtained through strain analyses and recordings of left atrial conduction times in patients with pEF. Regardless, retrograde VAC is not related to atrial dysfunction.

Double ventricular response in dual AV nodal pathways mimicking interpolated premature beat.

Double ventricular response in dual atrioventricular (AV) nodal pathways can result in nonreentrant supraventricular tachycardia. Since this condition was first described in 1979, around 20 cases have been reported. Here, we present the case of a patient with a confirmed diagnosis of double ventricular response in dual AV nodal pathways resembling an interpolated premature beat who underwent successful radiofrequency ablation of the slow pathway.

Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2.

Extrasystoles lead to several consequences, ranging from uneventful palpitations to lethal ventricular arrhythmias, in the presence of pathologies, such as myocardial ischemia. The role of working versus conducting cardiomyocytes, as well as the tissue requirements (minimal cell number) for the generation of extrasystoles, and the properties leading ectopies to become arrhythmia triggers (topology), in the normal and diseased heart, have not been determined directly in vivo. Here, we used optogenetics in transgenic mice expressing ChannelRhodopsin-2 selectively in either cardiomyocytes or the conduction system to achieve cell type-specific, noninvasive control of heart activity with high spatial and temporal resolution. By combining measurement of optogenetic tissue activation in vivo and epicardial voltage mapping in Langendorff-perfused hearts, we demonstrated that focal ectopies require, in the normal mouse heart, the simultaneous depolarization of at least 1,300-1,800 working cardiomyocytes or 90-160 Purkinje fibers. The optogenetic assay identified specific areas in the heart that were highly susceptible to forming extrasystolic foci, and such properties were correlated to the local organization of the Purkinje fiber network, which was imaged in three dimensions using optical projection tomography. Interestingly, during the acute phase of myocardial ischemia, focal ectopies arising from this location, and including both Purkinje fibers and the surrounding working cardiomyocytes, have the highest propensity to trigger sustained arrhythmias. In conclusion, we used cell-specific optogenetics to determine with high spatial resolution and cell type specificity the requirements for the generation of extrasystoles and the factors causing ectopies to be arrhythmia triggers during myocardial ischemia.

Electrophysiological relation between the superior vena cava and right superior pulmonary vein in patients with paroxysmal atrial fibrillation.

INTRODUCTION: The superior vena cava (SVC) is a main source of nonpulmonary vein (PV) ectopies initiating atrial fibrillation (AF). Empiric SVC isolation may improve rhythm outcomes after catheter ablation of AF. Because the SVC passes immediately adjacent to the right superior PV (RSPV), an electrophysiological relation could be present between the two structures. The present study aimed to estimate the interrelation between the SVC and RSPV by evaluating arrhythmogenic activities observed during catheter ablation of AF. METHODS AND RESULTS: Study subjects comprised 121 consecutive patients referred for catheter ablation of paroxysmal AF. Isoproterenol infusion was used to induce ectopies and AF. Patients were divided into two groups depending on the presence of arrhythmogenic SVC: arrhythmogenic-SVC (A-SVC) and nonarrhythmogenic SVC (Non-A-SVC) groups. The prevalence of females was higher and body surface area was smaller in the A-SVC group (N = 22) than Non-A-SVC group (N = 99). Arrhythmogenic activities were observed in 60 (49%) RSPVs, 24 (20%) right inferior PVs, 72 (59%) left superior PVs, and 31 (25%) left inferior PVs. Arrhythmogenic RSPVs were more prevalent in the A-SVC group than Non-A-SVC group (86% vs. 41%, P = 0.0001), whereas these prevalences in the other three PVs were not different between groups (P >0.3). In multivariable analysis, arrhythmogenic RSPV was the only independent predictor of arrhythmogenicity of the SVC (OR, 8.53; 95% CI 2.31-31.46; P = 0.001). CONCLUSIONS: An electrophysiological interrelation may be present between the SVC and RSPV in patients with paroxysmal AF. Semiempiric SVC isolation limited to patients with an arrhythmogenic RSPV may be a more efficient treatment strategy.

Slow antegrade excitation and delayed retrograde activation through an "inexcitable zone": A basis for arrhythmia formation in infarcted myocardium ex vivo.

