Ablation of unmappable ventricular parasystole originating from the right ventricular outflow tract: a case report.

BACKGROUND: When the coupling interval is matched, ventricular parasystole can form a stable fusion QRS complex with sinus rhythm. Ablation of a fusion QRS complex has been rarely reported and is unexpectedly difficult. CASE PRESENTATION: We describe a case of ventricular parasystole from muscle sleeves of the right ventricular outflow tract. The patient was a 54-year-old woman who was admitted to the hospital because of frequent palpitations for 3 months. Anti-arrhythmic drugs had been ineffective, and she had no history of cardiovascular disease. Because the fusion QRS complex interfered with the conventional mapping technique, we could not eliminate the ventricular parasystole successfully. RESULTS AND CONCLUSIONS: Finally, we used the reversed U curve method and found that the source of ventricular arrhythmia was in the right cusp according to the special local potential. A fusion QRS complex formed by ventricular parasystole and nodal ventricular activation make mapping and ablation difficult. The special local potential was the only evidence available to confirm the target of ablation satisfactorily.

Ventricular arrhythmias in children with attention deficit disorder--a symptom of autonomic imbalance?

OBJECTIVES: Potential side effects of stimulants for attention deficit disorder are in the focus of scientific discussions, intensified by the higher number of prescriptions. Children with known arrhythmias or other severe cardiac problems should not receive stimulants because of their sympathomimetic effects. METHODS: This is a retrospective analysis of 24-hour Holter electrocardiograms from 100 consecutive children with attention deficit disorder from January, 2006 to April, 2012. RESULTS: In all, nine children had significant ventricular arrhythmia (mean age 11.4 ± 3.1 years, 77% male, 77% received methylphenidate). All these children had ventricular parasystole - four of them with an accelerated idioventricular rhythm. A significant circadian rhythm of premature ventricular contractions in seven children and the effect of standing and exercise clearly indicate the influence of the autonomic nervous system. In these children, hourly analysis of circadian rhythm within a 24-hour period showed a highly significant correlation between premature ventricular contractions and the vagal tone indicated by the heart rate variability parameter RMSSD (r = -0.83; p < 0.001). Ventricular arrhythmia was unaffected in seven children who received methylphenidate before diagnosis and decreased during metoprolol treatment in two children. CONCLUSION: By Holter electrocardiogram analysis, we observed a remarkably high incidence of ventricular parasystole and accelerated idioventricular rhythm in nine of 100 children with attention deficit disorder, which depends on autonomic imbalance and not on stimulant treatment.

The role of local voltage potentials in outflow tract ectopy.

AIMS: Discrete, fragmented, local voltage potentials (LVPs) have been observed in electrograms recorded at the ablation site in patients undergoing radiofrequency ablation for arrhythmias originating in both the right and left ventricular outflow tract; however, the incidence and the significance of the LVP with respect to arrhythmogenesis is uncertain. METHODS AND RESULTS: We studied 25 patients with outflow tract arrhythmias referred for radiofrequency catheter ablation and recorded high-amplified intracardiac electrograms close to the site of origin of the arrhythmia. Ten patients undergoing ablation for supraventricular arrhythmias served as controls. During sinus rhythm, LVPs were recorded in 24 of the 25 patients, 10-85 ms (41 +/- 19 ms) after the onset of the QRS complex, duration 33 +/- 11 ms, voltage 2.0 +/- 1.5 mV. The same potential was recorded 10-52 ms (mean 37 +/- 11 ms) prior to the V potential in the ventricular premature beats. In 10 patients, ventricular parasystole was suggested by varying coupling intervals >100 ms, and fusion beats allowing for the estimation of the least common denominator of R-R intervals. In 23 of the 25 patients, the 12-lead electrocardiogram (ECG) and intracardiac contact mapping located the arrhythmias to an area of 3-4 cm(2) in the septal region of the right ventricular outflow tract; in two patients, the site of origin was in the left coronary cusp. Radiofrequency ablation carried out in 24 of the 25 patients was successful in 21 patients, and after successful ablation, the LVP could still be recorded in all these 21 patients. The LVP was not present in 10 controls. CONCLUSION: Local potentials are recorded close to the site of origin of ventricular ectopy in >90% of patients with idiopathic outflow tract ectopy and imply successful ablation. The potentials may reflect an area of depressed conductivity known to be a prerequisite for experimental ventricular ectopy including parasystole.