INTRODUCTION: The electrophysiologic mechanism for rate-dependent PVBs associated with double potentials (DPs) was investigated in infarcted canine hearts using bipolar and intracellular microelectrode recordings. METHODS AND RESULTS: Dogs exhibiting rate-related ventricular ectopic beats (coupling interval, 390 ± 54 milliseconds) during sinus rhythm or atrial pacing were studied 4-5 days (N = 63) or 25 days (N = 16) following anterior descending coronary artery ligation. Sites of DP and rate-dependent arrhythmia formation were identified in vivo using bipolar recordings for subsequent ex vivo studies. Rate-dependent conduction delays with increasing duration isoelectric intervals representing very slow conduction were observed at sites of DP formation, frequently provoking both manifest and concealed reentry (non-stimulated beats) over a narrow range of paced cycle lengths. Both slow antegrade and retrograde activation across an inexcitable gap (reflection) were integral components of extrasystole formation. Retrograde reflection to a region of very slow conduction (mid-potential) during antegrade activation was routinely observed at 4-5 days (42 of 63 preparations, 67%) and 25 days (22 of 26 preparations, 85%) postcoronary artery ligation. Reflection and premature re-activation of the proximal site was then observed in 6 of 63 (9%), and 3 of 26 preparations (12%). CONCLUSION: The present experiments demonstrate DP formation and rate-dependent constant-coupled late epicardial premature beats in infarcted dog hearts. Microelectrode recordings at DP sites demonstrating prolonged isoelectric intervals display very slow conduction preceding distal activation and "reentrant" re-activation of more proximal sites, representing reflection as an arrhythmia mechanism in ischemically injured epicardium during subacute myocardial infarction.

[Trigeminy of ventricular bigeminy caused by reentrant mechanism: reentry of reentry]. / Trigeminia de la bigeminia ventricular por mecanismo reentrante: reentrada de la reentrada.

The process that follows an acute myocardial infarction generates an appropriate substrate for the formation of reentry circuits, considered to be the most frequent mechanism of ventricular extrasystoles and tachyarrhythmias. We present the case of a patient with an acute myocardial infarction unusually concurring with ventricular trigeminy coupled to ventricular bigeminated extrasystoles giving rise to a trigeminy sequence over the bigeminy, which indicates the existence of two reentry circuits (reentry of reentry) that trigger ventricular flutter.

Hisian extrasystole mimicking second degree atrioventricular block. a case report.

Hisian extrasystoles originate from the His bundle. They are rare and usually misdiagnosed. In fact, they manifest on the EKG, with a p' wave located before, in or after the QRS complex. More rarely, the extrasystole blocks the propagation of the influx to the ventricles simulating a Mobitz II atrioventricular (AV) block. We report the case of a 36-Year-old woman with no medical History, suffering from presyncope and palpitations at rest. Her physical examination and EKG were normal. The 24-hour Holter monitoring showed some long periods with unexpected blocked p waves but with no significant pause. Considering her young age and the absence of causes of AV block, we performed an intracardiac electrophysiological study which showed hisian extrasystoles with normal conduction tissue properties at baseline and under flecainide. The diagnosis of hisian extrasystoles simulating Mobitz II AV block was made. A simple monitoring with beta-blockers therapy was recommended. Hisian extrasystoles may simulate first or second degree AV block with different therapeutic and prognostic implications. Nevertheless, these hisian extrasystoles may be the marker of a vulnerable AV conduction, long-term follow up should be considered.

Mobitz type II second-degree atrioventricular block with narrow QRS and junctional extrasystoles: what is the mechanism?

A 74-year-old man underwent an electrophysiological study because of Mobitz type II second-degree atrioventricular (AV) block with narrow QRS and frequent junctional extrasystoles. During the study, there were very frequent single His bundle depolarizations with multiple coupling intervals that reproduce the ECG findings. In this case, some His bundle extrasystoles result in retrograde concealed conduction and prolonged local refractoriness in the AV node that manifest as block of the next atrial impulse.

[The influence of electrosleep therapy on the dynamics of the parameters of biorhythmic hormonal activity in the children presenting with extrasystolic arrhythmia in the course of the spa and resort-based treatment].

UNLABELLED: Heart rhythm disorders occupy a leading place in the modern structure of cardiovascular diseases in the children. At present, the role of stress-induced reactions in the development of more than a thousand diseases has been proved. Rehabilitation of systemic manifestations of extrasystolic arrhythmia (EA) in the children is only scarcely described in the literature. AIM: The objective of the present work was to improve the effectiveness of the spa and resort-based treatment of the children presenting with extrasystolic arrhythmia taking advantage of the available information about the different biorhythmic activities of the stress-realizing and stress-limiting systems. MATERIAL AND METHODS: The study included 60 children presenting with EA, who received a standard combination of spa and resort-based therapeutic modalities in conjunction with electro-sleep therapy. RESULTS AND DISCUSSION: The study revealed desynchronization of the endocrine functions in the children with EA that manifests itself as the increased secretion of cortisol and adrenaline, suppressed melatonin and ACTH production, mismatched daytime and nocturnal hormonal levels. The daily bio-rhythmic profile influenced the formation of circadian-type extra systola in the children. The most unfavorable clinical and electrocardiographic patterns were observed in the children with the mixed and night-type arrhythmia. The complex of rehabilitation measures practiced at the Evpatoriya health resort including electro-sleep therapy made it possible to balance the activities of the stress-limiting and stress-implementing systems of the body in the form of normalization of the altered levels of adaptive hormones, ordering of biorhythmical hormonal relationships, and reduction of the number of extrasystoles. The most pronounced effect of the treatment was observed in the group of children with a rare and day-type of arrhythmia to whom electrosleep was prescribed. It is concluded that the significant decrease in the frequency of night-type and mixed-type extrasystoles under effect of electro-sleeptherapy allows to recommend the treatment modality being considered for the correction of this type of heart rhythm disorders.

The effects of simulated obstructive apnea and hypopnea on arrhythmic potential in healthy subjects.

Preliminary evidence supports an association between OSA and cardiac dysrhythmias. Negative intrathoracic pressure, as occurring during OSA, may provoke cardiac dysrhythmias. Thus, we aimed to study the acute effects of simulated apnea and hypopnea on arrhythmic potential and measures of cardiac repolarization [QT(C) and T (peak) to T (end) intervals [TpTec]) in humans. In 41 healthy volunteers, ECG was continuously recorded prior, during and after simulated obstructive hypopnea (inspiration through a threshold load), simulated apnea (Mueller maneuver), end-expiratory central apnea and normal breathing in randomized order. The number of subjects with premature beats was significantly higher during inspiration through a threshold load (n = 7), and the Mueller maneuver (n = 7) compared to normal breathing (n = 0) (p = 0.008 for all comparisons), but not during end-expiratory central apnea (n = 3, p = 0.125). Inspiration through a threshold load was associated with a non-significant mean (SD) increase of the QT(C) interval [+5.4 (22.4) ms, 95 %CI -1.7 to +12.4 ms, p = 0.168] and a significant increase of the TpTcc interval [+3.7 (8.9) ms, 95 %CI +0.9 to +6.6 ms, p = 0.010]. The Mueller maneuver induced a significant increase of the QT(C) interval [+8.3 (23.4) ms, 95 %CI 0.9 to +15.6 ms, p = 0.035] and the TpTec interval (+4.2 (8.2) ms, 95 %CI +1.6 to +6.8 ms, p = 0.002). There were no significant changes of the QT(C) and TpTec intervals during central end-expiratory apnea. These data indicate that simulated obstructive apnea and hypopnea are associated with an increase of premature beats and prolongation of QT(C) and TpTec intervals. Therefore, negative intrathoracic pressure changes may be a contributory mechanism for the association between OSA and cardiac dysrhythmias.

[Investigation and treatment of premature beats]. / Sydämen lisälyönnit--miten tutkin, miten hoidan?

If a patient has premature beats, it is essential to clarify whether they are associated with a heart disorder or some other disease. The basis for an examination for all patients is the rest-ECG. Ultrasound examination is indicated, if the symptoms are severe or findings indicating a heart disorder are present. The occurrence of severe symptoms, such as episodes of tachycardia and attacks of unconsciousness, is mapped in an interview and they are an indication for further investigations within specialized care. Atrial extrasystoles as such do not require any treatment unless they are accompanied by atrial fibrillation.

Predicting fluid responsiveness with stroke volume variation despite multiple extrasystoles.

OBJECTIVE: To investigate the ability of a new stroke volume variation algorithm to predict fluid responsiveness during general anesthesia and mechanical ventilation in animals with multiple extrasystoles. DESIGN: Prospective laboratory animal experiment. SETTING: Investigational laboratory. SUBJECTS: Eight instrumented pigs. INTERVENTIONS: Eight anesthetized and mechanically ventilated pigs were monitored with an arterial line and a pulmonary artery catheter. Multiple extrasystoles were induced by right ventricular pacing (25% of heart beats). Arterial pressure waveforms were recorded and stroke volume variation was computed from the new and from the standard algorithm. The new stroke volume variation algorithm is designed to restore the respiratory component of the arterial pressure waveform despite multiple ectopic heart beats. Cardiac output was measured before and after 56 fluid boluses (7 mL/kg of 6% hydroxy ethyl starch) performed at different volemic states. MEASUREMENTS AND MAIN RESULTS: A positive response to fluid boluses (>15% increase in cardiac output) was observed in 21 of 56 boluses. The new stroke volume variation was higher in responders than in nonresponders (19% ± 5% vs. 12% ± 3%, p < .05), whereas the standard stroke volume variation was similar in the two groups (29% ± 8% vs. 26% ± 11%, p = .4). Receiver operating characteristic curve analysis showed that the new stroke volume variation was an accurate predictor of fluid responsiveness (sensitivity = 86%, specificity = 85%, best cutoff value = 14%, area under the curve = 0.892 ±, whereas the standard stroke volume variation was not (area under the curve = 0.596 ± 0.077). CONCLUSIONS: In contrast to the standard stroke volume variation, the new stroke volume variation algorithm was able to predict fluid responsiveness in animals with multiple ventricular extrasystoles.