Parasystole due to re-entry as the possible mechanism of ventricular parasystole with second-degree entrance block.

BACKGROUND: In 1974, Kinoshita reported a case of 'irregular parasystole' due to type I second-degree entrance block. Since then, many cases of such 'irregular' parasystole have been reported by us. To explain the mechanism of 'irregular' parasystole, two theories have been suggested, namely, 'electrotonic modulation' by Jalife and Moe, and 'type I second-degree entrance block' by us. On the contrary, in 1960, Kinoshita et al. reported a case of concealed bigeminy for the first time. The electrocardiographic findings in concealed bigeminy have suggested that there are dual re-entrant pathways with markedly long effective refractory periods in the re-entrant pathway. We have suggested that parasystole may be caused by re-entry in such re-entrant pathways. In this article, attempts are made to explain the mechanism of all the electrocardiographic findings in our cases of parasystole by 'parasystole due to re-entry'. METHODS: Using 24 studies on parasystole and 21 studies on concealed extrasystoles that we have reported over 50 years, as well as three exemplary cases in this article, attempts are made to explain all electrocardiographic findings in parasystole by 'parasystole due to re-entry'. CONCLUSIONS: The electrocardiographic findings in our previous clinical cases of parasystole and concealed extrasystoles, as well as exemplary cases and diagrams in the present article, strongly suggest 'parasystole due to re-entry' as the mechanism of ventricular parasystole with second-degree entrance block.

Nodal rhythm and ventricular parasystole: an unusual electrocardiographic presentation of mad honey poisoning.

Mad honey poisoning syndrome has been reported in the Eastern Black Sea region and Southeastern regions of Turkey. Herein we report a case of 70-y-old man presented with syncope and severe hemodynamic instability following ingestion of one teaspoon of honey and his unusual electrocardiographic manifestations: nodal rhythm alternating with sinus bradycardia and intermittant ventricular parasystole. In this report, we also tried to explain the possible mechanism responsible for these electrocardiographic findings.

Thalidomide causes sinus bradycardia in ALS.

OBJECTIVE: Neuroinflammation contributes to motor neuron degeneration in ALS. Thalidomide (THL) shows potent anti-inflammatory properties and increased the lifespan in ALS transgenic mice. Thalidomide was therefore suggested as atherapeutic intervention for the treatment of ALS.We conducted a pilot, randomized clinical trial of THL in patients with ALS to assess safety, feasibility, and preliminary estimates of treatment efficacy. METHODS: Patients were randomized to THL in combination with riluzole (n = 18) or riluzole alone (n = 19). THL was initiated at 100 mg per day for 6 weeks. Thereafter, the dose was increased every week by 50 mg until reaching the dose of 400 mg per day and planned to continue for another 12 weeks. RESULTS: Within 12 weeks of THL treatment, nine THL patients (50%) developed bradycardia defined as a heart rate below 60 beats per minute (bpm) and ranged from 46 to 59 bpm. Mean heart rate dropped by 17 bpm with THL treatment. Severe symptomatic bradycardia of 30 bpm occurred in one patient. A further patient died from sudden unexpected death. The study was terminated prematurely for safety concerns. The secondary outcome variables showed similar results for both groups. CONCLUSION: Bradycardia was the most common adverse event of THL treatment in ALS. THL-related bradycardia does not appear to be ALS-specific. It is conceivable, however, that the unexpected frequency and severity of THL-induced bradycardia may be related to subclinical involvement of the autonomic nervous system in ALS. The cardiac toxicity discourages further clinical trials and compassionate use of THL in ALS. ClinicalTrials.gov Identifier: NCT00231140.

Atrial parasystole in left ventricular noncompaction: a morphofunctional study by echocardiography and magnetic resonance imaging.

Isolated left ventricular noncompaction is a recently recognized age-independent cardiac genetic disorder caused by heterogeneous defects in endo-myocardial morphogenesis. Transthoracic echocardiography and cardiac magnetic resonance are the most reliable techniques to make a diagnosis of the disease, noninvasively. Arrhythmic atrial and ventricular disorders have been reported in 20-50% of these patients. The morphological and functional findings are described in a young woman in whom the exclusive clinical sign of isolated ventricular noncompaction was an atrial parasystole.