Successful catheter cryoablation of Hisian ectopy using 2 new diagnostic criteria based on unipolar and bipolar recordings of the His electrogram.

We describe the case of a 61-year-old woman who underwent successful catheter cryoablation of a symptomatic Hisian ectopy. Diagnosis was based on features of the HV interval assessed from a bipolar recording during mapping. The location of the arrhythmic focus was identified using simultaneous unipolar and bipolar recordings of the His electrogram. This case report highlights the use of 2 new criteria for the diagnosis and mapping of Hisian ectopy, and the successful use of cryothermia for the ablation of extrasystoles arising from the His bundle.

Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death.

Premature beats can trigger ventricular arrhythmias in heart disease, but the mechanisms are not well defined. We studied the effect of premature beats on activation and repolarization dispersion in seven patients with cardiomyopathy (57 ± 10 yr, left ventricular ejection fraction 31 ± 7%). Activation time (AT), activation-recovery interval (ARI), and total repolarization time (TRT) were measured from 26 unipolar electrograms during right ventricle (RV) endocardial (early) to left ventricle epicardial (late) activation in response to RV apical extrastimulation (S1S2). Early TRT dispersion increased significantly with shorter S1S2 (1.0 ± 0.2 to 2.3 ± 0.4 ms/mm, P < 0.0001), with minimal change in late TRT dispersion (0.8 ± 0.1 to 1.0 ± 0.3 ms, P = 0.02). This was associated with an increase in early AT dispersion (1.0 ± 0.1 to 1.5 ± 0.2 ms/mm, P = 0.05) but no change in late AT dispersion (0.6 ± 0.1 to 0.7 ± 0.2 ms/mm, P = 0.4). Early and late ARI dispersion did not change with shorter S1S2. AT restitution slopes were similar between early and late sites, as was slope heterogeneity. ARI restitution slope was greater in early vs. late sites (1.3 ± 0.6 vs. 0.8 ± 0.6, P = 0.03), but slope heterogeneity was similar. With shorter S1S2, AT-ARI slopes became less negative (flattened) at both early (-0.4 ± 0.1 to +0.04 ± 0.2) and late (-1.5 ± 0.2 to +0.3 ± 0.2) sites, implying less activation-repolarization coupling. There was no difference in AT-ARI slopes between early and late sites at short S1S2. In conclusion, high-risk patients with cardiomyopathy have greater TRT dispersion at tightly coupled S1S2 due to greater AT dispersion and activation-repolarization uncoupling. Modulated dispersion is more pronounced at early vs. late activated sites, which may predispose to reentrant ventricular arrhythmias.

Intrinsic cardiac autonomic stimulation induces pulmonary vein ectopy and triggers atrial fibrillation in humans.

INTRODUCTION: The induction of atrial fibrillation (AF) by pulmonary vein (PV) ectopy is well described. The triggers for these PV ectopy are not so well understood. The intrinsic cardiac autonomic nervous system (ANS) has been suggested as a potential upstream regulator that may cause PV ectopy and atrial fibrillation (AF). We hypothesized that activation of the ANS by high frequency stimulation (HFS) of atrial ganglionated plexi (GP) can initiate PV ectopy. METHODS AND RESULTS: During sinus rhythm in 12 patients undergoing ablation for paroxysmal AF, short bursts of HFS, synchronized to the local atrial refractory period, were delivered at presumed GP sites. Electrograms were recorded from catheters placed in the PV, coronary sinus (CS) and high right atrium (HRA). A total of 112 episodes of HFS were recorded, producing ectopic activity in 91 of 112 (81%) episodes. Of these 91 episodes, there were 46 episodes of isolated single ectopic beats, 5 episodes of double ectopic responses, 24 episodes of ectopy/tachycardia lasting <30 s, and 16 episodes of AF lasting >30 s. In 63 of 91 episodes, the PV catheter was placed adjacent to the stimulated GP, resulting in ectopy recorded earliest in the PV catheter in 48 of 63 (76%) episodes. In one patient, reproducible ectopy was shown to occur following AV nodal conduction delay in response to HFS. Without HFS, neither AV nodal conduction delay nor ectopy occurred. CONCLUSIONS: This study has demonstrated a direct link between activation of the intrinsic cardiac autonomic nervous system and pulmonary vein ectopy in humans.