Improved integrate-and-fire model for rsa.

A simple operational model of heart rate variability is described, accounting in particular for the respiratory sinus arrhythmia, and is fitted to some interbeat interval sequences recorded from normal subjects at rest. The model performance is evaluated using a test based on the nonlinear prediction approach. Moreover, a short comparative account of two similar models described in the literature is given.

Apparent disappearance of ventricular parasystole due to a marked difference between the long form and the short form of the ectopic cycles.

Electrocardiograms were taken from a 44-year-old man with irregular ventricular parasystole in whom pure parasystolic cycles without any intervening nonectopic QRS complexes were found. When a sinus impulse fell late in the parasystolic cycle, it hastened occurrence of the next parasystolic discharge. This suggested that type I second degree entrance block occurred in the re-entrant pathway containing the parasystolic focus. When a sinus impulse fell early in the parasystolic cycle, it delayed occurrence of the next parasystolic discharge. This suggested that electrotonic modulation occurred in the parasystolic focus. As a result, the difference in length between the short form and the long form of the parasystolic cycle became markedly great. When the length of two adjacent sinus cycles ranged between the short and the long parasystolic cycle, manifest parasystolic QRS complexes disappeared for a long time. In true ventricular parasystole with pure ectopic cycles, such long disappearance has never been reported before.

Variation in parasystolic cycle length.

At the time of the first visit to our clinic, an electrocardiographic examination of a 73-year-old female patient revealed ventricular premature contractions (VPCs) with variable coupling intervals that were diagnosed as parasystole. Characteristically many of the parasystoles had no sinus contractions between two consecutive VPCs, which we referred to as pure parasystole. We first repeatedly examined variations in the length of the parasystolic cycles between January 6, 1997 and March 2, 2003 using electrocardiography. The time courses recorded over this period showed that the length of the parasystolic cycle did not remain constant, but varied irregularly within a relatively narrow range. We also recorded the length of the parasystolic cycles over 3 hours using Holter monitoring. The interectopic intervals plotted against mean sinus cycle length showed that the cycle length of pure parasystoles remained almost constant at about 1,300 ms over the 3 hours. We also examined the cycle length during exercise and found that it was slightly prolonged thereafter, while the sinus cycle length was clearly shortened after exercise. The average of six deep breathing tests showed that parasystolic cycle length did not significantly differ between deep inspiration and deep expiration, whereas the sinus cycle length during expiration was significantly longer than that during inspiration. These results indicate that the responses to both exercise and deep breathing obviously differed between the parasystolic and sinus cycle lengths.

Model of bidirectional modulated parasystole as a mechanism for cyclic bursts of ventricular premature contractions.

Cyclic bursts of ventricular premature contractions (VPC) coming at minute-order intervals have been discerned by analyzing ambulatory ECG recordings, and their mechanism has not been clarified. The present study simulates this phenomenon by constructing a bidirectional modulated parasystole model. With Ts and Te as the intrinsic periods of the sinus and ectopic pacemakers, there are distinct and initial condition-dependent solutions in the model with Ts / Te values close to 1, 1/2, 1/4, etc. Typically, two distinct stable solutions are found existing together around Ts / Te = 1/2. We have verified theoretically the coexistence of different solutions and their dependence on the model parameters. The solution presented switches between those by a premature stimulus and those by fluctuations in the model parameters such as Ts. Patterns of RR intervals were generated by simulation with randomly fluctuating Ts. They included cyclic bursts of bigeminy of the "flat type" and the "dome type" reported by Takayanagi et al. (1999) and other transient types with Wenckebach or reverse Wenckebach rhythm of coupling intervals. This model provides a mathematical representation of the atrioventricular feedback mechanism and enables the modulated parasystole hypothesis to be applied to wider classes of VPCs.

Extrapotentials and allorhythmias as an expression of experimental parasystole.

UNLABELLED: The aim of the study was to investigate the dynamics of experimental parasystole taking into consideration the peculiarities of recurrent arrhythmias recorded in clinical settings. MATERIAL AND METHODS: The experiments were conducted on isolated right atria of seven chinchilla rabbits. Parasystolic arrhythmias using periodical one-site electrostimulation were provoked in one atrium, where the sinus node was not affected, and in two atria with the spontaneous low value activity of pacemakers. The parasystolic arrhythmias by the dual-site periodical pacing were provoked in four atria, in which the spontaneous activity had disappeared, while the membrane potential of cardiomyocytes remained at the level of 70 to 80 mV. RESULTS: The parasystolic arrhythmias of the shape of single extrapotentials were obtained in atria when the periods of excitation impulses were within the limits of 0.9-1.2 s, and the differences between these periods being relatively small (0.04-0.2 s). The increase of these differences resulted the various allorhythmias. In cases of single extrapotentials, the recurrence periods of arrhythmias reached 5.6-29 s; while in cases of allorhythmias they shortened to 2.4-4.8 s. CONCLUSION: The parasystoles in isolated atria of rabbits can be induced by two competitive excitation sources. They may manifest themselves through single extrapotentials or allorhythmias, whose form depends on the duration of the periods of excitation impulses, the difference between these durations, as well as on effective refractory periods of atrial cardiomyocytes. The determination and evaluation of the recurrence period of these arrhythmias can serve in any given clinical situation as a supplementary criterion.

[Parasystole]. / Parasystolie.

Parasystole is usually an extrasystolic rhythm which can occur at every level, but particularly in the ventricle. It is admitted that the parasystolic focus is protected from the environing myocardium by an entry block but can manifest itself. Actually, a pure unidirectional block does not exist and the environing myocardium affects the parasystolic rhythm by an electrotonic current which modulates the output. A non-parasystolic complex which occurs prematurely in the parasystolic cycle delays it. Conversely it accelerates the cycle when it occurs late. By this fact, a parasystole pacing is possible and can lead to a fixed coupling. This arrhythmia is frequently unknown and can be experimentally, reproduced by a sucrose gap preparation.

Ventricular parasystolic couplets originating in the pathway between the ventricle and the parasystolic pacemaker: mechanism of "irregular" parasystole.

This article explains the mechanism of "irregular" parasystole. Two theories have been suggested: "electrotonic modulation" and "type I second degree entrance block." This study attempts to clarify the mechanism of irregular parasystole in cases of true ventricular parasystole associated with ventricular parasystolic couplets. Cases associated with ventricular parasystolic couplets were selected from 37 clinical cases of true ventricular parasystole in which one or more pure parasystolic cycles with no intervening nonectopic QRS complexes were found. Of the 37 cases of true ventricular parasystole, ventricular parasystolic couplets were found in 4 cases. In none of the other 33 cases, ventricular parasystolic couplets were found. In all the cases coexisting with ventricular parasystolic couplets, the latter ectopic QRS complex of the couplet failed to reset the parasystolic rhythm. The above findings suggest that the latter ectopic QRS complex of the parasystolic couplet originated not in the parasystolic pacemaker but in the pathway between the ventricle and the parasystolic pacemaker. It seems that when a sinus impulse fell late in the parasystolic cycle, it passed through the site of second degree entrance block and that the parasystolic couplets originated from the reentrant pathway between the ventricle and the pacemaker. This strengthens our previous suggestion that the mechanism of irregular parasystole is governed by "type I second degree entrance block" and not by "electrotonic modulation."

Clinical evaluation of excitability measures in sensory nerve.

A recently described method for recording multiple excitability parameters of human motor nerves has been adapted to the study of sensory nerves. The protocol measures stimulus-response behavior using two stimulus durations (from which the distribution of strength-duration time constants is estimated), threshold electrotonus to 100 ms polarizing currents, a current-threshold relationship (indicating inward and outward rectification), and the recovery of excitability following supramaximal activation. The method was tested on 50 healthy volunteers, stimulating the median nerve at the wrist and recording the antidromic compound sensory nerve action potential (SNAP) from digit 2. The excitability measurements were similar, where comparisons were possible, with published sensory nerve data, and confirmed differences from motor nerves, particularly in strength-duration behavior and recovery cycle, likely to reflect functional differences between sensory and motor nerves. Although slower than for motor nerves, the sensory nerve recordings were sufficiently quick (16 to 18 min) to allow them to be included in routine clinical studies. We propose that this method, which provides quite different and complementary information about nerve function to conventional conduction studies, provides a useful new approach for exploring the pathophysiology of sensory neuropathies.