Doubling of the ventricular rate by interpolated junctional extrasystoles resembling supraventricular tachycardia.

In a study of seven cases of paroxysmal supraventricular tachycardia, it was noted that the fast rate was not caused by the mechanism of rapid firing, reentry, or dual atrioventricular nodal conduction but by an abrupt doubling of the rate by interpolation of junctional extrasystoles between adjacent sinus beats while the sinus mechanism remained undisturbed. Dual ventricular response to a single atrial depolarization was seriously considered in each case. The intervals separating the junctional extrasystoles tended to be quite fixed, thus conforming to the pattern of junctional parasystole with an intrinsic rate very close to the rate of the dominant sinus rhythm. The paroxysms of tachycardia were transient, lasting a few seconds to 3.5 minutes. The onset and termination of the paroxysms were completely unpredictable and appeared unrelated to any change in the basic sinus rate or other identifiable mechanism. In only one case, case 7, the concept of dual ventricular response appeared tenable. However, as will be discussed later, the mechanism of junctional parasystole was found to be physiologically more acceptable.

Circadian and ultradian extrasystole rhythms in healthy individuals at elevated versus lowland altitudes.

We defined chronobiologic norms for supraventricular and ventricular single extrasystoles (SV and VE, respectively) in healthy older males in lowland areas. The study was extended to higher altitudes, where hypobaric hypoxia was expected to increase extrasystole frequency, while perhaps not changing rhythmicity. In healthy men (lowland n = 37, altitude n = 22), aged 49-72 years, mean numbers of SVs and VEs were counted over a 24-h period. Cosinor regression was used to test the 24-h rhythm and its 2nd-10th harmonics. The resulting approximating function for either extrasystole type includes its point, 95% confidence interval of the mean, and 95% tolerance for single measurement estimates. Separate hourly differences (delta) between altitude and lowland (n = 59) were also analysed. Hourly means were significantly higher in the mountains versus lowland, by +0.8 beats/h on average for SVs, and by +0.9 beats/h for VEs. A relatively rich chronogram for VEs in mountains versus lowland exists. Delta VEs clearly display a 24-h component and its 2nd, 3rd, 4th and 7th harmonics. This results in significantly higher accumulation of VEs around 8.00 a.m., 11.00 a.m. and 3.00 p.m. in the mountains. The increase in extrasystole occurrence in the mountains is probably caused by higher hypobaric hypoxia and resulting sympathetic drive. Healthy men at elevated altitudes show circadian and several ultradian rhythms of single VEs dependent on the hypoxia level. This new methodological approach--evaluating the differences between two locations using delta values--promises to provide deeper insight into the occurrence of premature beats.

Circa(ultra)dians of single extrasystoles in chronic respiratory failure versus health at lowland.

BACKGROUND: The circa- and ultradians of the single extrasystoles' frequency in patients with chronic respiratory insufficiency (CRI) in lowlands (Kosice 210 m) were studied by the testing of following null hypotheses: their average frequency as well as rhythmicity is the same as at health. METHODS: In 54 elderly males with CRI, mean numbers of supraventricular (SV) and ventricular (VE) extrasystoles were calculated for each 24 hours. The Halberg cosinor regression was used to test the presence of the 24-hour rhythm and its 2nd to 10th harmonics, i.e. ultradians with the period lengths of 12 to 2.4 hours. The resulting approximating function for either extrasystole type included its point, 95% confidence for mean and 95% tolerance for one individual. The results were compared with those obtained at health at alpha = 0.05. RESULTS: The daily mesors in CRI were 20.9 for SV, for VE 17.6 extrasystoles per hour and subject. This was significantly (20.3 (SV) and 17.0 (VE)) higher than at health. Significant periodic harmonic components were 3 in CRI versus 6 at health for SV and 6 in CRI versus 1 at health for VE. The dominating CRI rhythm was the 8 hour ultradian for SV and circadian for VE while at health the circadian rhythm was leading for every type of extrasystoles. CONCLUSION: The most remarkable effect of CRI versus health at lowlands is a marked increase of the frequency of every type of extrasystoles. SV extrasystoles exert more rhythmicity at health while the VE in disease (Tab. 1, Fig. 1, Ref. 20).